Lecture 10

Autonomic Nervous System 

 
 

1. The Autonomic Nervous System:
   
   1. Sympathetic Nervous System
      
   2. Para-sympathetic Nervous Systems 
      

       
       

• They both have a system of the upper motor neurons going to pre-synaptic neurons and post-synaptic neurons (and then go to the target tissue) in place of the lower motor neuron (note: upper motor neurons went to lower motor neurons in the CNS). 
  
• The Sympathetic nervous system can trace its pre-synaptic neurons to the sympathetic trunks
  
  • This is the anatomical definition of the Sympathetic nervous system
    
• The Para-sympathethic Nervous system cannot trace any of its neurons to the sympathetic trunks
  
  • This is the anatomical definition of the Para-sympathetic nervous system
    

     
     

• The two systems differ in neurotransmitters that they use at the target tissue
  
  • Pre-synaptic neurons in both Sympathetic and Parasympathetic secrete ACh (Acetylcholine)
    
  • The Parasympathetic system uses ACh at both the pre-synaptic and post-synaptic spaces
    
  • The Sympathetic uses Norepinephrine as the post-synaptic on or near the target tissue
    
  • There are 3 exceptions to this rule that the SNS uses Norepinephin
    
    • The SNS post-synaptic neurons, during flight or fight, are going to dilate the blood vessels to the skeletal muscles and use ACH. When you sit down and then stand up – your blood pressure was changed by the SNS – that is called Vasomotor Tone. When it changed the blood pressure it used Norepinephin.???At presynaptic???
      
    • Sympathetic post-synaptic neurons that innervate the Sweat Glands use ACH.
      
    • Sometimes there are no post-synaptic fibers.  When this happens the pre-synaptic fiber goes all the way to the adrenal medulla.  There the pre-synaptic fibers synapse (raining ACH out) on:
      
      • Chromaffin cells
        
        • These are endocrine cells that secrete hormones and they get released into the blood stream
          
        • Secrete things called Circulating Catecholamines - which are 80% epinephrine and 20% norepinephine
          

           
           

• The effect of the Parasympathetic system:
  

   
   

  • Constricts the pupils of the eye
    
    • it is the only one innervating the circular smooth muscles of the iris)
      
    • Contracts the ciliary muscle of the eye, which is attached to the lens of the eye. 
      
    • The lumen is getting smaller since this is a circular muscle. 
      
    • There are suspensory ligaments going to the lens, and it allows the lens to bulge (for close vision) and get fatter. 
      
    • The Sympathetic system does not innervate the ciliary muscle of the eye. 
      
  • It decreases the heart rate
    
    • When you sit down, your heart rate decreases b/c of the PNS b/c it has increased the firing rate to do that.  But when you stand up and increase your heart rate, it increases b/c of a decreasing the firing of the PNS. The SNS kicks in through regulating your heart rate, and there is a constant sending through there.  All you have to do to increase it or decrease it is change the PNS up and down.
      
  • It constricts coronary blood vessels
    
  • It increases the activity of the GI tract
    
    • it relaxes the sphincters to allow movement, it will increase the secretions, and it will increase the smooth muscle contractions in the GI tract.
      
  • It constricts the bronchioles of the lungs 
    
  • It is responsible for the contraction of the bladder, but it does not effect the kidneys (the PNS does not innervate the kidneys) 
    
  • It causes sexual excitation in both males and females
    

     
     

1. The effects of the Sympathetic system
   
   1. It dilates the pupil of the eye. 
      
      1. It innervates the radial muscles of the Iris, making the pupils larger. 
         
      2. During flight or fight, we will dilate your eyes, but when we walk into a dark room your eyes will dilate too, which is not flight or fight.  During the Sympathetic stimulation of flight or fight, if we monitor the lens of the eye, we do find that the lens of the eye does flatten some.  This is probably due to the change in the blood flow/circulation or the changing of the firing of the PNS, b/c there is no ciliary muscle to do that.
         
   2. It constricts and dilates all the necessary arteriole and venous systems for fight or flight (to accommodate for changes in the blood flow)
      
   3. It increases the heart rate, and increases the force of the heart beat. 
      
   4. It dilates the arterioles of the heart and skeletal muscle (you are thinking more about flight or fight when you do this)
      
   5. It constricts the arterioles of the:
      
      1. GI tract
         
      2. Kidney
         
      3. Skin
         
      4. Sex organs
         
   6. It constricts the arterioles to the lungs
      
      1. When running, you are expanding the lungs.  When you start to take deeper breathes, this will drop your blood pressure.  This is why we constrict our arterioles to make the blood pressure rise and stay at the proper pressure of the lungs.  You don't want your blood pressure to drop.  
         
   7. It dilates the Bronchioles of the Lungs (allowing more in)
      
   8. It shuts down the GI tract completely (this is definitely a flight or fight thing), closing sphincters, decreasing secretions, and relaxing the smooth muscle contractions.  
      
   9. It relaxes the bladder (this is not urinating) and closes the sphincter urethra (this is a flight or fight thing too)
      
   10. It increases Renin secretion by the kidney, making more Angiotensin II available giving you increased blood pressure.
       
   11. It increases sweating and pilli muscle contraction (Haripilation occurs – goosebumps)
       
   12. It stimulates fat break down in adipose tissue 
       
   13. It mobilizes glycogen stores of the liver raising blood glucose levels
       
   14. It also contracts the spleen, this does not make much of a difference in humans. 
       
       1. In larger animals, like a horse, if they contract the spleen they raise their Hemoatocrit by 5 points, because they have large stores of RBC's in the spleen. 
          
   15. Causes sexual orgasm in both male and female. 
       

• The Sympathetic system cannot shut down the sexual excitation that the Parasympathetic system created; the only way to end the excitation is through orgasm. 
  

 
 

• The sympathetic system is usually the winner over the parasympathetic system. 
  

   
   

• Sympathetic Tone – is the tonal firing of the sympathetic systems, especially the heart. 
  
  • When we talk about Sympathetic tone we only think of the Sympathetic Vasomotor tone, b/c there are no innervations of the blood vessels that are responsible for blood pressure regulation
    

     
     

• Parasympathetic Tone - is not due to the lack of Sympathetic innervations, it just sits there doing the same thing with the exception of when you have flight or fight.   
  
  • The heart has Parasympathic Tone firing and constant sympathetic tonal firing to blood vessels, increasing and decreasing tonal firing of sympathetic fibers – Sympathetic Vasomotor Tone
    
  • Regulating the blood pressure as you are walking back and forth. 
    
  • This is not in fight or flight. 
    
  • 3 systems of Parasympathetic Tone
    
    • these systems are generally regulated by the Parasympathetic system, except in the case of fight or flight. The Parasympathetic system is the ruler, unless we have fight or flight.
      
    • The heart is run by the parasympathetic system except you are in fight or flight (the PNS tells the heart to slow down and the SNS tells the heart to speed up: they are on both sides of the SA node)
      
    • The GI tract is under parasympathetic control except in fight or flight
      
    • The bladder is controlled parasympathtically except in fight or flight. 
      

   
   

• The Autonomic Nervous system: (we cover EEGs and Sleep)
  
  • Reticular Activating System (RAS): 
    

1. Reticular Formation is comprised of sensory afferents bound for the cerebrum going up to the brain stem (medulla, pons, and midbrain). 
   
2. The sensory afferents are going to have clusters of nuclei in white matter:
   
   1. As they go through the brain stem the more mid-line nuclei are called Raphe Nuclei.  
      
   2. Farther from the midline, but closer than the lateral line we have a medial group called a Large cell group. 
      
   3. Farther out from that we have a lateral group called a Small cell group. 
      
   4. The neurons of virtually all the senses send neurons to this area. (Such as from the eye or ear, they are above and go directly to the brain and talk to it).  They send messages into the reticular formation down into the brain stem.
      
3. The Reticular formation is an integral part of the RAS, but it is only one single part of the RAS system
   
4. The RAS sends a continual stream of impulses to the brain
   
   1. The messages change but the flow is continuous
      
5. It keeps the brain alert or puts the brain to sleep
   
6. The RAS system filters out what it considers unnecessary information. 
   
   1. You don't feel something if you are not paying attention to it.  (ex. Can you feel your socks?)
      
7. The RAS has the cerebral cortex disregarding 99% of the sensory stimuli that are sent to the brain. If we did not have this filter, the brain could not handle all the messages. 
   
   1. The filtering of the RAS system is shut down by LSD, and then you can feel more of the sensory stimuli. 
      
   2. Bad trips – take LSD and something scares you and you stay scared (LSD stops itself)
      
   3. You don't have flash backs, but there is only a sense of flashbacks
      
      

 
 

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Lecture 6

Synapses, continued

 
 

• vesicle has synaptotagmin (synaptic vesicle protein)
  
  • can interact with syntaxin (protein in neurolemma), interact only after priming of vesicle
    
• if put calcium in, it will come down and bind to synaptotagmin, changes the shape of synaptotagmin and can now interact with syntaxin, this causes the vesicle to open and NT is released
  
• synaptotagmin can bind to clathrin which is found surrounding the vesicle, when this binds it causes endocytosis or pulling away of the vesicle and the closing of the vesicle
  
• Ca can be pumped out by ATP-powered pumps, but typically think there is 3 Na in for one Ca out called an antiport
  
  • functions to remove most of the Ca
    
• Ca can also be taken up by mitochondria in the synaptic knob
  

   
   

• Autonomic Varicosities
  
  • receptors all over the cells, varicosities rain there NT around the receptors
    
  • use similar method to synaptic knob to release NT
    
  • takes time for NT to cross the synaptic cleft this delay is called the synaptic delay
    
  • the more synapses between start/end of excitation and wherever sending the impulse, the slower the signal will go
    
  • like reflexes to go through one or two synapses, so they go as fast as possible
    
  • response to NT, is dependent upon the receptor that the NT hits
    
    • Response not based on neurotransmitter
      
• if have excitatory receptor, bringing closer to threshold called Excitatory Post Synaptic Potential (EPSP)
  
  • EPSP's typically Na and Ca channels opening
    
  • Can also get EPSP by K channels closing
    
• if have an inhibitory receptor, bringing further away from threshold called Inhibitory Post Synaptic Potential (IPSP)
  
  • IPSP get closing of Na and Ca channels
    
  • opening of K channels, sometimes also see opening of Cl channels (Cl follows Na around, when Na pumped out Cl went without, have higher level of Cl outside of cell and whne open these channels, Cl flows in and hyperpolarizes the cell)
    
• sometimes see synaptic knob with another synaptic knob on top of it, the synaptic knob on top is regulating the amount of NT coming out of the second one
  
  • Synaptic knob on top is called presyanptic facilitation or presynaptic inhibition
    
• Presynaptic facilitation will increase the amount of NT leaving and it does this by either opening more Ca channels or prolonging how long the Ca channels are held open
  

  -can also close K channels, if it closes K channels, this will enhance action potential and will kick out more Ca
  

• Presyanptic inhibition will close the Ca channels, restrict them so they can't let in as much Ca, dampen action potential (if dampen the action potential, they will then open Cl channels, influx a negative)
  

 
 

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• A wants to get X to fire:
  
  • sends excitation
    
  • Doesn't work…fires again….doesnt work…..
    
  • NEEDED rapid firing
    
    • TEMPORAL Summation
      
• B wants Y to fire
  
  • Needs C to fire at same time to cause firing.
    
    • SPACIAL Summation
      

       
       

• temporal summation = rapid firing of two or more neurons or an individual neurons that causes excitation
  
  • temporal rapid firing can be adjusted, but with temporal firing all you can send is I fired
    
  • temporal summation in bursts used to send messages is called temporal patterning
    

     
     

• spatial summation = not rapid firing, but neurons fire once and then firing across three or more neurons is summed to achieve excitation
  
  • spatial pattern = tells you which neurons are firing
    
    • detect smell through spatial patterning
      
    • 10,000 odors spatially patterned in brain
      
      • when have a twitch fire a summation
        
      • summation in a multipolar neuron is in the axon hillock (where dendritic positives and negatives get summed), multipolar neuron will taper down to become an axon, this is the first initial segment of axon
        
      • unipolar and bipolar neurons summation occurs at the initial segment of the axon
        
      • to send a message regulate firing rate and how often it occurs
        

     
     

   
   

• NT made up in soma
  
  • sent down a microtubule railway microtubules
    
    • have vesicles attached to them which move back and forth
      

       
       

• protein called kinesin moves vesicle towards the synapse
  
  • Calcium combined with calmodulin will cause phosphorolation of vessle and release NT in synapse
    
  • Antegrade transport
    
• protein called dynein moves vesicle back up the microtubule to the soma to be refilled
  
  • Retrograde transport
    
• each of the microtubules have both proteins associated with it but only one works at a time
  
• some neurons have co-transmitters
  
  • don't come out of active sites, can come out anywhere around the synaptic knob
    
  • typically think they facilitate the main NT in some way, but they are not necessarily all the way
    
  • can enhance the NT when excitation high or low it depends on the neuron
    
  • Neuron needs certain firing rate to release co-transmitters (maybe)
    

     
     

NEUROTRANSMITTERS & RECEPTORS

• See Handout!!
  

   
   

• if NT binds directly to receptor and opens the channel  ionotropic receptor
  
  • NT directly opens/closes channel
    
• If NT activates a secondary messenger and is linked to something else 
  metabotropic
  
  • NT can hit a receptor, but it causes a metabolite to increase/decrease and can open/close a channel
    
  • two major metabotropic systems
    
    • cyclic AMP
      
      • See handout...
        
    • IP3-DAG
      
      • See handout...
        

 
 

Name	Chemical	Receptor	Receptor Type
Acetylcholine	Esther	Nicotonic – receptor find on skeletal muscle (5) Muscarinic M1-M5	1. Ionotropic     Metabotropic
Norepinephrine	Catecholamine	α 1-2 β 1-3	Metabotropic Metabotropic
Dopamine	Catecholamine	D 1-5	Metabotropic
Serotonin (5-hydro trptomine = 5-HT))	Indolamine	5-HT 3 5-HT 1, 3, 4-7	2. Ionotropic Metabotropic	Opens non selective channel
Histamine	Indolamine	H1-H3	Metabotropic	H3 in synaptic knob
GABA (gamma amino butyric acid)	Amino Acid	GABA A GABA B	3. Ionotropic Metabotropic	Opens Cl channel = inhib
Glycine	Amino Acid	Glycine Receptor NMDA	4. Ionotropic 5. Ionotropic	Opens Cl channel = inhib Has to bind BOTH gly/glut
Glutamate	Amino Acid	AMPA Kainate Metabotropic Receptor of Glutamate (11 subtypes) NMDA	6. Ionotropic 7. Ionotropic Metabotropic     5. Ionotropic	Opens Na channel Opens Na channels         Has to bind both glycine and glutamate
Endorphins/Enkephalins	Peptides	μ (mu) κ (kappa) δ (delta)	Metabotropic Metabotropic Metabotrpic	All called opiate receptors
Substance P/Neurokinate	Peptide	NK-1 Receptor	Metabotropic
Somatostatin (SST)	Peptide	SSTR 1-5	Metabotropic
NO	Gas	1 receptor	Metabotropic	Increase cyclic GMP
CO	Gas	1 receptor	Metabotropic	Increase cyclic GMP

 

Lecture 9

Audio recording started: 12:04 PM Wednesday, February 04, 2009

 
 

Lecture 9 – More Senses:

 
 

•    The Ear – has 3 closely linked sensors 

o    1.) The Semi-circular canals - detect rotational acceleration

•    They are filled with Endolymph

•    The Capulla (a gelatinous membrane that seals off the Crista Ampularis) sits on top of the Crista ampularis

•    There are hairs that protrude into the gelatinous mass of the Capulla. 

•    When we turn our head, the Endolymph pushes on the Capulla (billows like a sail) and pushes the hair cells to Distortion, and that is what it is detecting

•    Since Semi-circular canals lie in each plane of space, the anterior on one side is the same plane as the posterior on the other side. 

o    2.) Utricle and Sacule – detects head position and linear acceleration

•    They are at right angles to each other

•    Utricle – front to back and side to side – detects head position and linear acceleration

•    Sacule – front to back and up and down - detects head position and linear acceleration

•    The gelatinous mass is sitting on top of the Macula.  There are Calcium carbonate stones called Otoliths (which are acting as weights) sitting on here and they shift in response to gravity or acceleration, and they pull the membrane back and change the hair cells.

•    The induced bending of the cilia (shifting the membrane back and forth) is doing the detection of the motion. 

 
 

• Cochlea – detects Sound
  
  • Hair cells:
    
    • Vestibular Hair Cells-The hair cells are embedded in the Macula and in the gelatinous membrane of the Macula. 
      
      • The hair cells have clumps of Cilia on them (these are Vestibular Hair cells)
        

  There is a single very large cilia called the Kinocilium, this cannot depolarize, it cannot function, other than it is there.  
  

  •    The small away you move from the Kinocilium, the smaller the cilia (the Steriocilia) become shorter and shorter.
  

  •    The rest of the cilia are called Steriocilia – there are rows of the Seriocilia moving away from the Kinocilium, with each row getting smaller and shorter and shorter.  The tallest cilia will be the Kinocilium. 
  

  •    There are Cross-links between the Sterocilia, this is from 
  

  •    The Cross-links make sure that everything bends in the same direction at the same time. 
  

  •    There are Tip-links between the Steriocilia – from the tip of a small Sterocilia to the tip of the next highest one.
  

  •    The Tip-links open channels in the side of the larger cilia
  

  •    When the Sterocilia (the hair cells that are doing the electrical event) bend towards the Kinocilium there is a depolarization of the afferent nerve. 
  

  •    When the Stereocilia bend away from the Kinocilium, there is a hyperpolarization of the afferent nerve. 
  

  •    The hair cells rain out Neurotransmitters, and you are just increasing or decreasing the amount of Neurotransmitter over time
  

  •    The whole thing is considered a hair cell because it has the hairs sticking out of it. 
  

  •    The hairs sticking out of the cell are bathed in Endolymph, and the rest of the hair cell is being bathed in Perilymph. 
  

  •    Endolymph – is high in Potassium, and is much like intercellular fluid.
  

  •    Perilymph – is like extracellular fluid. 
  

  •    When the Sterocilia bends towards the Kinocilium (due to a depolarization) and opens the Distortion channels (a potassium channel), potassium is flowing into the cell. This is very unique because this is the first place where Potassium has a higher concentration gradient outside the cell than inside of the cell. Potassium is going into the cell. This is the only place in the human body where you find this.
  

  •    There is a high level of K in the Endolymph
  

  •    The Potassium (came in from the Endolymph) is going to cause a depolarization and cause the voltage gated Calcium channels to let Calcium into the cell.   The Calcium will flow into the cell from the Perilymph – this influx of Calcium increases the Neurotransmitter output.  The Neurotransmitter will bind to the Potassium channel and the Potassium will go out into the Perilymph.
  

  •    Support cells will pass this to other support cells, and then it will work its way back into the Endolymph and the cycle will restart again
  

  •    Hair cells don't fire action potentials, they just increase and decrease their Neurotransmitter output. Their afferents will fire action potentials.  
  

  •    The Voltage gated Calcium channels kick out Calcium, which binds to a Potassium channel, which kicks the Potassium out into the Perilymph. 
  

  •    The Potassium Distortion channel is pulled open by the Tip-link
  

  •    Endolymph is formed by dark cells. 
  

  •    Potassium is picked up in the Perilymph by support cells, and it is passed along to the dark cells, and then recycled into the Endolymph. 
  

  o    In the Semi-circular canals, the Kinocilium of the Crista Ampularis all face the same direction. 
  

  •    In the Lateral Semi-circular canals – the kinocilia face towards the utricle. 
  

  •    In the Posterior and Anterior Semi-circular canals – the kinocilia face away from the utricle. 
  

  •    In the utricle and sacule, the macula will have hair cells that go up into the gelatinous membrane. 
  

  •    There is an area in the utricle and sacule that does not have any hair cells coming out, and this is called the Striola. 
  

  •    The ridge of Otoliths is above this Striola. This is not the snowy ridge that sits above it. 
  

  •    In the Utricle the Striola is C-shaped 
  

  •    In the Sacule it is S-shaped or hook-shaped. 
  

  •    In the Utricle the Kinocilia face toward the Striola (the Kinocilia will be on both sides of the C)
  

  •    In the Sacule the Kinocilia face away from the Striola (the Kinocilia will be on both sides of the S)
  

  •    There are 2 types of Vestibular hair cells in the Macula of the Utricle and the Sacule. 
  

  o    Type I hair cells – it only connects to 1 afferent neuron, and it sits in a cup, and the axon comes up and wraps right around this cup.  This is a sensory axon. 
  

  •    There is Efferents going down and end on the outside of the cup, but they never actually touch the hair cell.
  

  •    The Afferent neuron is firing Tonally (it is always firing, and it just changes its firing rate based upon how much Neurotransmitter is being released; it speeds the firing up and down). 
  

  o    Type II hair cells – hair cells which directly connect to both efferents and afferents neurons; we have a bunch of efferents coming to it, and we have a bunch of afferents leaving it. 
  

  •    Type II - These cells fire Phasically (they have to be stimulated with enough Neurotransmitter to get a firing rate), they are NOT firing tonally 
  

   
   

   
   

• Cochlea and your Hearing: 
  
  • Sound is comprised of air vibrations. 
    

  o    The air vibrates and vibrates the Tympanic membrane, what we refer to as the eardrum. 
  

  o    The Tympanic membrane vibrates the Ear ossicles. 
  

  o    The Ear ossicles (the Stapes) vibrates the Oval window. 
  

  o    The Round window opens to the air filled middle ear. 
  

  o    See drawing (straightened cochlea). 
  

  •    The role of the Round window is that you cannot compress a fluid.  This is the only way the vibration can come in. 
  

  •    If one part pushes inward, something has to push out. 
  

  •    The Round window pushes out. 
  

  •    The vibrations are entering into the Perilymph and the vibrations get the Scala media to move up and down. (The Scala media has the vibrations going to it)
  

  •    As it moves up and down it causes a lateral movement of the Tectorial membrane. 
  

  •    The hair cells are below the Tectorial membrane
  

  o    There are 2 types of hair cells in the Cochlea:
  

  •    1.) Outer hair cells – there are 3 rows of them, and they stick up into the Tectorial Membrane
  

  •    2.) Inner hair cells – there is 1 row of them, and they don't stick up into the Tectorial Membrane
  

  •    Sometimes you can get up to five rows of outer hair cells in some regions of the Cochlea. 
  

  •    There are 3 rows of Outer hair cells, and they don't have a Kinocilium.  All the rows have Sterocilia.
  

  •    Within each row the Stereocilia are the same size/height. But the rows get shorter and shorter, arranged from tallest to smallest
  

  •    There are also Cross-links and Tip-links present. 
  

  •    Outer hair cells are V or W shaped, and the opening will face the inner portion of the spiral of the cochlea. 
  

  •    Inner hair cells are U shaped, but a flattened U-shape and the opening faces the inner portion of the spiral of the cochlea. 
  

  •    There are NO Type I and Type II cells 
  

  •    The inner hair cells only have afferent connections and they don't sit in a cup. Inner hair cells will have 10 or more synaptic connections, but all of them will be afferent.  
  

  •    Outer hair cells have both efferent and afferent connections.  (like Type II cells with no cillia)
  

  o    Inner hair cells are what we are hearing with
  

  o    Outer hair cells are for Amplification. 
  

  • These are what get damaged to cause deafness
    

   
   

   
   

  •    The Theories of Hearing: A human range of hearing is from 20Hz to 20,000Hz
  

  o    The Place Theory of Hearing (only works in the high notes well)
  

  •    The Basilar membrane that the Organ of Corti sits on is about 100um wide at the base, and about 500um wide at the apex. 
  

  o    The Organ of Corti is what you are hearing with, and it sits on a Basilar membrane 
  

  •    The tension is the same throughout its length, but it is stiffer at the base than at the apex. 
  

  •    This allows waves to travel one direction from base to apex. (there is no echoing and the wave cannot be returned back)
  

  •    If sound is vibrating the Oval window, we get a sigmoid (S) shaped wave in the vestibule, and it passes it all the way up towards the helicotremia, it will grow in size until it quickly disappears. 
  

  •    Where it peaks and dies, it what you hear as a tone. 
  

  •    If it peaks down close to the base, you hear a high note, if it peaks down towards the apex, you hear a low note. 
  

  •    Where the Maximum deflection occurs is where you hear the note. 
  

  •    There is a long flat part where the brain cannot discern the notes anymore. 
  

  •    Below 500Hz the peak of the traveling wave is too broad for pitch discrimination, so this theory does not work below 500Hz. 
  

  •    This theory is only good from about 20,000Hz to 500Hz. 
  

  •    It starts to fade out, as it gets closer to the 500Hz, and then dies. 
  

   
   

  o    The Phase Locking Theory of Hearing
  

  •    Below 500Hz the hair cells will vibrate at the same Hz frequency as the note/sound wave 
  

  •    Listing to the low notes because the hair cells are vibrating at the same frequency as the sound itself.  You are listening with the cells that are vibrating. 
  

  •    This is good from 20Hz to 500Hz. 
  

  •    We have this transition here b/c Phase Locking does not go above 500Hz.   At this 500Hz level the Absolute Refractory Period of the Afferent neurons prevent firing faster than 500 times a second. 
  

  •    The Place Theory is starting and isn't doing a good job of listening, and that's where the Transition Theory kicks in, which we call the Volley Theory of Phase Locking.
  

   
   

  o    The Volley Theory of Phase Locking
  

  •    Rows of hair cells, one hair cell fires, and then the next one up fires, until the first one can fire again. This is a Volley of firing. The brain analyzes and counts (counting how many hair cells that have gone by) the pattern of the Volley and interprets into sounds. 
  

  •    This transition from Phase and Place happens at 500Hz, switching to the Volley Theory, and that is doing a good job of hearing 
  

  •    The Volley Theory starts to phase out between 2,000Hz to 6,000Hz (this is variable between people)
  

  •    This is good from about 500Hz to 4,000Hz. 
  

  o    20Hz to 500Hz – only Phase Locking. 
  

  o    500Hz to 4,000Hz – both Volley theory and Place theory (with the Place increasing its ability as you move up further away from 500Hz towards 4,000Hz)
  

  o    4,000Hz to 20,000Hz – only the Place theory. 
  

  o    Most of the sensory input from the inner hair cells of the ear are sent to the opposite hemisphere of the cerebrum. If you are following the excitation of this, it will go to the opposite hemisphere. A small amount of information will be sent on the same side (Ipsolateral).  (Ex. This is useful for EEGs)                    End of Exam I Material
  

   
   

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Lecture 8

-EYE

• Detects electromagnetic waves from wavelength of 400-750nm (visible light)
  
• Detects EM waves using rods and cones
  
  • Rods  function in dim light, they're very sensitive, can respond to a single photon of light, doesn't see colors (black and white are colors), all you see is shades of grey with a rod
    
  • Cones  function in bright light, record color images
    
    • White = all colors at once
      
    • Black = none of the colors
      

• a rod has free floating discs in outer segment
  
  • each of these discs has a photopigment in the outer surface of its membrane, this pigmented membrane is going to pinch off the end of the rod and consume discs and and three new discs are made every hour, discs are made at the bottom and migrate upward
    
• photopigment called rhodopsin (is 11 cis-retinale + scotopsin)
  
  • 11 cis-reinale goes through a series of shape changes
    
    • One is the
      

    This opsin is called scotopsin in rods (the opsin of rhodopsin)
    

    -when only looking with rods (not enough light stimulating cones) using scotopic vision
    

  -if we turn up the light to bright light, the rod gets flooded with too much light and can't function and you are only using cones, this is called photopic vision
  

  -when use both rods/cones  mesopic
  

  -which one, rods/cones, is based upon how much light is available
  

  -rod has peak absorption of 505 nm
  

  -in dark the rod fires, ion channels open and Na and Ca flood in
  

  -the ion channels are held open by cyclic GMP and Na/Ca come in
  

  -think of Na as the main thing that causes the release of the NT
  

  -Ca plays a special role in NT release
  

  Cyclic GMP formed by glymulate cyclase, but is inactivated by Ca entering the cell, this causes cyclic GMP to be reduced and the amount of Ca coming in is reduced, when Ca is reduced more cyclic GMP is made
  

  THIS IS A CYCLE, it does not open or close it just finds a happy medium
  

  -when get rid of the light, hitting the rod, this process changes
  

   
   

  ______________________________________________________________________________________________________________
  

  http://en.wikipedia.org/wiki/Photoreceptor_cell
  

   
   

  ONE photon works for rods, not for cones
  

  • CAN change one rodopsin molecule, making one metarhodopsin
    
  • One meta can change 100s of transductions
    
  • One transduction can stimulate 1000s of
    

     
     

  Scotopic vision
  

  • No color, only the rods were working
    

   
   

  Photopic vision
  

  • In normal light, rods are maxed out and not really functioning
    

   
   

  Mesoptic vision
  

  • Transition period between the 2
    

   
   

  Types of cones:
  

  • Long wave cone
    
    • Peaks at 557 nm
      
    • Only one to see red
      
    • In yellow spectrum
      
    • longwaveconeopsin
      
  • Medium wave cone
    
    • Peak at 535 nm
      
    • mediumwaveconeopsin
      
  • Short wave cone
    
    • Peak at 420 nm
      
    • Shortwaveconeopsin
      

       
       

  660 nm - bright red (paper)
  

  410 nm - bright violet - (disk on it)
  

  TINY dot is a hole in disk
  

  Put you in dark room, with strobe light
  

  If we can get DOT in center of foveola, since there are no short wave cones…it disappears!
  

  Analysis AT BRAIN, not receptors - it sees what it wants
  

   
   

  Daishi
  

  € Invar
  

  it
  

  
   

  or
  

   
   

   
   

   
   

   
   

   
   

   
   

   
   

  Light hits Cone A center
  

  hyperpolarizes
  

  Glutamate coming out of A slows down
  

  A bipolar cell Na channels held down by glutamate
  

  Therefore more Na channels open and increase output of A
  

  Therefore ON CENTER
  

   
   

  B hit by light
  

  B bipolar cell Na channels held open by glutamate
  

  Therefore reduction in glutamate closes channels, output is decreased
  

  THEREFORE OFF CENTER
  

   
   

  Center surround antagonism
  

   
   

  ROD bipolar cells are only ON Center
  

   
   

  http://en.wikipedia.org/wiki/Bipolar_cell_of_the_retina
  

   
   

  Ganglion cells
  

   
   

  W - 40%
  

  • Connect mainly via amacrine cells?
    
  • Directional movement
    
  • Important in scotopic vision
    

   
   

  X - parvo cells - 55%
  

  • Color
    
  • Shape
    
  • Firing tonally
    
  • Main transmitter of visual image
    

   
   

  Y - magno cells 5%
  

  • Rapid changes in visual field
    
  • Movement
    
  • Intensity
    
  • Phasic bursts
    

     
     

   
   

  Uri is
  

   
   

  http://en.wikipedia.org/wiki/Visual_system
  

   
   

  Layers of LGN
  

   
   

  End in layer 4
  

   
   

  LGN and cortex have visual maps
  

  • Foveola has largest mapping
    

     
     

  Cortex
  

  • Blobs
    
  • No blobs - layers 2 and 3 - interblob areas
    

     
     

     
     

Parvo blob	Color
Parvo - interblob	Shape
Magno - movement	Depth of field, location

 
 

 
 

 
 

EAR

 
 

• Inner ear has sensors to detect rotational acceleration
  
  • Semicircular canals
    
• Head position and linear acceleration
  
  • Utricle and saccule
    
• Choclea
  
  • Sound
    

Semicircular canals have endolymph

•  
  

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

5

n

 
 

Lecture 7

Lecture 7:  Reflexes 

 
 

-polysynaptic reflexes = withdrawal reflex

-ESPS  flexor

-IPSP  extensor

      If touch hot pot you pull your hand away

      These feed to lower motorneuron in spinal cord

-polysynaptic means going through an interneuron

-if get strong withdrawal reflex you get a crossover response

      EPSPs go to the extensor on opposite side

      IPSPs go to the flexor on opposite side

      If touch a hot enough pot when you pull the hand away that you touch the pot with you push down with your opposite hand (crossover response)

-reflexes can be overcome by concentration

-Touch Receptors:

      -Pacinian corpuscle = has an axon into it, myelin sheath, Schwann cells encapsulate it creating lammaeli

            When push down on this get an indentation of these layers, layers filled with a gelatinous fluid, pushing down causes distortion and distortion channels, Na channels, will open

            Summation occurs at the first Node of Ranvier NOT at the initial segment and then it will fire 

-adaptation = happens rather quickly, fluid flows back in and is redistributed

      Occurs because of the cocktail onion shape of the lammaeli and this is why even if constant pressure is being applied you don't feel it (adaptation)

-other touch/pressure receptors will adapt by inactivating Na/Ca channels or by activating K channels

-receptors that adapt are called phasic

-receptors that don't adapt and can't send a message = tonic

-hot/cold sensations:  can only detect calories of heat

      You detect the flow of calories

      If calories flow out of the body sense COLD

      If calories of heat flow into the body sense WARM

-individual naked nerve endings that function as temperature receptors respond to absolute temperature

      Two groups of naked nerve endings responding, have a warm and cold receptor

            Warm receptor functions between 30 and 45 degrees Celsius

            Cold receptor function between 10 and 38 degrees Celsius

      We will adapt to temperatures between 20 and 40 degrees Celsius (about 68-104 degrees Fahrenheit) – like when jump in a pool that is 75 degrees you perceive the pool as cold

-hypothermia is what kills people and not drowning – takes approximately 10 minutes

-below 20 degrees Celsius it is COLD

-above 40 degrees Celsius it is WARM 

-PAIN

      -two pathways to the brain

            1.  quick, sharp pain followed by dull, achy sensation

      -autonomic nervous system is a strictly efferent system

-TASTE

      -five basic tastes:

            1.  sweet = sugar, sucrose (fructose, glucose)

                  Bind to metabotropic receptor, increase cyclic AMP

Activates protein kinase A in cytoplasm and phosphorylates a K channel causing it to close and this allows you to say "sweet"

1. sour = actually detecting acids, at the apex of the cell have K leak channels, hydrogen ions from the acids come in through the leak channel and block the exiting of the K and you taste sour
   
2. bitter = alkyloids
   

   bind to metabotropic receptor which utilizes the IP3-DAG system, IP3 is released into cytoplasm, opens Ca channels in the ER and you taste bitter
   

3. salty = have an ungated passive Na channel in the outer membrane of the taste bud and when Na passes into it you taste salty
   

   no Na in do not taste salty
   

   if eat a high salt diet and then eat a salty potato chip you say that is too salty
   

   if eat a low Na diet and stay on it for a few days and are give the same chip to eat you don't think it is as salty 
   

   if stay on low Na diet for weeks you won't have this craving a salt
   

4. umami = amino acids
   

   detects L-aspartate and L-glutamate
   

   (like the MSG test)
   

   -taste is delicious or savory
   

-tongue most sensitive to bitter, sour, sweet, salty

-taste buds are not different histologically, they can respond to all tastes, but each taste bud has a specific taste it responds the best to

-within the taste bud individual gustatory cells only respond to one taste

-there is a sweet pathway (attraction) and a bitter pathway (aversion) to brain

-can only taste things soluble in water 

-OLFACTION

      -80% of what you consider flavor is actually smell

      -ciliated cells in the nasal mucoso constantly sitirring and waving in a nonsynchronous manner to mix the molecules so that the receptors can detect the molecules

      -moleucules bind to metabotropic receptors in the nose

            Some are cyclic AMP others are IP3-DAG, in most cases they serve to open Ca channels

      -each bipolar cell contains only one type of receptor

      -each receptor can bind several odorants

      -the different types of receptors that are firing are doing so in a spatial form

      -using spatial patterning to send a message to the brain to tell it what you're smelling and this allows humans to identify 10,000 dif odors 

-EYE

      Detects electromagnetic waves from wavelength of 400-750nm (visible light)

      Detects EM waves using rods and cones

            Rods  function in dim light, they're very sensitive, can respond to a single photon of light, doesn't see colors (black and white are colors), all you see is shades of grey with a rod

            Cones  function in bright light, record color images

                  White = all colors at once

                  Black = none of the colors

-a rod has free floating discs in outer segment

      -each of these discs has a photopigment in the outer surface of its membrane, this pigmented membrane is going to pinch off the end of the rod and consume discs and and three new discs are made every hour, discs are made at the bottom and migrate upward

-photopigment called rhodopsin (is 11 cis-retinale + scotopsin)

      This opsin is called scotopsin in rods (the opsin of rhodopsin)

      -when only looking with rods (not enough light stimulating cones) using scotopic vision

-if we turn up the light to bright light, the rod gets flooded with too much light and can't function and you are only using cones, this is called photopic vision

-when use both rods/cones  mesopic

-which one, rods/cones, is based upon how much light is available

-rod has peak absorption of 505 nm

-in dark the rod fires, ion channels open and Na and Ca flood in

-the ion channels are held open by cyclic GMP and Na/Ca come in

-think of Na as the main thing that causes the release of the NT

-Ca plays a special role in NT release

      Cyclic GMP formed by glymulate cyclase, but is inactivated by Ca entering the cell, this causes cyclic GMP to be reduced and the amount of Ca coming in is reduced, when Ca is reduced more cyclic GMP is made

            THIS IS A CYCLE, it does not open or close it just finds a happy medium

-when get rid of the light, hitting the rod, this process changes

 
 

Pasted from <http://mail.google.com/mail/?ui=2&ik=e56a7a2463&view=att&th=11f526f856d7e467&attid=0.1&disp=vah&realattid=f_fqwqqokr0&zw>

 
 

Lecture 5

Muscle Fiber Types

 
 

Muscle fibers vary by the myosin

Heavy chain

Light chain

Troponin (isoforms of Tn-I, Tn-C, Tn-t)

Tropomyosin (isoforms)

Myoglobin (like hemoglobin, a singular thing instead of four, holds oxygen in muscle, has iron makes it red)

Varies how many enzymes are set up for aerobic and anaerobic activity

 
 

Classify fibers according to myosin heavy chains

 
 

Different types of fibers:

Type I

• Slow
  
• high aerobic capacity
  
• red – high myoglobin content
  

Type IIA

• Faster
  
• fairly high aerobic capacity
  

Type IIX

• Faster still
  
• Good deal MORE aerobic capacity (used to be called Type IID)
  
• Smaller animals can get an even faster fiber called Type IIB
  

Type IIB

• Fastest greatest anerobic capacity
  
• Called White cell
  
  • Still has myoglobin and is actually light red in color
    
• ONLY PLACE Type IIB fibers: in eye muscle in human
  

 
 

TypeIIX and Type IIB – low aerobic ?????????

 
 

Fibers originally genetically determined when first produced

• however what they become from then on is dependent on the activity of the motor neuron that innervates them
  

   
   

All types can switch back and forth depending on how much activity

I <--> IIA <--> IIX <--> IIB

If we unhook one and attach to a different nerve, will slowly switch to firing rate of new nerve

 

There are also intermediates - when transitioning.

Called IIX, IIB

 
 

If do endurance training, push fibers to Type I (aerobic)

If do strength training, push fibers towards Type IIB or Type IIX in humans

Idleness will also push to Type IIB/Type IIX (aerobic)

 
 

Can use fiber names to name motor units

 
 

Each skeletal muscle is mixture of motor units

Every muscle has types up to IIX, but have different ratios

 
 

During a slow initiated contraction motor unit incorporation is sequential

Slower fibers activated first

During fast contraction motor unit of all types are activated at the same time

 
 

Can monitor electrical event and can produce a single twitch, if let muscle rest for a while and we do a twitch and allow twitch to come all the way back down (completely relaxed), but before it gets to far and then produce a second twitch the second twitch goes up higher, this stair-step effect called:

Treppe

• see it in muscle that is relaxed
  
• Definition comes from Boddich (1881), first to describe treppe in hearts that had been stopped for a while and were restarted and then they would go a greater contraction each time until it got to a certain level
  
• Treppe will go higher and higher until it reaches a certain level and then it will plateau
  
• Classical explanation of treppe: when first open ryanodine receptor have efflux of Ca which will bring Ca off of calsequestrin which will increase amount of Ca, then pump Ca back into sarcoplasmic reticulum which will diffuse over back to terminal cistern and now have greater concentration of Ca for next fire and will come out faster
  

   
   

Summation:

• If fire twitch and before it relaxes, twitch it and will go higher and higher =
  
• Kicking Ca out faster than Ca can come back in, more Ca have out in a muscle up to a certain point will increase the contractability and will get more movement
  

   
   

If fire very fast so the level doesn't come down at all have a tetanus and the twitch flatlines

• Can't stay up there forever, b/c it will run out of ATP and start to see it drop and that line dropping is called fatigue (due to lack of ATP)
  
  • Called Fatigue
    

    Other types of fatigue such as fatigue of neuromuscular junction
    

 
 

When these muscles contract, they make noise

• William Wollatson determined the frequency of this sound
  
  • Got in a carriage with a horse in london with cobblestone street
    
  • Marking system to mark start and 1 second later
    
  • Stick his fingers in his ears - relaxed thumbs, contracted fingers
    
  • Went until pace of horse matched the noise in his ears
    
  • Counted cobblestones - 23
    
  • Late 1800's
    
• 23 Hz sound produced by muscle, actual number is 25 Hz
  

   
   

 
 

Synapses:

-two types of synapses

Electrical (like a gap junction) - quick

Chemical – prolonged, constitutes most synapses we look at, use

• Neurotransmitters
  

   
   

-some synapses both electrical (quick) and chemical (slow)

Both - conjoint

 
 

-space between is the synaptic cleft (20-30nm wide),

• NT cross the cleft and are released by synaptic vesicle cycle
  
• Delay called synaptic delay
  

 
 

synaptic knob

-have endosome, have railway from the cell body b/c NT are made up in the soma, sometimes made up as precursors in the soma and change on the way down

 
 

• Budding
  
  • very end of endosome will pinch off and (called budding)
    
  • called a synaptic vesicle, but is empty: NO NT
    

   
   

• Neurotransmitter Uptake
  
  • NT taken into the synaptic vesicle by active transport (burning ATP)
    

   
   

• Translocation: vesicle going down to active site
  
  • when vesicle full with NT, goes down to active site
    

   
   

1. Docking: proteins on the synaptic vesicle bind to proteins of the neurolemma (plasma membrane of neuron)
   

    
    

2. Priming
   
   1. series of protein bindings and dissociations that form a partial fusion of the synaptic vesicle to the neural lemma
      

   Primed synaptic vesicle waiting there for the completed spinal fusion and will do that in response to electrical stimulation
   

    
    

3. Full Fusion/Exocytosis: release NT into synaptic cleft and will diffuse down to the target tissue
   
   1. Action Potential induced
      
   2. Opens a hole and NT flows into the synapse
      

      -this dumping may be a calcium-calmodulin? regulated process
      

       
       

4. Endocytosis:
   
   1. sarcolemma closes back and synaptic vesicles break away
      

       
       

5. Translocation 2: empty synaptic vesicle binds to the other end of the endosome
   

    
    

6. Endosome Binding
   

    
    

7. Endosome Revamping: vesicle reattaches and gets ready to bind again
   

 
 

PROCESS CAN BE COMPLETED IN ONE MINUTE

 
 

Electrical event causes all of this

• Causes Ca influx
  
• Amount of Ca determined by intensity of electrical impulses
  
• Amount of NT directly proportional to Ca released
  

 
 

-CONTINUE ABOUT Ca Process Later….

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

Lecture 4

Audio recording started: 12:21 PM Friday, January 23, 2009

 
 

WENT OVER PAPER HANDOUT

 
 

• Action potential for a wave front traveling across skeletal muscle -90 – 0mV
  

   
   

• When goes down does not have hyperpolarization does not happen in muscle
  

   
   

• Depolarization due to influx of Na
  
• Repolarization due to efflux of K
  
  • Open Na channel and Na flows in bringing positive charge in, when open K positive charge goes outside and brings membrane potential back down to resting potential
    

  Wave of excitation goes over surface of the cell, sarcolema and heads down the T-tubule
  

  t-tubules have terminal cisterns
  

  AP travels down and hits a dihydropyridine receptor
  

  Dihidropyridine receptor made of four subunits and between subunits 2 and 3 you find a loop that goes down
  

  The loop goes down to ryanodine receptor between second/third subunit, loop is a physical link to ryanodine receptor
  

  http://en.wikipedia.org/wiki/Ryanodine_receptor#Physiology
  

  Terminal cistern is filled with Ca
  

  Ca is taken in by ER and went into terminal cistern and is waiting ot be released
  

  Dihydropyridine receptor has four loops/four subunits (this is one receptor)
  

  Four loops go down to ryanodine receptor, but only every other ryanodine receptor has a tetrad above it
  

  Every other ryanodine receptor has a physical link to open calcium, electrical event changes shape of tetrads and the loops go up and will open the ryanodine receptors and calcium will be effluxed and will open other ryanodine receptors (negative feedback system)
  

  Ryanodine receptor has a high affinity Ca receptor that will open if that is stimulated, it will bind Ca in low levels, when Ca comes out from ryanodine receptor and it will release Ca and this will increase Ca in the area and it will bind to low affinity Ca ryanodine receptors
  

  Troponin of the Thin filament (two rows of globular actin strung in a row)
  

  Tropomyosin covering active site
  

  Troponin keeps tropomyosin in place
  

  There are three troponin proteins:
  

  Tn-C
  

  Tn-T
  

  Tn-I
  

  Tn-C has two globular ends and one is called the C(carbon) end and the other is the N(nitrogen) end
  

  When making an amino acid you have a carboxyl and an amine end and you just stick these together to form a peptide chain
  

  Tn-C already bound to Tn-I
  

  N part of Tn-C not bound to anything
  

  If add Ca N end will bind to Tn-I
  

  When bind causes troponin to change shape and will break Tn-I off of actin molecule and will slide off of strip of tropomyosin and this will slide off of active site and expose
  

  Actin has an outer and an inner site, actin in the outer domain and it slips into inner site, exposing the active site
  

  Ca enters into cytoplasm bind to N part of globular Tn-C which will bind to Tn-I to cause shape change to expose the active site
  

  What does the active site do?
  

   
   

  Motor Unit = one neuron supplying several muscle fibers in a muscle
  

  If fine control muscle have as few as three fibers for one neuron
  

  Support/weight bearing muscle several hundred fibers per neuron
  

   
   

  During isometric contractions find that the lever arm is unmoving, ADP
  

  Lever arm in rigor state, but Pi has popped off and is in a great deal of tension, Z-disc can't move
  

  More tension want to put in that isometric contraction, the more subunits you initiate
  

   
   

  Isotonic contraction  the farther you want to go the more subunits you initiate and fire
  

   
   

  Can monitor the electrical activity in the muscles using an EMG (electro myogram)
  

  Have two electrodes, which attach to arm and will monitor electrical activity and will acquire a bipolar reading, sometimes you will see a plus associated with these
  

  Electrodes are attached to an amplifier which is attached to a pen, which will be making a recording on a piece of paper
  

  When one electrode sees a positive charge it tells the pen to move in one direction, when the other electrode sees the positive charge it tells the pen to move in the opposite direction (BIPOLAR RECORDING)
  

   
   

  If have muscles see positive on outside, but can't see negative on inside, have some excitation traveling across it, front of the wave is positive and back is negative therefore have positive wave front
  

  If have positive wave front traveling parallel to electrodes, pen doesn't move
  

  If have wavefront and doing a bipolar reading, if running parallel the wave front is imaginary and can use this idea to determine direction
  

  If have wavefront perpendicular to electrodes, get max deflection
  

  Able to rotate electrodes and observe raise/fall of deflection to determine direction of motor neuron
  

   
   

  Raw EMG = very rough, NOT smooth
  

   
   

  If not enough Ca, Mg will replace
  

   
   

  occurs on chain
  

  Neck changes shape and picks motor core up and puts it closer to active site - doesn't have to travel as far…quicker contraction time
  

  Ca stays for about 30ms
  

  1/2 life of phosphorolation = 1.3 seconds
  

   
   

  Cardiac muscle cannot sustain a contraction
  

   
   

  Myosin can only move in ONE direction
  

   
   

  2 types of contractions:
  

  Isotonic - same tension
  

  All sarcomeres are contracting in an all-or none fashion, however overall movement is SMOOTH
  

  Motor units are responsible for smoothness (primary cause for smooth movements)
  

  Group of muscle fiber cells that are innervated from many collateral axon fibers from a single axon
  

  …….3
  

  Fine control
  

  Fingers, eye muscle
  

  Or single nerve can innervate several hundred fiber
  

  When ONE nerve fiber fires, all motor units contract at once and smooth movement results
  

  Isometric - same length