Exam 2 Flashcards
Electrical Signaling Via Membrane Potential Changes
- look at graph
- signal is a very brief change in voltage in membrane at one spot
- start at depolarization: Na+ dominant but only open for a little bit then they inactivate and close which causes repolarization: K+ open and brings potential back down then hyperpolarization: so much K+ in brings potential down even more negative than beginning point
Graded Potentials
- congressman example
- as a congressmen you get inputs from many constituents telling you how to vote. One vote is smaller than two votes
- hyperpolarizing is when you vote no and there’s a dip; if there’s a yes it goes up and is depolarizing
- look at graphs
- threshold is the decision point when the congressman he has enough votes to act and action potential is the actual casting of the congressman’s vote
- a transmitter binds to a receptor to trigger some leakiness of ions; each unit of activation makes a change in membrane potential
- graded potentials get the membrane to threshold which then starts the action potential
- excitatory signal is when Na+ open and inhibitory is when K+ open
Action Potential
- when you decide to vote-it’s the actual action
- look at graph
Explain how graded potentials can summate to reach the threshold for an action potential on either a spatial or temporal basis.
- spatial: different neurons influencing cell-vote yes-pushing toward threshold
- temporal: one neural input repeatedly
How do changing ion conductances occur?
- resting membrane potential: activation gate closed but capable of opening, inactivation gate open–>depolarization opens activation gate and inactivation gate open–>1 ms activation gate open and inactivation gate closed (incapable of opening until return to resting state
- can’t use it again till it goes through period of recovery (refractory period) which is why the gates slam closed
- the change in molecular shape means they have to reconfigure to go again
All-or-none Law
- 1 kind of action potential that either happens all at once or not at all
- has nothing to do with gradation/amplitude of the action potential, it’s either there or it isn’t
- all action potentials are identical
Refractory Period
-takes a while to recover to be ready to go again
Why is there an absolute refractory period-a time during which now stimulus can elicit an action potential
-after the peak of action potential all the sodium channels close and they cannot open until they go through this period
How can nervous system distinguish between different stimuli like light touch vs. heavy touch or sharp pain vs. sharp pain?
- number of action potentials per time
- pattern of action potentials
- change in sensitivity-long term effect
- how many receptors are activated
- number of classes of receptors
Coding for Stimulus Intensity
- look at graph
- number of potentials influenced by the strength of the stimuli
Conduction of the Impulse
- positive attracted to negative which changes threshold and signal continues to move down neuron
- look at image
Axon Potential Propagation in Myelinated Axons
- enough insulation that when it reaches threshold it is enough for current to jump to next node
- voltage spreads a distance and if it goes far enough the signal is able to jump from node to node thus skipping the myelinated sections
- the myelinated sections allow the voltage to spread far enough for the jump to happen
MS attacks and destroys myelin sheath of CNS neurons and oligodendrocytes that form the myelin. What are some symptoms of MS that might be expected and how these might arise from loss of myelin?
- action potentials cannot move quick enough down axons to deliver stimulus
- loss of control
- slower rate of AP means you lose energy and there’s a delay
- makes motor and sensory pathways slower
- weakened muscles, touch receptors are numb
- lose coordination
How Chemical Synapses Work
- AP travels down axon and tells Ca2+ channels to open and Ca2+ ions allow neurotransmitters to be released into synapse
- neurotransmitters attach to receptor which gives a signal to cell which results in response
3 Ways to End Synaptic Activity
- diffusion away
- reuptake
- enzymatic breakdown
If action potential frequency increases, what adaptations could occur to either increase or decrease the response of the postsynaptic neuron?
-change numberof Ca2+ channels, change number of receptors, change sensitivity of receptors, change number of neurotransmitters released
Excitatory and Inhibitory Post-Synaptic Potentials
- EPSP’s and IPSP’s
- these are the “votes” received from constituents
- excitatory increases voltage and inhibitory decreases voltage
- bumps in the membrane potential when an interaction happens with the congressman
Divergent Neuronal Integration
-one neuron has effects on many separate neurons
Convergent Neuronal Integration
-on neuron is affected by many separate neurons
Spatial and Temporal Summation
- multiple inputs happen at same time to increase the potential more than a single input would=spatial
- have two EPSP’s and one IPSP on an axon so one EPSP will cancel with the IPSP and will be left with one EPSP which generates the response
- temporal is when one neuron repeatedly sends the same message in a short period of time
Pre-synaptic Facilitation and Inhibition
- one neuron is a part of another neuron that’s attached to the cell body and together they cause a higher spike in the membrane potential thus bringing it to threshold more easily and producing an AP
- opposite could also be true where one inhibits voting of other and then hyperpolarizing could happen thus bringing it further away from threshold and AP
- look at image
Why did dogs learn to salivate every time Pavlov’s assistant came into room even without food? What neural adaptations underlie this phenomenon?
- assistant became presynaptically linked with being fed
- neurons that fire together wire together
- neuronal circuits are plastic
In certain areas of the brain neurons are difficult to activate a first time, but repeated activation makes subsequent activation much easier. List some reasons why this fits with our experience of how learning develops.
-repetition reinforces information gathered
Would you like to see potentiation (greater and greater neural activation) of all incoming stimuli if the same synapses are used? List examples of sensory inputs that adapt to repetitive stimuli with decreased neural activation
- seeing unchanging things (nose on face)
- sounds you hear constantly (fans, trains if near tracks, sirens in bloomington)
- getting used to sharp smell after some time
- pressure/touch
Acetylcholine
-ACh as a neurotransmitter plays a role in motor nerves to muscles
Nicotinic and Muscarinic Receptors of ACh
- nicotine activates high effects in both directions-used in skeletal muscles
- muscarinic has different effect and plays a role in GI tract-differentiates from skeletal muscle
- point is that different classes of cholinergic receptors that all have different essential functions in the body
How would you design a drug that would slow the heart rate by mimicking the action of acetylcholine on cardiac muscarinic cholinergic receptors?
-make an analog which has similar shape/structure to portion that goes in the binding site of the receptor
Nicotinic and muscarinic cholinergic receptors are also found in the CNS. Is there any way to predict the actions of acetylcholine
No, it’s not about the neurotransmitters, it’s about the receptors
Alpha and Beta Adrenergic Receptors
- adrenaline activating
- can make more active or fit in receptor and do nothing
Based on effects of adrenaline in the body, what would be the effects of using a drug that inhibits the actions of adrenaline (e.g. a beta blocker)
- diminished response/alertness
- decreased heart rate
- decreased blood pressure
- relaxed
- lethargic
Agonist vs. Antagonist
- agonist does what endogenous neurotransmitters does in the body
- antagonist blocks receptor but does nothing but block NT binding
List some ways that SSRI’s might alter the level of activation of the post-synaptic serotonin neurons in the brain
- would activate many more receptors
- increase activity means more serotonin in synaptic cleft which increases activation of post-synaptic receptors
What do you suppose would be the effect on mood of a drug that was a serotonin reuptake enhancer?
-decreased serotonin levels means unhappiness and depression
Given that GABA is the most widespread inhibitory neurotransmitter in the brain, what would be some of the expected actions of drugs that mimic actions of GABA?
- decreased pain perception
- anti-anxiety
- decreased emotional response
Concussion
- only 20% of athletes that have had a concussion know they had one
- first concussion increases risk for second and cumulative risk increases steadily
- result from rotation of cerebral hemispheres in anterior/posterior plane-no rotation, no concussion
- happens right around midbrain-brain rocks forward and backward like on a hinge=concussion
- linked to depression
- symptoms: headache, nausea, disorientation, dizziness, memory loss, light sensitivity
What could explain the association of depression with repeated episodes of concussion?
-areas associated with mood get messed with/knocked around during a concussion
Postconcussion syndrome can be disabling. What are some of the most important symptoms?
-headaches, depression, difficulty focusing, decreased cognitive ability, brain response to special senses changes–>more sensitive
CNS Blood Supply
- needs a lot of blood and eats only sugar (glucose) and does not need insulin to get it into the cells
- the reason you regulate blood glucose is for the brain
- will eat ketone bodies if not enough glucose
Blood Brain Barrier
- tight junctions and astrocytes mean only certain things can get across to the brain
- protects brain from harmful toxins/drugs and regulates brain ECF
- oxygen, water, glucose by facilitated diffusion, salt (NaCl), carbon dioxide (out) and amino acids are what can enter
Gray Matter vs. White Matter
- gray is dendrites, cell bodies, axon terminals of presynaptic cell
- white is myelinated axons and oligodendrocytes
Spinal Nerves
-almost all mixed: have motor and sensory side to each
Explain why bulging spinal discs often cause both numbness and muscle weakness.
-They press on nerves and prevent effector functions to muscle/part of body and also affect sensory function resulting in numbness or pain
Axon Regeneration
- can occur if you cut a peripheral neuron
- if scarring occurs it cannot regrow
What are some factors that make axon regeneration in the spinal cord so difficult, given that the human spinal cord contains about 1 million neurons.
- sheer number of axons that would have to regrow
- complex network that exists in a web
- spatial concerns-density
- usually have scaring
Broca’s and Wernicke’s Areas of Brain
- Broca’s deals with speech formation/expression
- Wernicke’s deals with language comprehension
Motor and Sensory Areas of Cortex
-mapped out in a very specific way on the brain so that each part of the cortex relates to a specific motor/sensory response when activated
Why doe symptoms of a stroke tell us what portions of the brain have been damaged?
- portions damaged result in certain symptoms like loss of speech
- ask patients to do tests and if they can’t that’s the area that has been damaged
Phineas Gage
- got super mean; impulsive, hot-headed, and irresponsible
- after a while personality returned-plasticity; brain was able to make new connections and adapted around the injury; rewarded for making new connections via conditioning for correct response
What are some possible CNS and peripheral neural factors that may contribute to phantom limb pain?
-connections to spinal cord/brain still exist–>signals still sent from distal end of remaining neuron that is still mapped on the sensory cortex the same way–>typical pre-loss response
Functions of Hypothalamus
- appetite
- water balance (ADH)
- body temp regulation
- libido
Limbic System
- plays role in emotion and motivation
- primitive emotional brain at core of brain
- hippocampus and amygdala are important here
Hippocampus
- plays role in short term memory
- interacts with emotions-specifically fear (amygdala)
- if no fear/anxiety/emotional factor is present in a memory in short term it is erased
- if fear/anxiety/strong emotion is present it gets put into long term and may last for a while in the cortex
What parts of the brain may be involved in PTSD
- amygdala and hippocampus
- memory is too emotional so it goes from hippocampus to the long-term storage in the cortex that sticks around for a very long time, possibly forever
- loss of kappa opioid receptors in PTSD** important
- body’s endogenous versions of heroin or morphine cannot be used to relax a person because their receptors are gone
What does the limbic system do?
- regulates emotional responses
- don’t have to have a perfect system in order to feel emotions but it does have to be intact to respond correctly with regulation
What are some situations for which involuntary control of motor activity is advantageous or essential?
- breathing
- blinking
- withdrawal from pain/reflexes
- shivering
Muscle Spindles
- look at images
- stretched releases the most action potentials per time
- relaxed releases fewer action potentials per time
- contracted releases very few action potentials per time
Patellar Reflex
-stretching the muscle spindles feeds back to the spinal cord that then goes out to leg again and leg extends
Voluntary Movement
- idea: have to decide to do it–>
- primary motor cortex: activates other areas–?
- midbrain, basal ganglia–>
- lower motor neuron (spinal cord)–>
- muscle–>feedback
- feedback to sensory part-cerebellum to previous portions of sequence
Feedback
- need sensory systems to give sensory feedback to tell us where we are in space
- main part that does this is cerebellum and basal nuclei
Cerebellum
-plays a role in fine movement accuracy
Basal Nuclei
- midbrain
- feed into both feedback and motor attention
- damage to these cause Huntington’s and Parkinson’s
- Huntington’s: genetic, characteristic shaking action in limbs (circular)
- Parkinson’s: problem with tremors and inability to activate (facial) muscles (mask like face); damage to both sides of basal nuclei; trouble walking
After an injury that completely severs the spinal cord, why do spinal reflexes persist both above and below the point of transection of the cord?
- they don’t travel to the brain
- goes to spinal cord and right back-no CNS
- if the cord that gets chopped is the one that goes to the brain it doesn’t matter and will just feed into the reflex
List some possible reasons why spinal reflexes often become more pronounced after cord transection.
- loss of feedback
- keeps repeating signal
Reticular Activating System
- turns off when asleep
- essential for consciousness but not for brain activity
Circadian Rhythm and Homeostatic Sleep Drive
- all built to have circadian rhythm that works on a 24 hour + ~5 min cycle
- accomplished by monitoring cortisol levels and body temperature
EEG-Stage 4 Sleep and REM Sleep
- stage 4: non-REM slow wave sleep; essential for recovery and learning; consolidate memories that matter into long term during this
- REM: dreaming happens here; also plays a role in recovery and learning
- deny these two cycles you don’t learn
- also play role in refreshing
Symptoms of sleep deprivation and what do they tells us about functions of sleep?
- loss of cognitive function, fatigue, lack of motivation means decrease in creativity, inability to concentrate, forgetfulness, hungry, liable mood, sleep latency decreases
- need to sleep to regulate these feelings and refresh your brain and body
- decrease in sleep latency means your sleep cycle gets messed up so you can fall asleep almost instantly and at inopportune times
Appetite in Sleep Deprivation
- increases due to hormone called ghrelin which is made in stomach wall
- increases production when you’re sleepy
How would you accumulate a sleep debt? What prevents a person from “paying off” the entire debt in one night?
- lack of sleep for many continuous nights-less than your sleep need
- piles up hour for hour
- circadian rhythm won’t let you sleep for entire length of sleep debt
Synaptic Changes
- long term potentiation; synaptic plasticity
- making neuron fire more at same stimulus
- happens in hippocampus-cortex, once activated it gets easier and it doesn’t go away for a long time
Coma
- have electrical activity in brain but can’t be aroused
- gray area of life/death
Law of Specific Nerve Energies
-every type of receptor is most sensitive to one type of stimulus and will elicit the same response every time to a stimulus
Types of Receptors
- direct contact-has to activate neuron and sends AP to brain
- separate cells-uses NT to activate pathway to brain
Sensory Adaptation
- can happen quickly or slowly
- process by which receptors become less sensitive to stimulus as is the case with cutaneous receptors
- detect changes but not constant non-interesting information
Receptive Fields
- if you activate any of the branches it will converge onto one cell
- this determines the size of the receptive field which can vary
- TPGD of cheek and forearm
- TPGD means how far apart are two sharp points before you can say it’s two not one
- age decreases ability to discriminate declines
- receptive fields in cheek are smaller than forearm-more sensitive
- there is more convergence of neurons in cheek-all go to one point which makes it harder to distinguish one point from two
For photoreceptor in retina, list some advantages and disadvantages to having individual cells with very small receptive fields.
- advantages: more precise response-more detail and you can pack more receptors in
- disadvantages: damage will cost a lot, too much information and too sensitive
Receptor or Generator Potentials, and Coding for Stimulus Intensity
- look at graphs
- can tell the sensory receptor is adapting because AP’s get further apart and receptor potential sliding downward in response
How is stimulus intensity coded by this sensory system?
-more action potentials per unit time (frequency of APs)
List some ways that the CNS could get additional stimulus intensity info from the periphery of the body, in addition to that supplied by this particular sensory neuron?
- more sensory neurons-more receptors activate (can be same kind or different kind)
- increase in other factors
Do you want pain receptors to be adapting or non-adapting?
- non-adapting because you can then eliminate pain and avoid damage
- there are things to distract you from pain but it’s there to tell you something
- pain receptors NEVER adapt
What role do receptors in the skin play in the problem of development of soes on feet of people with long-term diabetes?
-nerve damage means loss of receptors which means loss of pain so damage can advance before you know it
Stimulation of pain receptors typically cause fear, anger, or aggression. What part of the brain is linked to sensory input from nociceptors and why is this “hard-wired” into our brains?
- amygdala
- protect yourself from harmful situations
- activates fight or flight
For any given pain stimulus, a number of factors influence how much pain is actually perceived. What are some of these factors?
- distractions
- block of receptors
- expectation
- sense of control
Implication of lack of pain sensation for daily life of Georgia? How is it caused?
- can cause severe damage without knowing so must be constantly monitored]
- mutation in single gene that codes for sodium channels
Fast and Slow Pain
- fast: A delta fibers carry but eventually fade away and slow fibers activate
- slow: C fibers; slow acting that may last a while
Referred Pain
- pain from one part of the body is felt by another part because they converge onto the same nerve
- gives a pain in the wrong anatomical position from where the problem is
- ex: heart and skin
Modulation of Pain Signals
- pain signals don’t adapt very much but can change very slightly or slowly via modulation
- pain fiber hasn’t adapted but has been modulated so it doesn’t do the thing it wasn’t supposed to do
- can also happen in spinal cord or brain-central pain modulation
What are some actions of opioid agonists (morphine) that mimic the actions of endogenous molecules in brain that modulate and reduce pain sensations.
- you have endogenous opioids but they’re not cutting it and need help
- pain killers that change perception in brain; increase center modulation
- euphoria that’s addictive
- slow heart rate and breathing that can lead to respiratory arrest
Fovea
- no blood vessels only photoreceptors in high concentration
- clearest vision
- damage causes macular degeneration: can only see periphery
Pupil
- lets light in
- controlled by autonomic feedback of ANS; sympathetic dilates and parasympathetic constricts
Accomodation
- changes your vision depending on location of object; parts adjust to make clearest image possible
- lens gets thicker as you get older and can’t accommodate as well
- presbyopia: old age leads to not being able to focus close up
What classes of drugs could an optometrist use to dilate eyes? Side effects if it gets in blood stream.
- sympathetic agonist
- parasympathetic antagonist (blocker/inhibitor)
- sympathetic agonist side effects: increased heart rate, blood pressure, breathing, anxiety, muscle tension and suppression of immune system eventually
Rods and Cones
- transduce light energy into action potentials
- photons of a certain energy activate them
- retinal Vitamin A is a protein and photons come in and activate a change in conformation which activates rhodopsin which activates rods or cones
Different Photoreceptors
- have 3 kinds of cones (red, green, blue) and rods
- loss of one kind of cone leads to color blindness, loss of two means no color in vision at all
Color Vision
-have to have a comparison of two different signals from two different types of cone photoreceptors
Depth Perception
-comparison of images from each of the two eyes
Rod/Cone Bleaching
- can happen in bright light like snow
- so much energy comes it that they become hyperpolarized and consequently stop working
- photoreceptors rendered inactive by too much light stimulus
Rod Monochromat
- no functioning cones but normal rods and rod function
- sees black and white and shades of gray
- lack of focus because there is no fovea so sees best in peripheral
- cannot see with too much light on
No convergence of foveal cones onto bipolar cells. So each cone in fovea has each ganglion cell. Outside fovea ratio is much higher (1000:1). What advantage does a lack of convergence provide at the fovea?
-each receptive field is tiny which means you can see in greater detail
Glaucoma
- tunnel vision
- can only see central items
- loss of information from rods means that you have damage in your peripheral ganglion cells
Neural Pathways from Retina to Brain
- cross over
- 75% what–>visual cortex
- 25% where–>down spinal cord
Horizontal Gaze Nystagmus refers to lateral or horizontal jerking of eye when gaze is directed to side. Standard field sobriety test. What is alcohol affecting in the brain that causes this problem?
- semicircular canals
- brain interpretation: still vs. moving
- depressant-slows down basically everything including brain
Conduction deafness includes all causes of hearing loss that involve an inability to transmit sound waves to the oval window of the cochlea. What are some causes?
- damage to tympanic membrane
- misshapen pinna
- damage to ossicles
- infection in middle ear
- blockage of ear canal
Sensory and Motor Tracts
- sensory ascend to the brain from the senses
- motor descend from the brain to the appendages/effectors
Motor Control Pathway-Reflexes
- involuntary movement through reflexes
- stimulus–>sensory receptor–>afferent neuron–>integration center (CNS)–>efferent neuron(s)–>effector organ (muscle, gland)–>response
Sleep Stages
-heart rate decreases as you go from stage 1 to stage 4 but then spikes back up when in REM which is higher than stage 1 but lower than when awake
Sensory Pathways
-stimulus–>receptors–>afferent neuron (first order neuron)–>spinal cord or brainstem–>second order neuron–>thalamus–>third order neuron–>cortex
Hearing aids are placed in outer ear at external auditory meatus. Do hearing aids help in treatment of conduction deafness? Why or why not?
- complete hearing loss-does not help-sound waves can’t be transmitted
- partial hearing loss-would help-increases in sound signals
Cochlea
- respond to waves of pressure in atmosphere with mechanoreceptors
- on membrane of cochlea there are sensory cells that have hair and when the hair is bend it signals to the cell and hearing is activated
- damage to hair cells can’t be repaired and if one is damaged often times the surrounding cells die off too
Sound Wave Conduction
- pressure wave vibrates everything starting at your canal to the tympanic membrane to the ossicles then the oval window to the cochlea
- in the cochlea some portion of the hair cells is bent which then transmits to an AP
- hair cells bent activates and heads back to cochlear nerve and ultimately auditory cortex in the brain
Sensorineural Deafness
- all causes of deafness from cochlea to brain
- can be caused by loss/damage of hair cells, damage to round/oval windows, damage to cochlea (structures other than hair cells like membranes or liquid composition) or damage to cochlear nerve or auditory cortex
Stereocilia and Sound Transduction
-when one bends they all bend which causes transduction which means ion concentration changes and signals an AP
Frequency Coding
- higher frequency sounds vibrate proximal end of cochlea so hair cells here are only ones activated at a high pitch
- lower frequency sounds vibrate at the distal end so only hair cells down there are activated at a low pitch
- volume is how much the cells bend
How does your body know where you are in space?
- proprioceptors
- vestibular apparatus
- vision
- when theses all agree everything is good but when they don’t agree is when you get motion sickness and nausea etc.
Vestibular Apparatus
- plays a role in equilibrium
- has 3 semicircular canals in 3 planes of movement/rotation
- utricle and saccule detect acceleration in a straight line/up/down
- all have hair cells being bent to determine position in space
Hair Cell Structure and Responses
- at rest or constant rate of motion have few signals in change of membrane potential
- head rotation-acceleration-get pressure from endolymph and less signals in change of membrane potential
- head rotation in other direction-acceleration-pressure from endolymph moves to other side of canal and lots of signals in change in membrane potential happen
Menieres Disease
- inflammation in labyrinth (inflammation in a system that’s supposed to be quite)
- vertigo and nausea
- inflammation in labyrinth can also cause neural activation of things nearby which means can result in auditory symptoms like ringing ears as in the case of labrynthitis
Taste
- bitter, sweet, and umami have receptor binding as triggers for changes
- sour responds to H+ ions and opens H+ channel and salty responds to Na+ ions and opens Na+ channel
- bitter is a taste related to toxin detection
- sweet responds to glucose which is response to energy needs
- umami is a response to proteins
Studies show that decreasing salt in the diet decreases desire for salt. What could explain this change?
-sensitivity adaptation change
Taste researches divide people into three groups non-tasters, medium tasters, and supertasters based on ability to detect bitter chemical called PROP. What could account for individual differences in taste sensitivity?
- genetics: # receptors, threshold differences and sensitivity differences
- different isoforms, density of receptors
In what ways might taste sensitivity affect diet and health?
- bad: healthy veggies are bitter and yucky and typically have lower body weight because they’re picky eaters
- good: lots of other food that are bad for you may also have a taste that is too much (too sweet for example) so also yucky
Smell
- affected mainly by olfactory bulb and olfactory epithelium
- easily damaged which means you can lose your sense of smell fairly easily
- part of taste sense as well-mouth feel and flavor have some ties with taste
We have about 350 different genes coding for 350 different receptor proteins for detection of 350 different odors. Why is it possible then for humans to distinguish up to 10,000 different odors?
-contribute variable amounts of each protein to change the kind of smell produced
Autonomic Nervous System
- by and large no voluntary control
- sympathetic and parasympathetic divisions
- many organs have dual innervation by both of these divisions
Adrenal Gland
- has cortex which secretes cortisol and other things
- has medulla where epinephrine is made (so is norepinephrine)
- norepinephrine comes from all sympathetic nerve endings but epinephrine does not
Sympathetic Nervous System Neurotransmitters
- adrenergic (relating to adrenaline/epinephrine) receptors
- major neurotransmitter is epinephrine
- fight or flight division
- comes from medulla
Parasympathetic Nervous System Neurotransmitters
- muscarinic cholinergic receptors
- major neurotransmitter is acetylcholine
- muscarinic cholinergic receptors differentiate these muscles from skeletal muscles (nicotinic cholinergic receptors play role in skeletal muscles)
- rest and digest division
19 year old woman develops tumor of adrenal medulla that secretes medullary hormone at ten times the normal rate. What hormones are found at excessive amounts in the blood? What symptoms will she experience? What might be some possible treatments?
- epinephrine and norepinephrine
- increased heart rate, increased blood pressure, anxiety, hot/sweaty, insomnia; fight or flight activated for no reason
- remove tumor or adrenal medulla that’s affected
ANS and Blood Pressure
- bunch of changes happen
- reciprocal activation and deactivation of parasympathetic and sympathetic systems helps to regulate and manage blood pressure
- all automatic
What are some benefits of having antagonistic parasympathetic and sympathetic effects on a given organ?
-helps you regulate and modify bodily functions more effectively
Cardiac cells control heart rate with “antagonistic” autonomic innervation. Heart rate would increase with use of what?
-muscarinic cholinergic antagonist
Potentiation
- increasing effect or power of something
- in neurons: similar to facilitation (decreasing threshold for activation) but effect can linger long after initial actions
What are some emotional and cognitive correlates of fight or flight response? What parts of the brain are activated?
- amygdala: fear/anxiety
- limbic system: regulates emotions; aggression
- prefrontal cortex: hyperalertness
- hypothalamus: stress response (cortisol)
- hypothalamus, amygdala, and limbic system all controlled by adrenal medulla: releases epinephrine and norepinephrine
Muscarine is an agonist at muscarinic cholinergic receptors in peripheral nervous system. What are some effects of eating them and why can it cause death?
- decreased heart rate
- contract bronchial muscles
- stimulates intestines
- bladder contraction
- die because you can’t breathe
Antagonist Effects of Sympathetic and Parasympathetic Influences
- heart rate
- one speeds up and the other slows down
- opposite effects=antagonistic
Complementary Effects of Sympathetic and Parasympathetic Influences
- salivary gland
- both make you salivate but sympathetic has enormous effect while parasympathetic has a trivial effect
Cooperative Effects of Sympathetic and Parasympathetic Influences
- sexual function
- one system does one aspect and the other system does the other
- parasympathetic does erection and sympathetic does ejaculation
Only One Innervation
- adrenal medulla (sympathetic)
- most blood vessels (sympathetic)
- sweat glands
Control of Autonomic Nervous System
- sensory input, medulla, hypothalamus, and limbic system inform parts of ANS on how to react
- certain heart rate, respiratory rate, etc.
- Medulla: has simple influence over cardiac control system but has total control over respiratory control center
Give an example of limbic system influencing autonomic nervous system activity.
-emotions like aggression influence cardiac control system which has autonomic sympathetic influence over heart rate (increases)
Skeletal Muscle Motor Units
- part of somatic nervous system
- each muscle fiber is innervated by motor neuron that branches and when it fires all the branches fire too
- can have large or small effect
Neuromuscular Junction
- in skeletal muscle it is a nicotinic cholinergic receptor and is an ion channel that ACh binds to and allows Na+ in and K+ out
- ACh is destroyed by acetylcholinesterase
What is the effect of auto-immune ACh receptors on the post-synaptic membrane at the neuromuscular junction?
- no action potentials so get weakness of muscle over time
- severe effect is paralysis
What is the effect of botulinum toxin on muscle strength? (Blocks ACh release from the presynaptic nerve). Why is it used to treat tension headaches and wrinkles?
- decreases muscle strength and tension
- blocks excessive muscle action
- weakness because prevents contraction
- basically paralyzes the muscles
- botulism poisoning ends in paralysis of the diaphragm
What is the effect of acetylcholinesterase inhibitors on muscle strength in patients who have lost AChE receptors? Can you explain how this effect happens?
- higher ACh levels which increases muscle strength
- ACh not degraded by AChE
Curare is a poison that binds to the ACh receptor but does not allow that receptor to increase the flux of Na+ and K+ ions. How does curare affect muscle strength?
- Na+ can’t get in so the cell can’t reach threshold which means there is no action potential so there’s no response in muscles
- paralyzed
Sliding Filament Theory
- generate force by sliding together and making cross-bridge formations
- myosin has actin binding sites and when given the chance will bind to the sites on actin and form cross bridges
Crossbridge Formation and Force
- crossbridge that forms involves ATP and conformation change in protein
- bond made between actin and myosin which goes under conformational change that generates force ans shortens it
- amount of force is the number of crossbridges formed
Rigor mortis is defined as the “stiffness that occurs in dead bodies” It is caused by specific effect at cross-bridge level in skeletal muscle. At what stage would the cross-bridge cycle have to stop to create a state of constant tension?
- after the binding of actin and myosin but before conformational change that causes shortening
- there is no ATP to contract to make force to shorten the fiber cause you’re dead
What are we trying to couple together in excitation-contraction coupling? How is it done?
- linking action potentials (membrane voltage charge) with contraction (actin and myosin bonding with ATP in crossbridges; proteins conformational change)
- AP–>NT release–>nicotinic cholinergic receptors–>AP–>T-tubule which allows whole muscle to depolarize at same time
- when AP comes down calcium is released and does real activation of contraction. Ca+ binds to troponin and induces a conformational change and exposes binding sites by pulling tropomyosin off of binding sites
- calcium is what links the AP to contraction through troponin binding
Role of Calcium (detailed)
- lots of Ca2+ outside and less inside
- calcium contained in sarcoplasmic reticulum inside the cell
- to make the muscle contract you have to release calcium ions from SR into the cytosol where there is low calcium.
- when you want to stop contraction use ATP to put it back in the bag
- the AP reaches voltage gated Ca2+ channels on SR that opens the bags and it comes out
Young woman begins a strength exercise program and increases her lean muscle mass by 10%. How much did she change her body’s total amount of myosin, actin, tropomyosin, troponin and Ca2+? Did her blood Ca2+ concentration change?
- myosin, actin, tropomyosin, and troponin increase by 10%
- Ca2+ increases (not quite 10%) in muscle but overall has a trivial Ca2+ increase in the body
- blood Ca2+ levels stay the same
Do you think gain or loss in muscle mass would affect the intramuscular concentration of Ca2+ required for activation of the crossbridge cycle?
- no-same concentration of Ca2+
- want more Ca2+ outside than inside because this gives you increased possibility for things to happen
Studies of patients with chronic fatigue syndrome show that this illness may stem in part from defects in excitation-contraction coupling. Defects in what specific processes could contribute to problems with excitation-contraction coupling?
- tropomyosin won’t move out of way of binding site
- Ca2+ not released from SR
- Ca2+ not binding to troponin
- crossbridges not forming properly
- ATP issue
Duration and Intensity of Exercise
- determine which source of energy you use
- light/easy activity uses fat
- harder activity uses carbohydrates
Maximal Oxygen Uptake
-how much aerobic energy can I produce/how much oxygen can I use
Creatine phosphate supplements would be most effective for increasing work output for what kind of exercise?
-maximal intensity for short duration
Isometric Twitch Contractions
- single stimulus=single contraction for a twitch
- no shortening of muscle/constant length
- ex: trying to lift something that can’t be moved
Isotonic Twitch Contraction
- constant force
- get shortening of muscle
- tension matches mass of weight
Concentric Contraction
-shortening due to sliding filament theory throughout length of muscle
Eccentric Contraction
- resists stretch-form crossbridges and external force pulls it in the opposite direction
- crossbridges being formed in the wrong direction
- lengthening muscle even though generating force
Delayed onset muscle soreness is much greater after eccentric than after concentric work. What are some potential mechanisms for the greater soreness seen after this kind of work?
-break cross-bridges mechanically (not with ATP) as you lengthen them and this seems to be more damaging to the muscle and cause the inflammation
Relationship of Action Potential to Force Generation
-delay is caused by release of Ca2+ and waiting for it to do its thing
Force Summation and Tetanus
- can pack in multiple AP before muscle stops contracting-AP releases Ca2+ and builds up in cytosol
- force rises and eventually comes to a plateau=tetanic
- brings you up to a high and stable force because multiple AP’s happen before contraction stops
Length Tension Relationship
-there is an optimal length for optimal tension
For a heart-which contains muscle fibers arranged in a sphere-changes in fiber length will change what aspect of the shape of the sphere?
- increase length will increases size of heart which changes force of contraction
- influences BP
- bigger=weaker (congestive heart failure)
Motor Units and Recruitment
- stereotyped
- smallest unit fires first and largest comes last
Why do you suppose that training cannot change recruitment order of motor units in skeletal muscle?
- easier to activate smaller motor neurons because of the lower threshold and as you work you way up to higher thresholds the lower ones will be activated
- takes a lot more spatially to get the larger ones to threshold
- this is the size principle
Endurance of Fibers
- smaller have more endurance because you use them every time
- higher endurance means they work slower in regards to respiration
- more oxidative less glycolytic
How do several factors contribute to high fatigue resistance of slow oxidative fibers
- high mitochondria density-more ATP
- high capillary density-brings in oxygen rapidly
- low force generation-don’t need fast contraction
- high myoglobin content-binds to oxygen
Adaptations to Training
-everything fatigues if given chronic load that’s manageable for awhile but small fibers are more resistant to fatigue
Smooth Muscle Units and Filament Arrangement
- single: bladder-all contracts at once
- multi-unit: small intestine-different parts contract at different times
- actin and myosin are thick and thin filaments and can be arranged in many different ways
- often arranged as circle (blood vessels, bronchial tubes) and when it contracts it gets smaller
- tubes to transport air, blood, fluids etc.
Excitation-Contraction Coupling for Smooth Muscle
- different from skeletal in that it has myosin light-chain kinase (MLCK instead of troponin
- all contractions of muscle involve Ca2+
- all have some sort of reticulum to hold onto Ca2+ in cell, in smooth muscle it’s endoplasmic reticulum
- same general principle of activation
Activation of Smooth Muscle
- a lot is spontaneous in action
- AP generates on its own sometimes and sometimes there is no AP but still has contraction
- cyclical membrane leakage of ions that results in the rhythm of contraction–>spontaneous depolarization
A class of drugs called calcium-channel blockers is often used to treat high blood pressure. How do Ca2+ channel blockers affect smooth muscle activity?
- block release from ER (more difficult) or from channel on membrane (more easily affected)
- block certain smooth muscles from functioning
