EPHE 160 exam 1

Body Functions are integrated (pp1)

-parts of the body work together.
-Proper function of 1 part depends on func of a diff part or parts.

Integrated body functions example (pp1)

-Muscle requires o2 provided by erythrocytes in blood that are manufactured in bone marrow.
-Erythrocyte synthesis requires erythropoietin which is secreted by kidneys.
-O2 is extracted from air breathed in by lungs.
-Lung expansion is controlled by the n.s. -Blood is pumped by the

Homeostasis (pp1)

-ability to maintain a relatively constant internal enviro. -Components of internal enviro that are regulated \= temp, volume, composition. -Requires organ systems integration. -Disruption of @ is the basis for disease and death and exercise training responses.

Feedback system (pp1)

-feedback loop is a cycle of events in which a parameter of the internal enviro is monitored, evaluated. changed, remonitored, reevaluated.
-Stimulus (disrupts homeostasis by ^ or decreasing a...) -\> Controlled Variable (that is monitored by...) -\> Receptors-input (that send a.p's or chem signals to a...) -\> Control Centre - output (that receives the input and provides action potentials or chemical signals to) -\> Effectors (that bring about a change or...) -\> Response that alters the controlled variable -\> Return to homeostasis when the response brings the controlled variable back to normal -\> controlled variable -\> etc.

Homeostasis terms (pp1)

-regulated variable.
-set point
-error signal

regulated variable (pp1)

-the aspect which is maintained.
-in relation to homeostasis.
-ex. blood glucose concentration, blood pH, plasma levels of sodium or calcium.

Set Point (pp1)

-expected value of a regulated variable.
-in relation to homeostasis.
-ex. core body temp \= 37 degrees
-ex. blood glucose (sugar) \=100mg/dL.
-ex. blood pH \= 7.4

Error signal (pp1)

-diff b/w the value of the set point and the value of the regulated variable.
-in relation to homeostasis..

negative feedback control of a regulated variable (pp1)

blood glucose normal -\> blood glucose rises; error signal ^ -\> regulatory mechanism activated -\> blood glucose decreases; error signal decreases -\> blood glucose normal.

Photo except the curve goes up not down. and speed is blood glucose

Positive feedback (pp1)

-strengthens or reinforces a change in a controlled variable.

feedforward (pp1)

-events occur in anticipation of a change in a controlled variable.
-ex. altoids at the sound of windows closing

homeostasis requires... (pp1)

signals* to:
-allow components to communicate.

- input signal is from a receptor to an integrating centre.
- output signal is from an integrating centre to an effector.
-signals are chemical messages or are sent via neurons.

Basic divisions of the nervous system (pp2)

-CNS: brain and SC.
-PNS: cranial nerves, spinal nerves, sensory receptors in skin

Divisions of the nervous system (pp2)

-CNS and PNS
-Motor output (away from CNS): somatic ns and autonomic ns.
-Somatic (efferent) \= skeletal muscle.
-Autonomic (efferent) \= sympathetic, parasympathetic, and enteric ns.
-Sympathetic and parasympathetic \= smooth, cardiac muscle, glands.
-Enteric \= smooth muscle of GI tract.

-Sensory input (to CNS): afferent division. somatic senses. special senses

Functions of the nervous system (pp2)

-sensory: sensory receptors detect external or internal stimuli, and relay sensory info to the brain and SC for integration.
-integration: CNS analyzes sensory info, and makes decisions for appropriate responses.
-motor: motor info is conveyed from the CNS thru cranial and spinal nerves of the PNS to appropriate effectors (muscle and glands)

Neurons (pp2)

Individual cells in the nervous system that receive, integrate, and transmit information.

Neuron structure and function (pp2)

-dendrites accept the information from neighbouring neurons
-the signal is then passed along the axon which carries out chemical reactions until it reaches the synapse
-this reaction creates chemical neurotransmitters which activate activity in the next neuron

neuroglia (pp2)

cells that support and protect neurons

Neuroglia CNS (pp2)

-Astrocytes: most numerous. help maintain blood-brain barrier. Maintain extracellular chem enviro. Guide neurons during development. Play role in synapse formation.
-Oligodendrocytes: Form and maintain myelin sheath in CNS.
-Microglia: phagocytes \= removes debris, damaged cells, and phagocytes.
-Ependymal cells: Produce and assist in the circulation of CSF.

Neuroglia PNS (pp2)

Schwann cell: form and maintain myelin sheath of PNS. Participate in PNS axon regeneration.

myelin sheath (pp2)

-the formation of a fatty sheath around the axons of a neuron
-the process by which axons become coated with myelin, a fatty substance that speeds the transmission of nerve impulses from neuron to neuron \= myelination

Functions of the myelin sheath (pp2)

-Electrical insulation \= ^ speed of conduction of a.p's.
-Found in both CNS and PNS \= schwann cell in PNS. Oligodendrocyte in CNS.
-Nodes of ranvier \= gaps in myelination.
-makes up white matter.

Neuron Repair (pp2)

-some neurons can be repaired through the processes of fragmentation, proliferation. elongation.
- plasticity \= ability to change throughout life.
-repair \= regeneration after damage.

Regeneration PNS (pp2)

occurs if:
-cell body is still intact.
- schwann cell remains active.

- schwann cells form regeneration tube. \= guides and stimulates regrowth of the axon.

Regeneration CNS (pp2)

-little to none can occur. possible reasons why \= inhibitory proteins released by neuroglia. Absence of growth stimulating cues. Scar tissue formation.
-CNS damage is permanent.

Functions of the nervous system (pp3)

-Sensory, Integration, and motor

Sensory nervous system function (pp3)

-sensory receptors detect external or internal stimuli, and relay sensory info to the brain and SC for integration.

Integration nervous system function (pp3)

-CNS analyzes sensory info and makes decisions for appropriate responses

motor nervous system function (pp3)

motor info is conveyed from the CNS through cranial and spinal nerves of the PNS to appropriate effectors (muscles and glands)

resting membrane potential of an excitable cell at rest (pp3)

negative on inside of cell, positive on outside. negative near edge, positive near edge. sodium wants to move in and k wants to move out. high to low concentration

ion channels (pp3)

-specialized channels in cell membranes that allow the passage of charged ions across the membrane. b/c the ions are charged, as the move they generate electrical current. Ions \= Na+ and K+

Ion Channels: leak (pp3)

gates randomly alternate b/w open and closed positions

Ion channels: ligand-gated (pp3)

opens or closes in response to a specific ligand (chemical) stimulus.

Ion channels: mechanically-gated (pp3)

opens or closes in response to mechanical stimulation in the form of touch, pressure, tissue stretching, or vibration.

Ion channels: Voltage-gated (pp3)

opens in response to a change in membrane potential (voltage). Eg certain voltage threshold

How do we use ion flow across the plasma membrane of the cell (current) to transmit information? (pp3)

1. graded potentials that communicate info over short distances.
2. Action potentials that communicate info over long distances.

Both result from the opening and closing of gated channels.

Graded potential (pp3)

-a small deviation from resting membrane potential.
-Depolarizing \= makes the membrane less polarized.
-Hyperpolarizing \= makes the mebrane potential more polarized.
-localized current changed cause by opening/closing ligand-gated or mechanically-gated ion channels.
-if strong enough give rise to ap's.
-all receptors, neurotransmitters, etc. cause @'s.

Why are graded potentials important? (pp3)

- they are generated by diff types of receptors to start the feedback cycle: thermal, chemical, pressure.
-they allow neurons to "pass" an electrical signal from one neuron to another.
-we have to have graded potentials in order to start an ap.

Types of ion channels (pp3)

-leak - resting membrane potential.
-ligand-gated - mechanically gated -\> graded potential.

voltage-gated \= ap's

a graded potential can be caused by (pp3):
a) ligand-gated channels
b) mechanically-gated channels
c) voltage-gated channels
d) all of the above
e) only two of a-c

E.
ligand-gated channel and mechanically-gated channel

Action potentials (pp3)

-rapid large changes in the membrane potential from depolarization to a reversal in polarity to repolarization to hyperpolarization.
-all or none and amplitude is always the same.
-used to communicate info over long distances.

How to generate an action potential? (pp3)

-have to open voltage-gated ion channels \= need to hit threshold voltage.

threshold (pp3)

membrane must be depolarized to -55mV (sufficient to open voltage-gated channels)

how do we get to threshold? (pp3)

-need to allow more positive ions in and move negative out.
- a stimulus (graded potential) causes a change in membrane potential that is equal to or larger than the threshold "target".

changes in the membrane potential (pp3)

subthreshold potentials fire but don't cause ap until reach threshold

all or none (pp3)

- the ap resultingfrom stimuli have exactly the same amplitude.
-once threshold is reached membrane events are no longer dependent upon stimulus strength.
-once threshold is reached, voltage-gated channels ALL open this SAME amount of Na+ goes in EVERY time.

drugs and ion channels (pp3)

-local anaesthetics eg novacaine and xylocaine block Na+ channels, preventing the rise of ap's.
-afferent signals of pain cannot reach the brains b/c not creating ap.

action potential propagation (pp3)

- one action does not itself travel along the membrane.
- the local current it produces stimulates an ap on the adjacent part of membrane.
-a Na+ positive feedback loop takes over.
-and so on, and so on, etc.

Triggering and propagating action potential (pp3)

Na+ in cell is high and cause depolarization...

Velocity of action potential propagation (pp3)

depends upon:
-fibre diameter \= large diameter is better b/c faster transition rate, less resistance for charge mvmt
-myelination \= myelinated is faster for conduction b/c need continuous conduction for unmyelinated so more energy. insulation causes pull of Na+ ions from further in -\> na+ moves down and changes membrane potential which helps reach threshold -\> jump from node to node

Conduction velocity (pp3)

the speed at which an action potential is propagated along the length of an axon

if the myelination serves to insulate an axon, decreasing the loss of electrical signal and increasing speed of conduction, then which of the following statements accurately predicts where myelin will have the largest effect? (pp3)
a) Neurons with short axons that relay information of minor importance.
b) Neurons with short axons that relay critical information.
c) Neurons with long axons that relay information of minor importance.
d) Neurons with long axons that relay critical information.

d) Neurons with long axons that relay critical information.
myelin has largest effect in areas of long axons and critical info relaying

how can one tell if action potentials are generated by a threshold or suprathreshold stimuli? (pp3)
a) the suprathreshold will have the largest amplitude
b) threshold stimuli will not always produce an action potential
c) the suprathreshold stimulus will create a higher frequency of action potentials
d) there in no difference in action potentials generated by either type of stimulus

c) the suprathreshold stimulus will create a higher frequency of action potentials.

can tell by looking at the frequency of the aps. higher frequency \= stronger stimulus

Synapse (pp3)

-func associationof a neuron with:
another neuron, effector organs (muscle or gland).
-types: electrical, chemical

neuron to neuron synapse (pp3)

-axodendritic synapse.
-axosomatic synapse
-axoaxonic synapse
-either at post -synaptic neurons dendrites, cell body or axon.
-presynaptic neuron will release neurotransmitter that will aid in communication signal, jump space b/w 2 neurons and continue on with transmission of post synaptic neuron

Axodendritic synapse (pp3)

-presynaptic - dendrite - axon - synsaspe at axon terminal and dendrites of post synaptic neuron \=

Axosomatic synapse (pp 3)

-presynaptic n - soma of cell body

Axoaxonic synapse (pp 3)

synapse from one axon to the post synaptic neuron's axon

anatomy of a synapse (pp3)

- pre syanptic neuron \=synapse moves \= changes potential - opens voltage gated ca channels - ca move into cell - promote release of synaptic vessicles \= dump out their neurotransmitter and release into synaptic cleft.
ligand gated receptor fits neurotransmitter - open channels for na or k movement - help generate graded potential which leads to AP on post synaptic neuron (only if meet threshold) (Threshold determined by amount of neurotransmitter released) - if threshold move synapse further down - have ap go to post synaptic neuron.
enzymes and reuptake molecules that help with clearance of neurotransmitter to reset

post synaptic activation (pp 3)

- a type of graded potential
-ligand gated channels
-neurotransmitter is the ligand
- leads to a postsynaptic potential
- some are excitatory (EPSP)
-some are inhibitory (IPSP)

inhibitory synases (pp 3)

-neurotransmitter binds to receptor
-channels for either k+ or Cl- open.
-if K+ opens: K+ moves out - IPSP
-if Cl- open, either: Cl- moves in - IPSP, or Cl- stabilizes membrane potential.

why do we have inhibitory neurotransmitters? Don't we always want to give rise to an AP on the post-synaptic neuron? (pp 3)

b/c want to be able to modulate things. eg don't always want increase - sometimes need to decrease the odds of a synapse

Neural toxins (pp 3)

-tetanus
-strychnine

-unchecked excitatory pathways lead to convulsions, muscle spasticity and death

Tetanus

-blocks release of GABA and glycine from inhibitory presynaptic inputs of neurons that supply sk.m
-lose ability to have inhibitory effect
-uncontrolled muscle spasms

strychnine

-competes w/ glycine (inhibitory transmitter) at post synaptic receptor site - blocks it - motor nerve fibres in the SC are more easily activated.

Producing an action potential on a post synaptic neuron (pp 3)

-divergence
-convergence
-axon hillock and threshold

Activation of the post synaptic cell (pp 3)

- a single excitatory postsynaptic potential (EPSP) is not enough to cause threshold to be reached.
-AP can only be initiated by combined effects of EPSPs

Divergence and Convergence (pp 3)

- go from 1 neruon to many
-many neurons converge into 1

Divergence (pp 3)

presynaptic neuron synapsing with many diff postsynaptic neuron
eg cochlea, visual

Convergence (pp 3)

a bunch of presynaptic neuron meeting with one spot of post synaptic neurons
eg respiratory centre of brain cell. lots of diff input, one result
eg neuromuscular junctions for movement in contractions

Neural integration (pp 3)

-the summing of input from various synapses at the axon hillock of the postsynaptic neuron to determine whether the neuron will generate ap's
-not just the value of potential but distance of hillock plays a role too (further from hillock \= lower value - even if started off really strong)

summation (pp 3)

-adding effects of graded potentials
-types of summation: temporal and spatial

Temporal Summation (pp 3)

one synapse at a time
-summing of a stimulus that is at one location at diff times.

Photo: when AA (close to each other) \= AP.
only A

Spatial Summation (pp 3)

several diff synapses at same time.
sum summation of a stimulus that is across a \# of diff locations that is coming in at exact same time.

photo\= a (EPSP), b (EPSP, and c IPSP) firing. come in at exact same time. A + B stimulated at same moment \= reach threshold \= AP.
If try to combine A + C they cancel each other out - still summation just no net outcome eg no movement

EPSPs and IPSPs/ postsynaptic neuron (pp 3)

not every EPSP causes ap.
-can sometimes take a lot to get to threshold
-IPSP + EPSP \= stay the same.
-temporal and spatial summation happen simultaneously to create an ap

Assume the potentials from the following combinations of dendrites reach the axon hillock/trigger zone at the same time. Which combination will have the greatest chance of generating an action potential? (pp 3)

A) 1, 2, 4
B) 2, 3, 4
C) 3, 4, 5
*D) 1, 4, 5
(photo in slides)

a \= 2 IPSP and 1 Epsp
b \= 2 IPSP and 1 epsp (far away from tigger zone)
c \= 2 Epsp and 1 Ipsp
d \= 2 epsp (closer to trigger zone than in c) and 1 ipsp

A scientist wants to study the effects of summation on graded potentials. Her assistant applies the stimuli, but there is no apparent result. Compose a situation that would explain these results. (pp 3)

A) The stimuli were given, but they did not reach threshold. (doesn't explain why there was no result)

B) The stimuli were given too soon after a trial run and the membrane was still in a refractory period.

C) The stimuli caused a hyperpolarization, but graded potentials are only depolarizing. (graded potentials can be depolarizing or hyperpolarizing)

*D) Two stimuli, equal in amplitude, but opposite in polarity were given and when summed they cancelled each other out.

presynaptic modulation mechanisms (pp 3)

-availability of neurotransmitter (amt of neurotransmitter results how many ligand gated channels on post synaptic side)
-[Ca++] (if change intracellular concentration of Ca - see change neurotransmitter release)
- drugs and disease
-presynaptic neuron only

Presynaptic facilitation (pp 3)

photo -
e isn't interfaced. only augments c so working together. E will c to increase neurotranmitter release \= presynaptic facilitation. also form of spatial summation b/c come in at same time but diff spaces/neurons coming in.
C and d \= graded potential
e \= not voltage change
c + e \= faciliation which will drive it to its treshold

Presynaptic inhibition

similar to presynaptic facilitation but stops what is happening (not positive effect).
(photo in slides)
f + g \= reach threshold b/c both EPSP
F+g+h \= f and h cancel each other out and only left with g.

postsynaptic mechanisms (pp 3)

-many types of receptors for each type of neurotransmitter eg acetycholine, epinephrine
-receptor desensitization eg insulin, cocaine
-electrical state of postsynaptic membrane
-drugs and disease

drugs and synapses (pp 3)

-most nervous system drugs work on synapses
- can bind to receptor and cause similar action to neurotransmitter -\> agonist
-can bind to receptor and block it -\> antagonists
-mostwill take effect in areas with synapses b/c that's the most vulnerable part of NS - no need to travel down synapse.
agonist\= similar action
atagonist \= prevents action/opposite

cocaine (pp 3)

-blocks reuptake of dopamine:
-binds w/ the dopamine reuptake transporter
-dopamine remains in synaptic cleft longer than usual and continue to interact with postsynaptic receptor sites -\> prolonged activation of neural pathways

-emotional responses (especially pleasure)
-cocaine 'locks on' in the neural pleasure pathway
-constant dopamine

cocaine is addictive (pp 3)

-Causes long-term molecular adaptations of the involved neurons -\> cannot transmit normally across synapses w/out higher doses of the drug
-Postsynaptic cells become accustomed to high levels of stimulation...they become 'hooked' or 'needy' :
◦ Desensitization of receptors
◦ User steadily increases dosage to get same 'high'
- can take a year to return to same sensitization

Parkinson's disease (pp 3)

-Development and progression of Lewy bodies (enteric system & olfactory bulb)
-Deficiency of dopamine in the basal nuclei (region of the brain controlling complex movements)
-Treatment is admin of the dopamine precursor levodopa (L-dopa) :
◦ Reduces symptoms
- l-dopa crosses blood brain barrier and converted into dopamine - helps with complex mvmt and maintain same lvl of dopamine in the body.

neurotransmitters (pp 3)

-chemical messengers
-Transmit a message from a nerve cell across a synapse to:
◦ Another nerve cell
◦ A muscle cell
◦ A gland cell

Cholinergic fibres (pp 3)

-present in both the CNS and PNS
- Release acetylcholine (ACh)
-Cholinergic system in brain plays major role in attention, learning, and memory
-alzheimer's disease -\> degeneration of these neurons: confusion, mem loss, language decline, etc.

Acetylcholine (pp 3)

-Major transmitter in CNS & PNS -Synthesized from acetyl CoA & choline -Packaged & stored in vesicles for release
-Two types of receptors for ACh:
◦ Nicotinic (nicotine is an agonist)
◦ Muscarinic (muscarine is an agonist)
-Short-lived response -\> broken down by acetylcholinesterase
-release for when wanted, broken down once have response so you don't have continued stimulation

Catecholamines (pp 3)

-Cell bodies lie in the brain stem
-Axons branch extensively & go to all parts of the brain & spinal cord
-Play essential role in: ◦ States of consciousness
◦ Mood
◦ Motivation
◦ Directed attention

catecholamine biosynthetic pathway (pp 3)

they are all very closely related.

Norepinephrine (pp 3)

-Found in the CNS & at neuromuscular junction between nerves & smooth muscle in autonomic nervous system. -Released by: adrenergic fibers
◦ Awakening from sleep
◦ Attention
◦ Mood regulation -Two major classes of adrenergic receptors ◦ alpha and beta receptors
◦ Influenced by different drugs -Amphetamine's promote the release of NE

Dopamine (pp 3)

-Neurons present in the brain (substantia nigra & ventral tegmental area of midbrain)
-Receptors -\> can be excitatory or inhibitory
-Involved in generating emotional responses
◦ Schizophrenia -\> linked to excess dopamine :
◦ Inappropriate or absent emotions, delusions, distortion of reality etc.
-Plays a role in addictive behaviours & pleasurable experiences.

ADHD (pp 3)

-Result of neurotransmitter deficiencies :
◦ Norepinephrine and dopamine
-Decreased blood flow and lower level of electrical activity in the frontal lobes (prefrontal cortex) :
◦ Solve problems, plan ahead, understand behaviour of others and control impulses
-Lower glucose metabolism in the areas of the brain that control attention and movement

How ADHD medication works (pp 3)

-Block reuptake of neurotransmitter by presynaptic neuron
◦ Stays in synaptic cleft longer
◦ More opportunity to bind to receptors on post synaptic neuron
-Considered a 'stimulant' drug because it increases the exposure of the post synaptic neuron to the neurotransmitter
◦ How would this effect EPSPs? \= increase EPSP b/c ligand gated chanels -\> open channels which increases graded potentials -\> allow for more channel to open \= increases graded potential.

Why does caffeine help? (pp 3)

-neurons produce adenosine
-high levels of adenosine make us tired
-adenosine restricts the release of dopamine
-caff is similar structure to adenosine so can act as an inhibitor
-caff blocks adenosine receptors (A1) so dopamine will continue to be released - allows dopamine to continue to be released - open dopamine gates.
for ADHD:
-already deficient in dopamine
-so taking caffeine increases levels of dopamine in the body.
-calms body - finds normal level of dopamine

Epinephrine (pp 3)

-Released from some neurons in CNS -Better known as a hormone
-Also binds to a & ß receptors

histamine (pp 3)

-CNS neurotransmitter -More commonly known for:
◦ paracrine actions (local increases in blood flow)
◦ neuromodulation (control of the release of other neurotransmitters)
-Main location :
◦ Hypothalamus
◦ Control of sleep-wake cycle (promotes arousal - ↓'s GABA & ↑'s epi and norepi levels)

Serotonin (pp 3)

-Synthesized from tryptophan
-Has at least 16 different receptor types
-Has excitatory effect on pathways involved in muscle control -Highest serotonin activity seen during alert wakefulness -Also has important functions in regulation of food intake & other homeostatic mechanisms

Glutamate and Asparate (pp 3)

-Excitatory amino acids
-Implicated in epilepsy, Parkinson's & Alzheimer' s -Damage to their receptors also follow strokes, brain trauma & brain damage due to low O2

GABA (gamma-aminobutyric acid) (pp 3)

-Inhibitory neurotransmitter
-3 types of receptors (GABA A, GABA B, GABA C) -\> open Cl- or K+ channels
-Cl- goes into cell
-K+ goes out of cell.
-driving membrane potential to more negative number, decreasing the chance of a graded potential reaching threshold
-Agents that enhance activity of GABA synapses depress CNS activity
◦ Sleeping pills
◦ Anti-anxiety medication (Valium) \= increase duration of opening Cl- channels
◦ Alcohol -\> enhances activity of GABA A receptors \= overall inhibition of the NS
-Taking a combo of any of the above is dangerous as all interact at the same receptor....synergistic effect.