neurophysiology

Question 1

2 types of electrical signals b/t neurons

Answer 1

action potentials - travel long distances

graded potentials local membrane changes

Question 2

Segments of a neuron

Answer 2

• Cell body = receptive segment–> binds neurotransmitters to create graded potentials
• Axon Hillock = initial segment - summation of graded potentials and initiation of action potential
• axon = conductive segment - propagation of action potential
• axon terminal = transmissive segment - AP causes release of neurotransmitters

Question 3

Types of Ion Channels

Answer 3

• Leakage = always open -> more K+ ones than Na+ ones
• Ligand gated = open and close in response to stimulus (results in neuron excitability)
• voltage gated = respond to change in membrane potential
• mechanically gated = respond to mechanical vibration or pressure

Question 4

RMP

• what is the #
• where’s + vs -

Answer 4

• the rmp is -70mV
• exists bc extracellular fluid is rich with Na+ and Cl- and inside is rich with K+, organic phosphate and AAs
• inward flow of Na+ can’t keep up with outward flow of K+
• Na+/K+ pump removes Na+ as fast in leaks in

Question 5

Graded potentials

Answer 5

• small deviations from -70mV
• vary in amplitude depending on strength of stimulus
• lovalized
• occur most often in dendrites and cell body

Question 6

2 types of graded potentials

Answer 6

1. EPSP
   - opens Na+ and K+ chem-gated channels
   - Na+ influx > K+ efflux
   - depolarization
2. IPSP
   - Neurotransmitter binding causes hyperpolarization
   - opens K and/or Cl chem-gated channels
   - K efflux and/or Cl influx

Question 7

Generation of APs

Answer 7

voltage gated na and k channels open in sequence

Question 8

all or none principle

Answer 8

if stimulus reaches threshold the ap is always the same –> a stronger stimulus won’t cause a larger impulse

Question 9

Depolarizing phase

Answer 9

• chem or mech stimulus causes graded potential to reach at least -55mV
• voltage gated na channels open and na enters cell
• Resting membrane: inactivation gate of na channel is open and activation gate is closed
• when -55mV is reached, both open
• inactivation gate closes again really fast–> 20,000 Na get in

-positive feedback process

Question 10

Repolarizing Phase

Answer 10

• When -55mV is reached, K channels open, but do it really slow
• K finally open once Na have already closed
• K outflow causes repolarization and often hyperpolarization to -90mV
• k channels close and rmp goes to -70mV

Question 11

Refractory period

Answer 11

• period when neuron can’t generate another AP
• absolute refractory = even strong stimulus won’t do anything –> inactivated Na channels have to go back to resting state first
• relative refractory period = a suprathrshold stimulus will start and AP –> k channels are still open, but Na channels have closed

Question 12

continuous vs saltatory conductions

Answer 12

continuous = step-by-step depolarization of each portion of the length of the axolemms

Saltatory = depolarization at nodes of ranvier where there’s high density of voltage gated channels –> current carried by ions flows through extracellular fluid from node to node

Question 13

Factors that affect speed of propagation

Answer 13

1. amount of myelination : more myelin = faster
2. axon diameter: bigger diameter = faster
3. temp: warmer = faster

NOT related to strength of stimulus

Question 14

fiber types, biggest to smallest

Answer 14

A fibers = 5-20 microns and 130 m/s –> myelinated somatic sensory and motor

B fibers = 2-3 microns and 15 m/s –> myelinated visceral sensory and autonomic preganglionic

C fibers = 0.5 - 1.5 microns and 2 m/s –> unmyelinated sensory and autonomic motor

Question 15

2 types of synapse

Answer 15

1. electrical = fast, 2-way, ionic current goes to next cell through gap junction
2. chemical= 1 way info transfer from presynaptic to postsynaptic neuron (axodendritic, axosomatic, and axoaxonic)

Question 16

chemical synapse

Answer 16

• AP reaches end bulb and voltage gated ca channels open
• ca influx triggers release of neurotransmiters
• neurotransmiters cross synaptic cleft and bind to ligand gated receptors (more neurotransmitters= bigger change in postsynaptic cell)
• synaptic delay = 0.5 msec

Question 17

neurotransmitters

Answer 17

• can be excitatory and inhibitory –> same one can be both depending on location
• acetylcholine, glutamate, aspartate, gamma aminobutyric acid (GABA), glycie, norepinephrine, epinephrine, dopamine

Question 18

Small molecule neurotransmiters

Answer 18

Ach = released by many PNS neurons and some CNS –> exitatory on NMJ, but inhibitory on others –> inactivated by AchE

AAs = glutamate= released by almost all excitatory neurons in brain --> inactivated by glutamate specific transporters
-GABA = inhibiting neurotransmitter for 1/3 of all brain synapses (valium enhances GABA activity)

Question 19

Ionotropic and Metabotropic receptors

Answer 19

• Ionotropic = ligand gated (channel-linked)

- Metabotropic = 2nd messenger protein (G prot linked)

Question 20

G-prot linked receptor

Answer 20

-neurotrans binds to it, activating G protein–> G prot controls production of 2nd messenger (cAMP/cGMP)–> 2nd messenger open/close channels, activate kinases, phosphorylate channel prots, or activate genes to induce prot. synth

• responses= indirect, complex, slow and prolonged
• involves transmembrane prot. complexes
• cause widespread metabolic change

Question 21

channel linked receptor

Answer 21

• ligand gated channel
• action is immediate and brief
• Excitatory receptors = channels for small cations (influx contributes to depolarization)
• Inhibitory receptors allow influx that causes hyperpolarization
• e.g. ach and aa

Question 22

Removal of neurotransmitter

Answer 22

1. diffusion = move down conc. gradient
2. enzyatic degradation = AchE
3. Uptake by neurons or glia cells = neurotransmitter transporters (prozac= seratonin reuptake inhibitor)

Question 23

Summation

Answer 23

• if several presynaptic end bulbs release neurotransmitters at same time, combined effect may generate a nerve impulse due to summation
• may be spatial or temporal

Question 24

spatial summation

Answer 24

multiple axon terminals release neurotransmitters to one neuron
-effects are added

Question 25

temporal summation

Answer 25

presynaptic neuron releases neurotransmitters in rapid succession, so the effects pile up on top of themselves

Question 26

results of summation

Answer 26

Excitatory > inhibitory but < threshhold = facilitation excitatory > inhibitory and threshhold = AP inhibitory > excitatory = Inhhibition

Question 27

Modifications of neurotransmitters

Answer 27

- Agonists = enhance the effects | - Antagonist = blocks its action

Question 28

types of neural circuits

Answer 28

- diverging - convergins - reverberating - parallel after-discharge

Question 29

regeneration/ repair

Answer 29

- limited ability for repair --> PNS can repair damaged dendrites or axons, but CNS can't repair stuff - Plasticity is maintained, though --> new dentrites/ proteins and changes in synaptic contacts

Question 30

Repair in PNS

Answer 30

- Damage causes chromatolysis = swelling of cell body (peaks 10-20 days aft injury) - Wallerian degeneration of distal portion of neuron days 3-5 - retrograde degeneration of proximal portion to first neurofibril node - Regeneration after chromatolysis = synthesis of RNA and proteins favoring rebuiding of axon (several months) --> schwann cell/neurolemma on each side of injury repairs tube and axonal buds grow down the tube

Question 31

requirements for PNS repair

Answer 31

- no damage to cell body - schwann cells remain active and form tube - scar tissue doesn't form too fast

Question 32

Neurogenesis in CNS

Answer 32

- formation of new neurons from stem cells doesn't happen - no neurogenesis in CNS - This is bc neuroglial cells inhibit it, no growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue