Slide Deck 3 - Nervous System

central nervous system

brain + spinal cord

peripheral nervous system

cranial nerves, spinal nerves, sensory organs

sensory organs

eyes, nose, tongue, ears, skin

neurons

structural and functional units

general neuron functions

a. Respond to stimuli
b. Generate and conduct electrochemical impulses
c. Release chemical regulators
d. Learning, memory, and control of muscles and glands

sensory nervous

receptors to spinal cord

somatic motor neuron

spinal cord to skeletal muscles

autonomic motor neurons

spinal cord to autonomic ganglion to smooth muscle, cardiac muscle, gland

nerve classifications

nerves and tract

nerves

axon bundle outside CNS; sensory and motor neurons

tract

axon bundle inside CNS

membrane potential (movement)

potential gradient (ion conc.) for ions to passively move in one direction

membrane potential attraction of charges

opposite charges attract

polarized

inside more negative than outside

neuron resting MP

-70mV

depolarization what is happening

membrane potential increases (more positive)

depolarization mechanism

positive ions enter cell (usually Na+)

repolarization what is happening

membrane potential decreases (more negative)

repolarization mechanism

pos ions leave cell (usually K+) or neg ions (Cl-) enter cell

depolarization excite or inhibit

excitatory

repolarization excite or inhibit

inhibitory

what changes membrane potential

flow of ions

oscilloscope

test measuring voltage inside and outside of cell

voltage gated Na+ channels (open, gradient, equilibrium, deactivation)

open: MP reaches -55mV (threshold)

electrochemical gradient: Na+ rushes in

MP climbs towards Na+ equilibrium potention

+30mV channels deactivate

depolarization steps

Threshold (−55mV) → voltage-gated Na+ channels open → Na+ rushes in → cell depolarizes, more Na+ channels open → more Na+ enters

depolarization (feedback loop and rapid reversal)

positive feedback loop

rapid reversal of MP: -70mV to +30mV

voltage gated K+ channels (opening, gradient, return)

~+30mV voltage-gated K+ channels open

electrochemical gradient: K+ rushes out

return to RMP

repolarization steps

+30mV → Na+ channels close → K+ channels open → K+ rushes out → cell repolarizes → more K+ channels open

repolarization feedback loop

positive feedback loop

hyperpolarization (reestablishment, mV)

a. Repol overshoots RMP to −85mV.
b. Na+/K+ pumps quickly reestablish RMP

all-or-none law (threshold, mV, duration)

a. Threshold = AP.
b. AP will always reach +30mV.
c. AP duration always same.

how does stimulus reach threshold

signal from another neuron, previous position from another neuron

what stimulus allows sodium channels to open

threshold → -55mV

all-or-none law stimuli

no matter strength of stimuli, action potential will always have the same amplitude

why is there no action potential when there is an extremely weak stimulus

did not reach threshold

stimulus intensity and AP

does not determine amplitude, duration, or magnitude of AP

what can stimulus intensity impact

frequency modulated of ap

recruitment of added neurons

refractory period limits

does not allow for another action potential to occur

absolute refractory period (Cause, what is happening)

beginning of AP, depolarization and repolarization

due to inactivated Na+ channels

relative refractory period

due to continued outward diffusion of K+

reestablishment of resting potential

only a strong stimulus can cause AP at this time

when membrane potential becomes more positive due to Na+ rushing into the cell, what is occuring?

depolarization

impulse

action potential

conduction of nerve impulses

action potential begins (depolarization, repolarization, resting potential)

what does stimulus do

causes graded potential and ligand gated cation channels open

what happens once threshold is reached

another graded potential reaches threshold

V-gated Na+ channels open and Na+ rushes in, depolarization occurs

what happens as depolarization comes to an end

V-gated K+ channels begin to open, V-gated Na+ channels begin to close

what happens after depolarization

repolarization begins

what happens after repolarization starts

V-gated Na+ closed, V-gated K+ open → K+ rushes out

what happens after threshold is reached after repolarization

V-gated K+ channels closing and the rush of K+ out slows down

hyperpolarization

all K+ leak channels open and some V-gated K+ channels still open

what happens after hyperpolarization

All V-gated K+ closed

inner vs outer membrane in resting potential

outside → more positive

inside → more negative

inner vs outer membrane in depolarization

outside → negative

inside → positive

inner vs outer membrane in repolarization

outside → positive

inside → negative

what are demyelinating diseases

myelin sheaths are attacked by the immune system

examples of demyelinating diseases

guillain-barre syndrome

multiple sclerosis

regeneration of cut neuron in PNS

distal nerve fiber degenerates and is phagocytosed, proximal end of injured nerve fiber regenerating into tube of schwann cells

growth → former connection reestablished

synapse

functional connection between neuron and cell

CNS synapse

second cell another neuron

PNS synapse

second cell muscle or gland → neuromuscular junctions

types of presynaptic neuron signals

dendrite (axodendritic)

cell body (axosomatic)

axon (axoaxonic)

What are the types of synapses, common direction, and common type

common type: axodendritic

1 direction

synapses are: electrical and chemical

what are electrical synapses also known as

gap junctions

what are gap junctions

span membranes between cells

what do gap junctions do and where are they found

pass ions and molecules

found in : smooth and cardiac muscle; brain

what do chemical synapses do and what are they made of

synaptic clefts (space between cells)

release neurotransmitter from axon terminal

synaptic cleft size and proximity

synaptic cleft is small

pre and post synaptic cells are held closely by cell adhesion molecules

release of neurotransmitter process

1. action potentials reach axon terminals

2. voltage-gated Ca2+ channels open

3. Ca2+ binds to sensor protein in cytoplasm

4. Ca2+ protein complex stimulates fusion and exocytosis of neurotransmitter

main actions of a neurotransmitter

diffusing across synapse → binding to a specific receptor protein

graded potential

neurotransmitter diffusing and binding (results and what is the neurotransmitter in this case)

neurotransmitter becomes ligand

results in opening of chemically regulated ion channels (called ligand-gates)

graded potential

ligan regulated gates open → MP changes depending on which ion channel is open

What graded potential channels are there

Na+ or Ca2+

OR K+ or Cl-

Na+ or Ca2+ channels open

graded depolarization called an excitatory postsynaptic potential (EPSP)

K+ or Cl- channels open

graded hyperpolarization called inhibitory postsynaptic potential (IPSP)

How is it decided whether or not an action potential occurs

summation of EPSP or IPSP at axon hillock determines whether AP occurs

EPSP roles

move MP closer to threshold; may produce AP

IPSP roles

move MP farther from threshold (no impulse produced)

presynaptic neuron parts

terminal boutons

terminal boutons functions

action potential conducted by axon → opens voltage-gated Ca2+ channels → release of excitatory neurotransmitter

parts of postsynaptic neuron

dendrite and cell bodies, axon initial segment, axon

dendrite and cell bodies steps

opens chemically ligand gated channels → inward diffusion of Na+ causes depolarization (EPSP) → localized decremental conduction of EPSP

axon intial segment

opens voltage-gated Na+ then K+ channels

axon function

conduction of axon potential

how does synaptic integration take place

via neural pathways

divergence of neural pathways

collateral branches form synapses with several postsynaptic neurons

convergence of neural pathways

Several presynaptic neurons can synapse on one postsynaptic neuron

voltage gated ion channel phases

closed - at resting membrane potential

open - by depolarization (AP)

inactivated - during refractory period

how are chemical synapses different than electrical synapses

chemical synapses are more common and complex

more detail about the chemical synapses

neurotransmitter goes across the cleft, binding to the muscle cell

what is summation and what can it do

summation is the combination of graded potentials and they can add EPSPs

what leads to AP or no AP, graded depolarization or repolarization

depolarization: strong EPSPs lead to AP, but if they’re weak or counteracted by IPSPs, nothing will happen

spatial summation

multiple synaptic neurons converge into one, release of neurotransmitters

temporal summation

successive release of neurotransmitter from one presynaptic neuron only

what can cause an IPSP

inhibitory neurotransmitter from neuron

what can cause an epsp

excitatory neurotransmitter from neuron

neuromuscular junction

connection point between a neuron and a muscular cell

where does depolarization occur

down the nodes of ranvier

what direction does an action potential move on a neuron

down the axon away from the cell body

all-or-nothing principle of action potentials

if we send something down an axon, it will reach the terminal

what connects gap junctions

neurotransmitters and electrical impulses