Neuron Function

Membranes, Potentials, Synapses, and Neurotransmitters

diffusion movement of concentration gradient

high to low

“down concentration gradient"

diffusion overview

rate depends on permeability + concentration gradient

lipids passively diffuse

non-lipids diffuse through pores

variable permeability

CHARGED IONS CANT DIFFUSE

passive transport

free diffusion through pores + ion channels

channel opened by trigger

integral proteins

what impacts free diffusion

size

hydration energy

charge

ion channels selectivity filter

pore diameter

binding site is chemical interaction-sufficient bond strength to offset water molecule loss

passive transport ions through ions channel

Na+ binding allows diffusion

channels are selective (K+ unable to bind/diffuse through Na+ channel)

ion channels can be gaited by

voltage (change creates threshold)

ligands (binding to gates)

light (eye)

mechanical stretch (muscle)

carrier assisted diffusion (passive transport)

binding to integral protein

equal affinity on either side of membrane

movement down concentration gradient + undergoes protein shape change/binding

diffusion rate based on conc. gradient + prevalence of carrier

Competitive + non-competitive inhibition

saturation (carrier-assisted transport)

substance>carrier

competitive inhibition (carrier-assisted diffusion)

similar substance binds + may/may not be transported

binds in channel

multiple solutes trying to enter

non-competitive inhibition (carrier-assisted diffusion)

a binding elsewhere shuts down channel

impacts cell function

Na+/K+ pump (active transport)

direct/primary AT

uphill against conc. gradient

ATP + ATPase binds to pump

ATP provides energy/creates diff affinity on each side

SUPER SLOW

(both pos. charge so inside becomes NEG)

indirect active transport

indirect/secondary AT

uphill against gradient (Na pushed up by ATP, needs more molecules to move)

indirect use of ATP/ATPase

need both molecules to open channel

membrane potentials 3 acting forces

osmotic force

concentration force

electrostatic force

osmotic force (egg experiment)

F of diffusion acting on water

2 fluids w/ diff osmotic conc. + separated by water permeable membrane cause diff. of water towards HIGHER osmotic conc.

imbalance can remain if oppo. by another F (water pressure)

concentration force (gradient/diffusion)

equalize conc. of each particle

selective permeability

conc. F imbalance can remain if opposed by another F (electrostatic)

electrostatic force

only cares ab charge

acts to balance # of pos. + neg. charges

imbalance exists if balance by conc. F (nernst equation)

goes against conc. gradient (same charges repel)

Nernst equation

V = (-60 mV / z) x log (Ci/Co)

v=electrostatic potential across cell membrane

z = valence of ion (K+ = +1)

Ci = ions conc. inside cell

Co = ions conc. outside cell

what does Nernst equation rely on

equilibrium

permeability to only 1 ion

conductance equation

Vm = g(ion1) x V(ion1) + g(ion2) x V(ion2)

proportion of total permeability

How are concentration gradients sustained (electronic potential)

No change in membrane permeability

Down membrane

Initiated at receptor/synapse by influx of ions

Cytoplasm is conductive

Around dendrites + cell body

Not effective signal process

Very fast + dissipates quickly

graded potentials (aka electronic potential)

passively propagated change in membrane potential (down membrane)

NO change in permeability

happens very fast + dissipates quickly

initiated at receptor/synapse by flow of ions

around dendrites/cell body + cytoplasm conductive

depolarization charge direction

less negative

action potentials (perturbation from resting membrane potential)

momentary alt. of membrane permeability (ion channels open)

happens around gaps in myelin + axon hillock

At depolarization: fast Na+, slow K+

All or nothing response

Large density of ion channels

AP depolarizing disturbance can come from

adjacent AP

neurochemical/drugs

artificial electrical stimulus

depolarization resting state + threshold

resting: -75 mV

threshold: -55 mV (all or nothing response)

reach fast for Na+ / slow for K+

where is the highest concentration of voltage gated Na+ channels

right before 1st node of ranvier

axon hillock

action potential process

Na opens first at -55 mV

inactivate gates close at peak AP (around 30 mV) + permeability drops

slow channels (K+) open

doesn’t go to full Nernst potential bc still permeable to other ions

AP propagation

movement of ions during AP cause very small intracellular conc. changes

many APs occur before na+/K+ pump is necessary

AP propagates + myelin creates saltatory conducction

saltatory conduction

voltage jumps from node to node

ions flow through nodes of ranvier

Vm jumps to next node speeding up conduction

synaptic transmissions general attributes

cell-cell comm.

membrane of presynaptic neuron meets w/ postsynaptic neuron

presyn. depolarization open Ca2+ channels (high conc. outside cell)

Ca2+ influx releases NT + diffuses across synaptic cleft

NT binds to postsyn. membrane receptors

ion channels open → post synaptic potential

PSP conduction is graded

types of membrane specialization: pre synaptic cells

release of NT into synaptic cleft

AP arrived + converts to chemical

types of membrane specialization: post synaptic cells

contains receptor channels + enzyme proteins

for NT to bind to ion channels

influx of Ca2+ at presyn. membrane

need 2 Ca2+ cell

• 1 Ca2+ causes release of vesicle from storage in cytoskeleton

• 1 Ca2+binds vesicle to membrane + opening of fusion pore

Type 1 transmitter release

Excititory

depolarizes cell

Happens in dendrites

Type 2 transmitter release

Hyperpolarizes cell (more neg)

Near cell body

Inhibitory

NT action classified through 2 mechanisms

direct

indirect

indirect gating

metabotropic

seconds to minutes

direct gating

ionotropic

fast

postsynaptic response

metabotropic acts to amplify signal

flux of ions through receptor channels create post syn. potential (graded)

inhib/exit depends on NT + receptor

size of potential prop. to amount on NT released

post syn potential summation

each neuron receives constant signals (pre)

ex + inh input cause fluctuating membrane potential

represents integrative capacity of neuron

integrative capacity of neuron

fire or dont fire

decided at axon hillock

• higher conc. of voltage gated channels

• lower threshold for AP

neurotransmitters (NT) life cycle

synthesis

synaptic action

metabolism

NT synthesis

fabrication in presynaptic neuron

NT synaptic action

ability to diffuse through clef + bind to postsynaptic membrane

cells can send NT back to presynaptic neuron to store by carrier

NT metabolism

diffusion, breakdown + reuptake of NT

2 main categories of NT

small molecule NTs

neuropeptides

small molecule NTs examples

acetylcholine

AA’s

biogenic amines ( monoamines)

purines

neuropeptide NTs

large molecule

7 major categories

3-36 aa sequence determines action

colocalized: released at same time as primary NT

glutamate

primary excitatory transmitter (depolarizes/EPSP) in CNS

synth. in neurons

excitatoxicity in brain injury (neurons die)

GABA + glycine

primary inhibitory transmitter in CNS

GABA: primary in brain

glycine: primary in brainstem/cord

GABA receptors permeable to Cl- (oppo direction in early development)

monamines (neuromodulators)

work through indirect gating (amplified + slower RT)

catecholamines

histamine

serotonin

receptors usually metabotropic initiating a 2nd messenger cascade (effects long + slow lasting)

catecholamines

dopamine

norepinephrine

epinephrine

neuropeptides

synth in cell body

large molecules

stored/released from co-localization

eg. opioids + substance P