activation gate

inactivation gate

activation gate:  closed at resting membrane pot. and is rapidly activated in depolarization

inactivation: open at resting potential and closes slowly in response to depolarization

Repolarization reverse the two processes

delayed rectfier

calcium activated Channel

fast, transient channel

M-type channel

K+ Channels

Calcium: activated by depolarization but its voltage sensitivity is a function of intracellular concentration od Ca2+

Fast: activated rapidly by depolarization, almost as rapidly as the Na+ channel, and inactivated rapidly if depolarization is maintained

M-type: activated very slowly by depolarization and deactivated by Ach.

Ca2+ enters the cell during falling phase and opens the K+ channels and deactivates Ca2+ channels.

Na: 8 - 18 pS

K: 4 - 20 pS

 Ca: 1 - 3 pS

4 transmembrane domains

w/ glutamic acid at outer part of openings

lysine and alanine on inner part for selectivity

GA attracts cations and repelling annions

.3x.5nm cations are too bulky to pass through the pore

alpha subunti forms pore

Goldfish tail flip response

 recieves input from sensory neurons via electrical synapses which rapidly depolarize Mauthner's Cell, Depolarization activates motor neurons through chemical synapse.

increased threshold

 lower resistance

fire in sync

all or none

gap junctions allow flow in between cells for ionsand close in response to low pH or high Ca2+ sometimes voltage=unidirectional

consist of a pair of cylinders called hemi-channels that connect the cytoplasm of the 2 cells 1.5nm diameter

each hemi-channel is a connexon made up of connexins which have 4 membrane spaning regions

isn't: Trasmitter is gate

is: Receptor activates GTP binding proteins (G-protein) which in-turn activate a 2nd mesenger cascade (cAMP or diaglycerol) that modulates ion channel activity directly (fast and short) or through serine-threonine proteins (slow and long)

located in the junction folds,  is a network of connective tissue consisting of collagen and glycoproteins, covers the surface of entire muscle

10,000 receptors per square micro meter

Ach diffuses away or it destroyed by AChesterase

Excitatory post-synaptic potential @ 70mv

Amplitude decays away from end-plate by leaking out

formed by Na+ flowing in and K+ flowing out

+mV = K and Na out = net current out = resting current inward

slightly +mV = small Na in, Large K out = net current out = resting current in

0 = Na out and K in=no current

slightly -mV = large Na in, small K out=net in=resting out

resting mV -90 = larger Na in, no K movement= net in=resting out

-100mv = larger Na in, K in, net in, resting out

Conduct unitary current

amplitude is the same but duration is random,

avg per plate is 1ms

four factors

- total number of channels

-probability channel is open (depends on transmitter concentration)

-conductance of an open channel

-driving force on ions

channel open simultaneously but close at different times

Ach bind to the amino terminus on each of the 2 Alpha subunits and opens pore

5 subunits total

alpha-bungarotoxin binds to ACh receptor sites ihibiting it

each subunit has 4 regions M1-M4

M2 region is lines the channel, has 3 rings of negatively charged glutamatefor selectivity for cations

large entrance, narrow pore, large exit

=Voltage gated have 2 seperate channels for na, k that open sequentially

-transmitter gated does both at once and sometimes Ca2+

=voltage gated are Na regenerative, depolarization causes more Na channel to open cause an all or none

- ACh channels varied response depending on concentration on ACh

=blocked by tetrodoxin

-blocked by alpha-bungarotoxin

Action potential in presynaptic neuron causes ACh to be released

ACh diffueses across cleft and binds to nicotinic ACh receptors

Channels open to cations, Na in and K out

influx na produced depolarization called end plate potential which activate voltage gated na channels

AP is made

GABAa: Ionotropic receptor that gates the Cl- channel, blocked by barbituates (phenobarbital + secobarbital) and benzodiazenpine (Valium + Librium)

-5 subunits, Alpha binds both barbituates and benzodiazenpine Beta bind only barbituates

Like ACh channel M1-M4

GABAb: Metabotropic that activates K+ channel

Ihibitory ionotropic receptor for Cl- channels

release in the spinal chord to inhibit antagonist muscles

Grey's Type I

Grey's Type II

Type I: excititory glutaminergic, contact dendritic shaft, larger

Type II: Inhibitory GABAergic, contact cell body

ionotropic receptors: 4 membrane spanning segments, M2 lines pore

-M2 flanked by aspare and glutamate its a nicotinic ACh Receptor = cations

-M2 clusters lysine and arginine GABA or Glycine = anions

Voltage Gated: 

-Na+ and Ca2+ are 1 large subunit with 4 segments

S1-S6 w/ S4 voltage sensor P region between S5-S6 lines pore

L-type - slow inactivation

N-type, P-type - rapid inactivation

mostly NEAR active zone anchored by actin filaments called synapsins made of four proteins (Ia,Ib,IIa,IIb)

proteins restrain vesicles to prevent accidental release, target freed vesciles to active zone, dock vesicles at active zone, allow fusion and exocytosis

Ia and Ib - substrates for both the cAMP-dependent kinase and the ca/calmodulin dependent kinase.

-when not phosphorylated it links the vesicle to actin Ca comes in and phos. releasing it

 Rab3a and rab3b traffic the vessicle to site

site recognition- Receptor proteins on the vesicle called VAMPS & P65 act like donor proteins NSF and SNAP are attachment protein the attach VAMPS &P65 to receptor proteins Syntaxins and Neurexins

release- pores on both membrane form a gap junction that dialates when Ca enters

-brief high frequency AP

potentiation - if postsynaptic potential increases

posttetanic potentiation - when postsynaptic potentials stay increased after the tetanic stimulation for minutes

1) Synthesized within a neuron

2) Present in presynaptic neuron and is release in sufficient amounts to cause AP in post

3) If administered in a drug it mimics the action

4) A specific mechanism exsists for removing it from the synapse

catalysed by choline acetyl transferase

choline derived from diet

acetyl coenzyme A: metabolic pathways

 syntesized in nucleus basalis

 tyrosine -(TH)> L-Dopa -(dopa-decarboxy)>Dopamine -(DBH)> norepinephrine -(PMNT)>epinephrine

Glycine, Glutamate

Glutamate- produced in krebs cycle, made into GABA

GABA - in the CNS, inhibitory, 

Glycine - synthesized from serine, used by inhibitory neurons, 

ATP converts to Adenosine, Adenine, Guanine

-in sympathetic neurons, some muscles, 

autoimmune disease in which the immune system attacks the ACh receptor which eventuaklly weakens the muscle

inhibitors of AChesterase reverse symptoms

-AP on endplate decreases rapidly causing not all NTs to barely above threshold

-T-cells bind and crosslink signaling the breakdown of the receptors

-reversed by neostigmine or edriphonium

-removal of thalamus helps or draining lymph nodes