neurobio exam 1

What even is the example of the zebra fish?

that the nervous system (NS) react rapidly to sensory stimuli. The fish responds to pulse in water quickly—>escape behavior—> speed is a crucial evolutionary selection

what are channels

aqueous pore that allows specific solutes to pass

what are transporters

2 separate gates that open/close, allowing movement from one side to another

which is faster, channels or transporters?

channels faster

what do channels and transporters support?

support net movement in one direction across the membrane

what is electrochemical gradient

combo of both electrical and chemical gradient, determines direction and magnitude of net solute movements

what is the chemical gradient and what does it determine

a difference in the [ ] of a chemical substance (like an ion, molecule, or nutrient) between two areas. Determines the direction of ion movement (H—>L [ ])

what is the electrical gradient

difference in electrical potential across the membrane

what is passive transport

solutes down their chemical gradient, req no external energy

what is active transport

against electrochem gradient (L—>H), using external energy

what if chem gradient alone

no membrane potential

what if both chem + e- gradient

driving ion force in same direction larger magnitude in driving force

what if chem grad + e- grad in opp directions

driving ion movement in opp directions, lowest magnitude of DF

Active transport (AT) type 1

ATP-driven pump where transporter is ATPase, chem E from ATP drives

AT type 2

light-driven pumps, Light E derived from photon absorption

AT type 3- Coupled transporters

symporter moves solutes in same direction, antiporter moves solutes in opp directions

nernst eq

calculates the cell potential (or electrode potential) of an electrochemical reaction under non-standard condition

calculates the membrane potential of a cell by taking into account the concentrations and relative permeabilities of multiple ions

transporter Na-K ATPases do what

pump Na out and K in against gradient

what is Ek

equilibrium potential is when electrical and chemical forces balance out so net net K flow. (-) charge increases electrical potential differences, stops K diffusion because K is (+)

What is driving force?

push ions in/out. equal to the difference between membrane potential (MP) and equil potential (Ek)

in electrical circuit what is a resistor (R)

opposes passage of e- current, produces a voltage across it’s 2 terminals when current flows thru

± on circuit

battery maintains voltage (electrical potential difference) across 2 terminals

what is capacitor

A capacitor is a device that stores electrical energy by holding opposing charges on two close surfaces separated by an insulator

what does I represent

current: flow of e- charge per unit time that passes thru resistor

in the cell what does the resistor represent

Cell Membrane. stores charge, keeping (+)/(-) ions separated on either side of cell wall

what does battery represent in the cell (E)

Ion concentration gradient, drives ion flow

in the cell what does the current represent

stream of ions, actial flow of charged ions crossing the membrane

Ohms law

I= V/ R. V is voltage across resistor, R is how hard it is for current to pass

what would happen if Resistance increases

Current decreases

what is the formula for conductance

g= I/R. measure of a resistor, the inverse of resistance. A good conductor decreases resistance

I = V x g

how easy current passes increased conductance = increased current

what da lipid bilayer do

its an insulator, a resistor w/ infinite resistance, no e- current thru

what happens when you have 2 resistors connected in a series

the current passing thru both is the same. V is the sum of V1 and V2, same for resistance, so when 2 1/g= 1/gi +1/g2: conductance decreases

what is the time constant

t= RC

time constant

gradually increase to approack max value of I_t. I_c is the exponential decay, witgh t equal to the product RC. V changes simalrly to I_R

what does conductance represent

how easily it si for ions to flow across Pm but this depends on the permeability + presence of ions

I = gX ( Vm - EX)

( Vm - EX) is the driving force. I is a product of conductance and driving force

in these circuits why is C_m (+)

because the equil of K is - inside

intracellular circuits

only permeable to K, has 2 paths, membrane capacitance and K⁺

time constant and circuits

is current flow thru R + C changes over time

what happens when circuit switched on

transient current charges capacitor until voltage across is the same as voltage across from the battery

what is the length constant eq

Experiment where you have a stim electrode, recording electrode a, b, c

t₁ gradually depolarized @ beginning of current pulse. Membrane potential changes are gradual, magnitude and speed of MP changes decay across distance

what if you have a smaller t

faster membrane potential changes. Becuase of capacitance e- signals evolve over time

extracellular circuit series

L_i magnitude decreases because of the leaky transmembrane current (i_m)

what happens to L constant when you decrease diameter (d)

Diameter and resistande are related in a forward direction. SO when diameter increases, resistance decreases

what happens if the length constant is longer

further distance equals decay of signals

what happens if you decrease R_m

more current flow down axial path so L with increase. R_I decr diamter= incr current = L

what are the key properties of neurons

T for the temporal spread of a signal, and L for attenuation across distance

what type of experiment is it if you have mV in Y axis and time on X

current clamps. controls (or "clamps") the electrical current injected into the cell. This current can be kept at zero (to observe natural resting state activity) or injected in specific pulses to stimulate the cell.

what happens in current clamp exp

use stim electrode to inject current w/ varying magnitude. Start iwth (-) inward current to hyperpolarize. Magnitude changes in MP proportional to mag of (-) current opposite is depolarization.

what are Na-K ATPases

they maintain [ ] of Na/K + resting potential by counteracting leak, against chemical gradient. reach treshold for stimulus

how are APs initiated by Depolar-induced inward flow of Na

If extracellular [Na] is reduced, based on nerst eq, that magnitude of AP would decrease with decreased external [Na] because depolarization could induce membrane permeability to Na—> influx—> depolar

what does the peak of AP show

membrane permable to Na @ peak inward flow that is responsible for rising phase. MP during rising phase of AP exceeded ) so AP not caused by transient breakdown of membrane

the green line increases once you add Na back in, the blue line is reduced when Na reduced. Basically tested the rising phase of AP is caused by Na+ influx

what is voltage clamp experiments

to measure ion flow in response to voltage changes. Compares intracellar MP with command voltage that is set.

what happens when feedback current is injected

when back into oscillator, rapidly changes intracel MP to the value of command ion flow change measure by how much current must be injected to keep MP @ certain point. This eliminated capacitive current (current that charges membrane in response to V)

the green initial inward current and then increase, the red is deducted Na current. Depolarization also increases K conductange by laggs behind NA. both depend on MP—>ion channels selectively permeable. conductance incr when axon depolar, now VGion channels becuase conductances change as a function of MP

Sequence of Na/ K conductance accounting for action potentials

1. V-gated Na channels activate, depolarization @ rising phase, Na down echem gradient

2. V-gated K channels activate during falling phase —>repolar. becuase increased K efflux

3. V-gated Na channels inactivate during falling phase

4. V-gated K channels deactivate. Na efflux > K = AP

what does all or none mean for APs

only after treshold constant waveform, shape determined by timing of Na/K conductance changes

what does regenerative mean for AP

Propogate w/o attenuation in amplitude. The rising phase depolarization that spreads down and brings adjacent region to treshold

what does unidirectional refractory period mean

Actoin potential, while depolarization is spread to other regions. delayed activation of K and inactivation of Na combine for refractory period, time when no ap appeared

Action potentials propagate rapidly with larger diameters and myelination why

Larger diameter = lower axial resistance = larger proportion of current moving forward, increase diameter = increase in length= further depolariszation at supratreshold to produce next AP. Myelin provides low capacitance for instant V and high resistance to prevent large current leakage

what does increase in Rm do

also increases t required to charge MP = slower AP—> compensate by dec Cm, membrane capacitance (myelination)

what does patch clamp do

form high resistance seal with smaller patch, clamps voltage, correspond for extracellular

what does TTX do

blocks VGNa channels

what does TEA do

selectively blocks VGK channels

what does the inward current represent in the patch clamp recordings

represents Na channels opening bc (+) Na flow inside

what does cloning of genes do

cloning genes that encode ion channels allows their structure function relationship to be studied

ball and chain model

voltage gated na channel inactivation, depolarization opens channel at same time moves AA so that inner poer more - , binding site for ball (+charge)

how is neurotransmitter release controlled at the presynaptic terminal

AP at presyn terminal triggers NT release

what does the ionophoresis experiment do

you inject current that depolarized motor axon and then apply positive current that deives + ACh out of th epipetter into the surface close to NMJ. The point is to measure depolarization of muscle fiber in response to nerve stim or ACh ionophoresis

what did the ionophoresis experiment show

for nerve stimulation, transient depolar is EEP, ionophoresis mimics motor nerve stim. when use TTX block VGNa channels but in ACh ionophoresis evokes EPP even when AP blocked—> AP in motor neurons is to trigger ACh release bind ACh to muscle membrane to cause depolarization in form of EPP

NT released in discrete packets

The experiment had low Ca activation and it sometimes produced depolarization (spontaneous). lower [Ca] reduced frequency of EPP but did not dec amplitude. shows that EPPs under normal conditions caused by many mEPPs—> NT released in uniform size

How does NT release @ presyn terminal occur

when a single presyn vesicle fuses with the PM—> dump NT content into the synaptic cleft and producing depolarization in the cell

How is NT release controlled at the presyn terminal: Ca²⁺ entry into presyn terminal

in exp used voltage clamp, @-70 mV a depolarizing step to -25mV applied to presyn terminal—> triggered Ca influx resulted in synaptic transmission. voltage at 50 no presyn Ca influx. at this point VGCa channels are open but since close the equil potential of Ca little driving force for Ca influx

what does the Ca2+ Nt experiment show

normal synaptic delay between Presyn and post syn response consist of delay due to time it takes VGCa channels (bypassed in tail condition bc channels alr open) and a delay between Ca entry and NT triggered post syn response

whats makes Ca entry also important

the short latency between Ca entry into presyn terminal + post syn events implies theres a pool of readily available vesicles ready to fuse with PM immidiately upon rise in intracellular Ca

sequence of events for NT and Ca

AP from axon—>depolarizaion of presyn terminal—>opening of VGCa channels—>Ca entry into presyn terminal—> fusion of SV with presyn PM—>NT release

what mediates synaptic vesicle fusion

SNARE and and SM proteins

what does synaptobrevin do and what is it

vesicle associated membrane protein that is a part of the SNARE complex.

what does syntaxin do and what is it

located on target membrane for vesicle fusion (t-SNARE), a part of the SNARE complex for vesicle fusion

what is SNAP-25 and what does it do

a t-SNARE attached to the cytoplasmic phase of PM via lipid modification

how does the SNARE complex work

the vsnare bends alpha helix releasing a lot of energy as well as the tsnares—>fuse membrane across

what blocks NT release

proteases that cleave SNARE proteins, it inhibits attachment of 4-helix to membrane blocking NT release

whats the partner to SNARE

munc18—>binds to SNARES throughout fusion

what does synaptotagmin do

serves as a Ca2+ sensor to trigger synaptic vesicle fusion

Syt experiment

knockout mice had syt-1 disrupted, in these mice, depolarization of presyb neuron had smaller post-syn response—> syt-1 req for normal synaptic transmission

why syt req

normally depolarization of presyn terminal causes AP to be fired resulting in inward current in post syn responses= success, a mutation decreases Ca binding. point mutations of Ca binding afficiency of single protein was able to move the ability of Ca to act to activate release

what does complexin do

activates both snare complex and blocking it at an intermediate step

syt binding affinity

needs lower binding affinity bc binds < time, has many of these so multiple sites needed to bind to Ca —> NT release

what impacts speed of Ca release

proximity of the VGCa channels. increased Ca in resp to depolar restricted to microdomains in AZ—> transiently to facilitate binding of Ca to multiple binding sites on syt

unc 13

binds and activates t-snares, tethers vsnares and SV to the releasing site

RIM

binds to RAB-3 (vesicle gtpase) bringing SV closer to VGCa channels

lifecycle of a NT ACh

made in cytoplasm, packaging requires 2 transporters: one is an V-ATPase to help acidify the vesicle and the other uses proton gradient to take in NT and placed into the SV. for release opening of VGCa channels—>Ca entry into presyn terminal—> fusion of SV with presyn PM using SNARE complex—>NT release. degraded

lifecycle of a NT GABA

made in cytoplasm, packaging requires 2 transporters: one is an V-ATPase to help acidify the vesicle and the other uses proton gradient to take in NT and placed into the SV. for release opening of VGCa channels—>Ca entry into presyn terminal—> fusion of SV with presyn PM using SNARE complex—>NT release. reuptake

LC of vesicle — kiss and run

form a pore, release NT—>membrane recloses—> vesicle pinches off

LC SV - full fusion

uses clatherin mediated endocytosis to remove the vesicle and its components has to use adaptor proteins

Bulk endocytosis

take of a huge portion of the PM, reclaim it , and sort out huge endosome the pieces that are needed using clatherin mediated endocytosis