Brain & Behavior Quiz #2

EEG vs implant vs ECoG

EEG: surface of head

implant: on top of brain

ECoG: within brain

axon charge

-70 comapred to outside. greater concentration of neg ions inside axon bc of membrain permeability. this polarization leaves potential for change

Na K pump

pumps out 3Na+ for every 2K+. them concentration gradient pushed even more K+ out

Action potential

Brief but large change in neuronal polarization (=depolarization) that arises in the initial segment of the axon and propagates (moves) at high speed along the axon’s length

All or none property

Increased frequency —> increased stimulus strength (not size)

triggering an AP

hyperpolarization - more negative inside, less likely to trigger

depolarization - less neg inside, more liekly to trigger AP (~-40 threshold)

postsynaptic potential (chemical —> electrical signal)

brief change in resting potential

1. Excitatory postsynaptic potential (EPSP): Positive ions enter the cell and produce a small local depolarization, pushing the cell closer to threshold (glutamate)

2. Inhibitory postsynaptic potential (IPSP): Negative ions enter the cell and produces a small hyperpolarization; pushes cell further away from threshold. (GABA)

spatial summation vs temporal summation

summing elec signals over space vs summing elec signals over time. can cause AP is sum big enough

How does depolarization lead to an Action Potential?

Na+ channels open when reach -40, Na+ rush in while activation gate open. inactivation gate closes and then rush stops. K+ channel opens and hyperpolarizes briefly, then back to resting

absolute vs relative refractory phase

no action potential could be produce vs, strong signal required to produce AP

is communication within a neuron electrical or chemical?

primarily electrical

mylenation benefits (AP)

Prevents ionic currents from flowing across membrane

Small gaps in the insulating myelin sheath where AP regenerates

AP travels inside the axon and regenerates from node to node

more myelin —> faster travel

Na+ channel blockers

anasthetics, numbing

otto loewi’s key experiment

found that when he electrically stimulated one heart and not another, the non electrically stimulated heart had a reaction, proving there is something involved in communication besides electricity (chemical signaling, neurotransmitter/vagusstoff/acetylcholine)

voltage gated calcium channels

in active zones of presynaptic neuron

active zone

region of presynaptic zone where vesicle dock and NT is released

exocytosis

Ca2+ entry allows vesicles fuse with membrane and release the transmitter into the synapse

SNAREs

tethers, VSNARES (vesicle) and TSNARES (target membrane). attach to things during docking

synaptotagmin

entering Ca2+ binds to synaptotagmin sensor, triggers zippering of SNARES (change shape) and bilayer fusion leading to transmitter release

botox

botulinum toxin cleaves SNARE proteins & disables exocytosis of acetylcholine (neurotransmitter that communicates with muscles)….so muscles “paralyzed”

weak vs. strong stimulus from AP

weak: less Ca2+ channels open

strong: more Ca2+ channels open

co-release

different types of neurotransmitters are released in the same vesicles

co-transmission

different types of neurotransmitters are released from the same axon terminal into the same synapse but are grouped into different vesicles

spatial segregation

different types of neurotransmitters are released from different axon terminals

sequence of synaptic transmission

1. Action potential arrives at axon terminal.

2. Voltage-gated calcium channels open and Ca2+ ions enter.

3. Ca2+ entry causes vesicles to fuse with membrane and release transmitter into synapse

4. Transmitter binds to postsynaptic receptor molecule in postsynaptic membrane, which opens ion channel

5. Ion flow creates EPSP or IPSP in postsynaptic neuron

6. Terminating synaptic transmission

postsynaptic receptors

recognize transmitters, adjust ion channels in postsynaptic membrane

ionotropic receptor

ligand gated ion channels, directly changes ion channel (postsyn recept)

metabotropic receptor

G-protein couples receptor (not ikon channel), contains G protein that indirectly alters ion channels (postsyn recept)

number of receptors

varies daily in adults, throughout development, drug use

up-regulation: inc in number of receptors

down regulation: dec in number of receptors

long-tern synaptic plasticity

more receptive channels up-regulation, good for learning and memory, inc strength

NTs are not only excitatory and inhibitory, can change fucnction depending on receptors

ex: ACh can be excitatory, opening channels for Na and K creating loal depol; ACh can be inhibitory bu opening channels for Cl-

Degradation (Ending Synaptic Transmission)

rapid breakdown by an enzyme/caspase, e.g., acetylcholinesterase (AChE) breaks down ACh and recycles it.

Reuptake (Ending Synaptic Transmission)

transmitter is taken up by presynaptic receptors called transporters

Diffusion (Ending Synaptic Transmission)

transmitter diffuses away from synapse

Autoreceptors

on presynaptic membrane bind transmitters; inform the cell about

transmitter concentration in the cleft, which can be adjusted = feedback loop

gap junctions

* Presynaptic and postsynaptic membranes are physically connected

• Axon potential jumps directly to the postsynaptic region without being transformed into a chemical signal.

• Ions flow directly through large channels, connexons, into adjacent cells, with no time delay.

• Electrical transmission is continuous

• Resembles Action Potential conduction down axon