Cells and Systems Fall 2023

Concentration of Na+ inside the cell

18 mM

Concentration of Na+ outside the cell

145 mM

Concentration of K+ inside the cell

140 mM

Concentration of K+ outside the cell

3 mM

Concentration of Cl- inside the cell

7 mM

Concentration of Cl- outside the cell

120 mM

Concentration of Ca2+ inside the cell

100 nM

Concentration of Ca2+ outside of the cell

1.2 mM

Room temp Nernst simplification

58

Body temp Nernst simplification

61.5

Equilibrium potential Na+

+56 mV

Equilibrium potential K+

-102 mV

Equilibrium potential Cl-

-76 mV

Equilibrium potential Ca2+

+125 mV

tau1

time constant (time for current to go through membrane)

tau2

time constant (time for current to go down cell)

lambda

space constant

capacitance

amount of voltage a cell can hold

what happens to membrane resistance when axon diameter increases (and why)

decreases, because there are more ion channels present

what happens to membrane resistance when axon is myelinated (and why)

increases, channels are insulated

what happens to internal resistance when axon diameter increases (and why)

decreases, lower charge density

what happens to internal resistance when axon is myelinated (and why)

nothing, myelin does not alter the inside of the axon

what happens to membrane capacitance when axon diameter increases (and why)

increases, surface area of the axon increases

what happens to membrane capacitance when axon is myelinated (and why)

decreases, the inter-plate distance increases

what happens to lambda when axon diameter increases (and why)

increases, internal resistance increases

what happens to lambda when axon is myelinated (and why)

increases, membrane resistance increases

what happens to tau1 when axon diameter increases (and why)

nothing, membrane resistance and membrane capacitance change by the same factor

what happens to tau1 when axon is myelinated (and why)

nothing, membrane resistance and membrane capacitance change by the same factor

what happens to tau2 when axon diameter increases (and why)

decreases, internal resistance decreases

what happens to tau1 when axon is myelinated (and why)

decreases, capacitance decreases

equation for lambda

sqrt(rm/ri)

equation for tau1

rm * cm

equation for tau2

ri * cm

equation for rm

Rm/2pia

equation for ri

Ri/(pi * a squared)

peptide ball and chain

mechanism by which K+ channels inactivate

hydrophobic IMF amino acids, cytoplasmic loop between motif III and IV

mechanism by which Na+ channels inactivate

CaM

mechanism by which Ca2+ channels inactivate

selectivity filter, p loop, carbonyl oxygen atoms of the polypeptide backbone

responsible for selectivity of K+ channel

DEKA P-loop sequence

responsible for selectivity of Na+ channel

negatively charged glutamate residues (EEEE) P-loop sequence

responsible for selectivity of Ca2+ channel

gap junction

site where the electrical current in one neuron passes without delay into the dendrite of another neuron, directly affects membrane potential

Active zone

specialized region of an axon terminal where synaptic vesicles come to fuse with the axon terminal’s plasma membrane and release their contents

postsynaptic density

the protein-rich region directly across from the active zone, regulates the proteins inserted into the plasma membrane, holds in place proteins that will respond to events in the synaptic membrane and produce long-lasting, global changes in the post-synaptic neuron

readily-releasable pool

small set of vesicles in the active zone that are docked to the plasma membrane

reserve pool

sizable population of vesicles that can be recruited to the presynaptic plasma membrane when the readily releasable pool is exhausted

cytomatrix of the active zone

hexagonal grid formed by triangular protrusions with spaces between them that are just large enough to accomodate a synaptic vesicle

actin filaments

reserve pool vesicles move along these to the CAZ to interact with the proteins at the CAZ and be docked at a specific spot in the presynaptic membrane

a long lambda

excitatory synapse at the tips of dendrites can produce a measurable depolarization at the initial segment as long as the dendrite has this

electronically compact

term for having a very impressive lambda

shunting inhibition

when the effect of the synapse is to redirect current from inside the cell to extracellular fluid

dendritic branch points, initial segment

most effective locations for shunting synapses

small axon terminal contact a single dendritic spine

simplest and most common arrangement of synapses

mossy fibers

axons end in a series of large axon terminals, each of which forms synaptic contacts with several dendritic spines

type I synapse

synapse where excitatory events occur, thick post-synaptic density, most common

type II synapse

synapse where inhibitory events occur, thin post-synaptic density, less common

qualities of type I synapse

complex of transmembrane receptors and cytoplasmic effectors held together by scaffolding proteins

primary dendrite

dendrites that come directly off the cell body, inhibitory

peripheral dendrite

dendrites that are excitatory

spatial summation

addition of currents across several active synapses

temporal summation

addition of currents produced at a single synapse over a short period of time

presynaptic inhibition

caused by axoaxonic synapse, limits the release of neurotransmitter from the postsynaptic axon terminal

2 causes of postsynaptic inhibition

1) induction of v.g. K+ channels opening prematurely in postsynaptic neuron, reduces depolarization so Ca2+ channels don’t open

2) v.g. Ca2+ channels are directly targeted

connexin

proteins that form channels in the plasma membrane at a gap junction

connexon

assembly of connexin proteins

method for closing gap junctions

anything that raises extracellular pH or permits intracellular Ca2+ to rise

formation of an inhibitory net between dendrites of inhibitory neurons

main purpose of electrical synapses

presence

neurotransmitter should be synthesized or otherwise taken up and sequestered in the presynaptic element

release

substance must be released by the presynaptic elemtns when that element is depolarized

effect

substance must have an effect on the postsynaptic neuron which must be able to be mimiced by artificially putting that substance on the postsynaptic neuron

pharmacological results

agent that either promotes or interferes with the actions of the substance must have the same effect at the synapse

termination

must be some means to stop a neurotransmitter from working shortly after it has been released

amino acids NTs

glutamate, GABA, glycine

biogenic amines

dopamine, norepinephrine, epinephrine, serotonin

means by which the action of a neurotransmitter ends

diffusion out of cleft, pumping out of cleft, breaking down

synthesis-regulating autoreceptors

receptors that control the enzymatic activities required to make neurotransmitter, stimulate the production of neurotransmitter when release occurs

release-regulating autoreceptors

receptors that limit the amount of neurotransmitter released by an axon terminal

probability of neurotransmitter release decreases

what happens to the probability of neurotransmitter release per action potential when the rate of action potentials goes up and stays up for a significant period

acetylcholinesterase

enzyme found in cleft that breaks acetylcholine into acetic acid and choline

acetyal-CoA and choline

precursor molecules for acetylcholine

choline acetyl transferase

cytoplasmic enzyme that catalyzes the reaction to make acetylcholine

3 subpopulations of cholinergic neurons

Motor neurons, retiuclar formation neurons whose axons innervate the thalamus, basal forebrain neurons whose axons innervate the cerebral cortex

volume neurotransmission

mechanism by which acetylcholine is transmitted in the thalamus and cerebral cortex; the axon of a single neuron provides a large volume of neural tissue with a neurotransmitter, require GPCRs

goal of volume neurotransmission

change the basal activity of all the neurons within a volume of neural tissue

tyrosine

precursor amino acid for dopamine, epinephrine, and norepinephrine

tyrosine hydroxylase

converts tyrosine to L-DOPA

LAADC

converts L-DOPA to dopamine and 5-HTP to serotonin

DBH (dopamine beta-hydroxylase)

converts dopamine to norepinephrine

PNMT

converts norepinephrine to epinephrine

NET

norepeinephrine transporter, terminates the actions of NE by reuptake

MAO (monoamine oxidase)

termiantes the actions of NE, dopamine, serotonin, and epinephrine by degradation

VMAT

transporter that pumps NE and serotonin back into vesicles

COMT (catecol-O-methyl transferase)

enzyme that breaks down all catecholamines

2 systems of dopamine

neurons of the substantia nigra that terminate in the basal ganglia, ventral tegmental area that terminate in the nucleus accumbens

tryptophan

precursor animo acid for serotonin

tryptophan hydroxylase

converts tryptophan to 5-HTP

SERT

transporters that pump serotonin back into the axon terminal

raphe

region in the pons and the midbrain where the majority of serotonin neurons are found

function of astrocytes for glutamate

pump glutamate out of the synaptic cleft, convert it to glutamine, and pump glutamine into the axon terminal

PAG (glutaminase)

mitochondrial enzyme that converts glutamine to glutamate