Week 2 Review Flashcards
which ions carry the early inward & late outward currents during AP?
during early part of AP, influx of Na ions across membrane briefly depolarizes membrane. brief inward sodium current is consequence of opening voltage-gated potassium channels after delay of 1msec.
why is AP referred to as all or none?
bc no partial AP exists. physical or electrical event opens Na permeable channels, but resulting influx if Na ions & resulting depolarization (generator potential) must reach threshold before axon generates AP. after threshold depolarization cell fires AP.
why do AP travel in only one direction?
membrane just behind AP is refractory due to inactivated sodium channels
there is higher potassium K+ concentration inside cell than outside. why, then is the resting membrane potential negative?
bc neuron is filled with negatively charged molecules, i.e. proteins, that don’t transverse cell membrane thru channels the way ions do
when brain is deprived of oxygen, mitochondria within neurons stop producing ATP. what effect would this have on membrane potential & why?
sodium-potassium pump, which requires ATP, will not function so resting potential membrane won’t exist & brain won’t function
why is excitatory synapse on soma more effective in evoking AP in postsynaptic neuron than an excitatory synapse on tip of a dendrite?
current entering sites of synaptic contact must spread to spike initiation zone & zone must be depolarized beyond threshold to generate AP. also, depolarization decreases as function of distance along dendrite. as a result effectiveness of excitatory synapse for triggering AP depends on how far synapse is from spike initiation zone (SIZ).
bc soma is closer to SIZ, excitatory synapse on soma is more effective in firing APs than synapse on dendrite
what is resting membrane potential?
difference in electrical charge across membrane at rest
which of the following is major charge carriers involved in conduction of electricity in neurons?
ions
how do the lipids of neuronal membrane contribute to neuronal membrane potential?
forms barrier to water-soluble ions & water
how do APs differ from passively conducted electrical signals?
APs are signals of fixed size & duration; passively conducted signals are not signals of fixed size & duration
which if the following is true of ion channels?
a) permit passage of ions thru cell membrane
b) composed of proteins that form pores in cell membrane
c) responsible for passive transport of ions thru cell membrane
answer is all of the above
which of the following might cause neuron to fire?
a) EPSPs triggered by activity @ five synapses @ same time
b) EPSPs triggered by activity @ five nearby synapses
c) multiple EPSPs @ same synapse triggered in rapid succession
answer is all of the above
golgi stain
labels only small fraction of all granules & processes in brain to see stained structures against clear background
neuron doctrine
developed by Cajal, idea that neurons are cells that transmit info across tiny gaps called synapses
resting membrane potential
voltage difference of -70mV between inside & outside of neuron
action potential
brief reversals of polarity (becoming positively charged) that neurons use to transmit info along axons
Na+/K+ -ATPases (sodium potassium pump) move
2 potassium ions in for every 3 sodium ions they move out of
resting potential of typical neuron
-70mV
what is major cause of neuronal resting potential?
push & pull of potassium ions across neuronal membrane
ion channels
pore-forming proteins
in the process of generating AP
electrical potential across membrane reverses polarity & briefly surges from -70mV to +40mV
depolarization
positively charged sodium ions generate inward current that causes inside of axon to become more positive
action potential threshold
membrane potential at which positive feedback between membrane depolarization & sodium influx kicks in (typically 10-20mV more positive than resting potential of -70mv)
equilibrium potential for potassium
-80mV
axon potentials initiated in
axon hillock
refractory period
voltage gated sodium channels that open during AP rising phase close automatically shortly after & voltage gated potassium channels open slowly on depolarization & stay open for a while; as long as potassium channels are open and sodium channels closed, membrane cannot generate another AP (this is known as refractory period)
how does myelination boost conduction velocity?
1) by increasing an axon’s length constant
2) decreasing axon’s membrane capacitance
synaptic vesicles
~50 nanometers in diameter & filled with thousands of NT molecules each
Neurotransmitters (NT)
for most excitatory neurons in the CNS, the NT is L-glutamate (ionic form of glutamate acid) generally referred to as glutamate
synaptic cleft
tiny gap about 20-25nm wide between pre & post synaptic cells
voltage gated calcium channels
AP comes into axon terminal, calcium channels open, calcium ions rush down concentration gradient, raising calcium levels in terminal causing some synaptic vessels to fuse w cell membrane & thru exocytosis release NT in synaptic cleft
Excitatory Post Synaptic Potential (EPSP)
when glutamate binds to AMPA receptors of neuron at rest, neuron experiences net influx of positive ions (mainly sodium) & is consequently depolarized
Inhibitory Post Synaptic Potentials (IPSP) caused by
15-40% neurons use NT GABA (gamma-aminobutyric acid)
EPSP vs IPSP
ipsp’s often located close to axon hillock of post synaptic cell, epsp’s mainly found on dendrites, making ipsp’s frequently more powerful in their effect than epsp’s
ionotropic receptors
class of receptors that contain central pore thru which ions flow, effects can be excitatory or inhibitory, depending on ions that come thru, but effects usually fast & brief
metabotropic receptors
class of receptors that don’t have central pore for ions to pass, but can open other close nearby ion channels indirectly by modulating intracellular signaling cascades that ultimately affect ion channels. most belong to fam of G-protein-coupled receptors & affect neuronal activity by activating enzymes that control production of secondary messengers. post synaptic effects of metabotropic receptors significantly slower but longer lasting than ionotropic receptors
