week 3 Flashcards
diff bw GPs and APs in terms of…
a) location
b) channel types involved
c) ions involved
d) duration
GPs vs APs:
a) dendrites/soma/sensory receptors vs axon
b) ligand and mechanically-gated vs voltage-gated
c) Na+, Cl-, or K+ vs Na+ and K+
d) few msec to seconds vs 1-2 msec
phases of an AP (3)
- depolarization
- repolarization
- after-hyperpolarization
when do Na+ channels open?
once threshold is reached (~-55mV)
do VGSCs operate in a positive or negative feedback system?
positive
why does the peak depolarization of an AP only reach +30mV? why not reach the EP of Na+ (+60mV)?
because soon after the VGSCs open, they inactivate
what causes repolarization? (2)
- at rest, K+ leaks out of cell, so cell becomes more negative.
- VGPCs open (recall: EC of K+ = out).
which are faster: VGSC or VGPC?
- VGSCs are faster.
- this is why the repolarization phase (which depends on VGPCs) takes longer and overshoots (after-hyperpolarization).
do VGPCs operate in a positive or negative feedback system?
negative
review: at rest, is Na+ or K+ more permeable?
K+
what brings the membrane to threshold?
sum of the graded potentials
what restores resting membrane potential?
Na+/K+ pump
are the activation and inactivation gates open or closed at…
a) rest
b) depolarization
c) repolarization
a) rest: activation = closed, inactivation = open
b) depolarization: activation = open, inactivation = open
c) repolarization: activation = open, inactivation = closed
why are threshold and suprathreshold stimuli equal in size?
bc all-or-none principle
what is a refractory period? whats the diff bw absolute and relative refractory periods?
refractory period: decreased excitability following an AP because VGSCs are inactive until membrane potential is at rest.
absolute: ALL VGSCs are inactive. spans all of de and most of repolarization. second AP cannot occur.
relative: SOME VGSCs are inactive. last part of re and after-hyperpolarization. second AP may occur with stronger stimulus.
what is most common local anesthetic dentists use to “freeze” you and how does it work?
- lidocaine
- works as VGSC blocker, preventing APs (pain)
can you completely block membrane from generating AP?
- yes
- keep membrane depolarized above threshold to stop influx of sodium.
- inject KCl to destroy concentration gradient for K+ (will keep inside of cell positive, keeping VGSC inactive).
if APs are all-or-none, how do we differentiate strong vs weak stimuli?
- frequency coding
- strong stimuli encoded in higher frequency of APs
what are the cons of an unmyelinated axon? (2)
- leakage of ions
- decreased conduction velocity
how does the propagation of APs work in unmyelinated axons?
- A = depolarized
- positive charge of A attracted to negative charge of B
- B = depolarized
- cycle continues
what makes the propagation of APs unidirectional?
absolute refractory period
what are the factors affecting propagation? (3)
- refractory period (makes it unidirectional)
- axon diameter (larger = faster)
- myelination (saltatory conduction = faster)
how does the propagation of APs work in myelinated axons?
- high density of VGSC at nodes of ranvier
- AP jumps from node-to-node
in electrical synapses, neurons are linked together by ___. what do these contain?
- gap junctions
- contain connexins that allow ions to cross
functions of electrical synapses in the nervous system? (5)
- rapid communication
- ions or second messengers
- usually bidirectional communication
- excitation and inhibition at same synapse
- identified in retina, cortex, brainstem (breathing), and hypothalamus (neuroendocrine neurons).
describe functional anatomy of chemical synapses (5)
- presynaptic neuron releasing neurotransmitter
- postsynaptic neuron accepting neurotransmitter
- synaptic cleft
- unidirectional communication
- usually axodendritic, some axosomatic or axoaxonic
describe the anatomy of a synapse (7)
- presynaptic axon terminal (AP arrives here)
- neurotransmitter-containing vesicles
- depolarization opens VG Ca2+ channels
- neurotransmitter dropped into synaptic cleft
- receptors
- enzymes
- reuptake molecules
how can leftover neurotransmitter be removed? (3)
- enzymatic breakdown
- diffusion
- reuptake
what is synaptic delay? what is it caused by?
- 0.5–5 msec between arrival of AP and change in postsynaptic cell.
- caused by changes in Ca2+ entry, vesicle docking, and release of neurotransmitter
what are the 2 types of receptors that allow signal transduction at chemical synapses?
- channel-linked (ionotropic): ligand-gated, fast acting, close as soon as neurotransmitter leaves.
- g-protein coupled (metabotropic): slow acting
describe the steps of…
a) direct coupling
b) second messenger systems
[discussing g-protein coupled receptors]
a) neurotransmitter binds, activates g-protein, opens/closes ion channels.
b) neurotransmitter binds, activates g-protein, activates/inhibits enzyme, produces second messenger, opens/closes ion channels or produces other cell responses.
whats a PSP?
change in membrane potential in response to receptor-neurotransmitter binding.
most common EPSP neurotransmitter? IPSP?
EPSP: glutamate
IPSP: GABA
what makes an EPSP fast or slow?
whether channel-linked or g-protein coupled receptors are used
in inhibitory synapses, what happens if K+ channels open? Cl- channels?
K+: moves out = IPSP
Cl-: moves in = IPSP (or stabilizes MP)
why are IPSPs more important than EPSPs? (3)
- more specific
- more accurate
- shape info
diff bw divergence and convergence?
divergence: axon of one neuron has several collaterals that communicate to several other neurons.
convergence: many PREsynaptic terminals converge onto one postsynaptic neuron.
recall: temporal vs spatial summation
temporal = one stimulus, close times.
spatial = multiple stimuli, same times.
more APs = more neurotransmitter released + ___ IPSP or EPSP in the next neuron.
greater
what is presynaptic modulation?
regulation of communication across a synapse on presynaptic neuron (axoaxonic)
what is presynaptic facilitation vs inhibition?
facilitation: modulating neuron results in modulated neuron releasing more neurotransmitter
inhibition: modulating neuron results in modulated neuron releasing less neurotransmitter
diff between axoaxonic vs axodendritic/axosomatic ???
axoaxonic excites/inhibits one synapse and is selective
others excite/inhibit postsynaptic neuron and is nonselective (“overall”)
what is Ach used for and where is it found?
- muscular contractions
- PNS and CNS (most abundant neurotransmitter in PNS)
how is Ach synthesized? broken down?
synthesis: Acetyl CoA + choline = acetylcholine + CoA (CAT = enzyme for synthesis)
breakdown: Acetylcholine = acetate + choline (AChE = enzyme for degredation)
what is the Ach competitive agonist? what does it do?
- curare
- blocks Ach, prevents voluntary movements
cholinergic receptors can be of what types? (2)
- nicotinic (ionotropic, EPSP)
- muscarinic (metabotropic, EPSP or IPSP)
which type of cholinergic receptor is abundant in CNS?
metabotropic (muscarinic)
name the 5 biogenic amines
- dopamine
- epinephrine
- norepinephrine
tyrosine ^
- serotonin (tryptophan)
- histamine (histidine)
serotonin (3)
- CNS (mainly brainstem)
- regulates sleep + emotions
- related directly to plasma concentration of tryptophan
histamine (3)
- CNS (mainly hypothalamus)
- regulates wakefulness
- commonly known for paracrine actions (allergies)
which amino acid neurotransmitters are at excitatory vs inhibitory synapses?
excitatory: glutamate, aspartate
inhibitory: GABA, glycine
name the 6 neuropeptides
- endogenous opioids
- TRH
- ADH
- oxytocin
- substance P
- orexin
name one unique neurotransmitter. why is it uniqe?
- NO (gas)
- unique bc cannot be stored; created on spot as needed.
is the effect determined by the receptors or the ligand for Ach?
receptor
