kenyon neurotransmission 1 Flashcards
gap jxn allow __(be specific)__ to move between cells
ions (and really small molecules according to the book)
“electrically coupled.” what does that mean?
this term refers to cells that are connected by GAP jxns and, therefore, have the same membrane potential
gap jxn structure
connexons that span both the presynapatic and postsynaptic neuron membranes
hallmarks of electrical transmission
- gap jxns
- bidirectional conduction
- can be either positive or -negative
- allows for SYNCRONIZATION
three examples of neurons that connect through electrical transmission
- cardiac m
- smooth m
- some CNS neurons, like those that release hormones in the hypothalamus
define synaptic vesicles
organelles!
membrane bound
MUST contain 1 or more NTs
synaptic cleft space parameter
wide but narrow
chemical neurotransmission… up the where NT is released into cleft
- NT packed vesicles chill
- AP depolarizes terminal, causing opening of voltage gated Calcium channels
- calcium then rushes through these channels
- calcium increase causes vesicles to fuse w/ presynaptic membrane
- NT is released into synaptic cleft
chemical neurotransmission after NT release into cleft
- NT binds to receptors on postsynaptic membrane
- ^^binding of NT will open OR close postsynpatic channels
- the post synaptic current will cause inhibitory or excitatory change in electric potential
- then NT gets removed by uptake or enzymatic degradation
lidocain
Na+ channel inhibitor, so it blocks the AP
Lambert-eaton
autoimmune disease where the body makes INHIBITORY antibodies against the voltage gated calcium receptors on the presynaptic membrane
conotoxin
a type of neuropeptide that inhibits voltage gated calcium channels on the presynaptic membrane
botulin and tetanus toxins
block vesicle release
curare
irreversibly binds and inhibits the nicotinic ACh receptor on neuromuscular junctions
benzodiazepine
binds to GABA receptor and inhibits it
myasthenia gravis
antibodies bind to ACh receptors at neuromuscular jxns.
similar effect to curare!
physostigmine
blocks acetylcholinesterase
prozac
serotonin reuptake inhibitor
slow axonal transport
FOR SMALL MOLECULE NT synthesis!!!
- enzymes are synthesized in the cell body
- enzymes travel down slowly along axon
- synthesis and packaging of NT happens at the presynaptic terminal
fate of small molecule NTs
usually, they precursor gets recycled by coming directly back into the terminal
fast axonal transport
FOR NEUROPEPTIDES:
- neuropeptides are synthesized and pre-packaged into vesicles of cell body
- these “loaded” vesicles are transported to the terminal
fate of neuropeptides
usually, they get degraded/diffused away
unconventional NT synthesis
the whole new school sequence: NT etiology, calcium FXN, and receptor location
just remember that the enzymes are synthesized in the cell body and then transported to terminal
list the three unconventional NTs
NO, C02, endocannabinoids
NT location: old schools vs new school
old: substance must be present in presynaptic vesicles
new (unconventional NTs): substance can be synthesized on demand–like in the case of unconventional NTs
calcium fxn: old school vs new school
old: release of substance MUST be triggered by an increase in [Ca++]presynaptic
new (unconventional NTs) … calcium-activated enzymes can synthesize NTs upon increase in presynaptic calcium; then these NTs diffuse out
receptors: old school vs new school
old: specific receptors must be present on postsynaptic membrane
new (unconventional receptors): specific receptors present, instead, on CYTOPLASM of postsynaptic cells
vesicle cycling
- vesicles originate off an endosome and are filled w/ NTs
- upon Ca++, vesicles bind to the plasma membrane
- and then these same vesicle membranes are retrived by clathrin-mediated ENDOcytosis
- then the clathrin comes off (uncoating)
- and finally the vesicles are at a position where they can return to the endosome
kiss and run
vesicles may transiently open pores to the synaptic space. this opening is very transient and only releases a small amount of contents. in kiss and run releases, vesicle does not have to get reabsorbed
kiss and run/classic mech effect on membrane
has an effect on membrane for sure, but looks smaller than quantal release
define cotransmission
when one neuron releases more than one NT
Differential release in cotransmission
preferential release is dictated by frequency of stimulation and concomitant increase in calcium concentration
at low frequency, usually, small molecules are released.
at high frequency, usually, neuropeptides are released
snap 25
a non-SNAP protein lol. it’s important to serve as a dock for synaptobrevin to syntaxin. it serves to dock the vesicle to the membrane
synaptobrevin and syntaxin
synaptobrevin (SNARE on vesicle)
syntaxin (SNARE on plasma membrane)
synaptotagmin
protein located on vesicle membrane.
fxn: once the SNARE complexes dock via SNAP-25, synaptotagmin is primed to accept the calcium.
once calcium binds, synaptotagmin catalyzes the membrane fusion!!!!. How? by binding to itself to SNARES and the plasma membrane
nerst equation
Ex=[58/z][logXo/Xi]mV
permeability effect on membrane potential
more permeability = heavier contribution to overall membrane
ACh example in terms of permability
ACh increased the permeability to a particular ion. NTs can increase or decrease it
iontropic
deals w/ muscles
permeability and gating: two cases–ionotrpoic and metabotropic
basically ionotropic is direct and metabotropic is indirect
ionotropic: NT binds to a receptor; that same receptor opens its channel; ions flow through receptor.
metabotropic: NT binds to receptor; G protein sequence; G protein subunits or intracellular messengers modulate the ion channels; ions flow through channels.
Suppose: channel opens to allow BOTH Na+ and K+ in. how will membrane potential change?
It’ll go somewhere between Ek and ENa
Define: Erev
the target potential associated w/ the opening of ANY particular channel
when you open more channels for a particular ion, you will be more closer to the Erev
effect of opening nonselective channels
should be around zero because of the positive and negative summations of Exs, like EK, and ENa
The general rule of NTs on membrane potential!
NT will drive the POSTsynpatic potential toward Erev for the SPECIFIC ion channel that said NT is activating
always think in terms of changing permeability
Types of channels in NT transmission
Common: non-selective channels for Na, K, or Ca++
Also common: Selective for Cl- or for Ca++
rare: selective for K+ and Na+
are the channels involved in NT different than those in the AP?
YES!!!!
as far as i know
Define EPSP
Erev is more positive than the postsynaptic neuron AP THRESHOLD mark
Define IPSP
Erev is more negative than the postsynaptic neuron AP THRESHOLD mark
Is a IPSP that causes depol more likely to reach threshold than a cell just chillin at resting threshold?
NOOO!
Coz the IPSP depol actually stabilizes, sort of electrically buffers, the membrane potential to FOR SURE keep it below the threshold
general threshold rules.
-Ion channels nonselective for cations or selective for
Ca2+ mediate EPSPs (Erev positive to threshold)
-Ion channels selective for K+ mediate IPSPs (Erev negative to threshold)
- Ion channels selective for Cl- mediate IPSPs if ECl is negative to threshold or EPSPs if ECl is positive to threshold.
- Recall the range of ECl given as -88 to -35 mV. See box 6D for gory details..
Define the summation phenomenom. what two factors are important too?
summation: neuron receives 100s/1000s of inputs and sums them up
location and timing are CRITICAL
define EPP
EPP=end plate potential, which is when ACh opens ligand gated channels and therefore creates an AP.
(ONLY REQUIRES ONE MOTOR END PLATE–NO SUMMATION NEEDED)
Are EPSP and IPSP additive?
yes BUT not linearly
list examples of NTs involved in retrograde signaling
NO, CO, endocannaboids, and prostagladins
retrograde mech
NT binds to post synaptic neuron; calcium concentration increases; increased calcium pushes endocannabinoid production; then that same endocannabinoid seeps back into the synaptic cleft to bind onto the presynaptic terminal.
good for like a negative feedback effect.
presynaptic receptors
fxn: receptors on presynaptic terminal serve to regulate release of NTs
source of the NTs that modulate these presynaptic receptors: (1) NT inhibiting itself and (2) NTs from other neurons
