NEUROTRANSMISSION IN THE NERVOUS SYSTEM Flashcards
in a synaptic cleft, what breaks down ACh? [1]
in a synaptic cleft, what breaks down ACh? [1]
acetylcholinesterase enzymes
what has to enter presynpatic terminals in order to allow vesicles to release NT across synaptic cleft? [1]
what causes this to occur? ^
- how do vesicle fuse with presynaptic cleft? [1]
- what causes vesicles to be recycled? [1]
1. calcium ions - through voltage gated channels - triggered to enter by AP
- vesicles dock with the presynaptic membranes: they fuse via SNARE complex: releases vesicles into synaptic cleft
- vesicle membrane is recycled: taken up via clathrin. make more vesicles
which two pieces of evidence suggest that AP starts with at NMJ in skeletal muscle? [2]
- the latency of AP increases the further move from NMJ.
- source of greatest depolarisation in the NMJ is closest to the axon terminal
what are minature End Plate Potentials caused by? [1]
what are EPPs made from in NMJ? [1]
why do you sometimes get no response at all from activating synpases? [1]
what are minature End Plate Potentials cause by? [1]
spontaenous release of NT from vesicles sporadically binding with membrane
- *- EPPs are built of whole numbers of miniEPPs
- when you reduce probability of vesicle release - sometimes get no response at all from activiting synapses**
NT release in the CNS:
- what type of post-synaptic potentials? [2]
- what determines ^? 2]
NT release in the CNS:
- what type of post-synaptic potentials? [2]
- *EPSP & IPSPs**
- what determines ^? 2]
if NT is E or I
type of receptor binds to
where do you find more K:
inside / outside nerve?
where do you find more Na:
inside / outside nerve?
what determines this ^? [1]
where do you find more K:
inside / outside nerve?
where do you find more Na:
inside / outside nerve?
what determines this ^? [1]
Na/K ATPase !!
what drives the upswing of an AP in nerve? [1]
[during rest, which ion causs negative charge?]
sodium electrochemical gradient
- at rest, the cell has resting K ion permeability - it carries a negative charge outwards. this leaves behind a negative charge inside cell
how does EPSP occur in CNS cell? [4]
- K+ is greater inside cell, Na+ greater outside
- at rest, K can move across membrane (leak out of the K+ channels): leaves behind a negative resting potential
- nicotinic Ach receptor is permeable to both Na- & K+ ions
- Ach binds to Nicotinic Ach R: causes conformational change: gives rise to depolarisation (bc Na move in?)
- activation gives rise to depolarisation of cell
describe how IPSP occurs xx
NT released that are associated with inhib: GABA & Cl-
- GABA binds to GABAa receptor
- this activates causes an increase in **membrane conductance: Chloride ions moves inwards
- **causes inhib.
when GABA binds to GABAa receptor, a change occurs to the receptor. which ion can then subsequenlty move into the CNS cell?
Na-
K+
Ca2+
Cl-
H+
when GABA binds to GABAa receptor, a change occurs to the receptor. which ion can then subsequenlty move into the CNS cell?
Na-
K+
Ca2+
Cl-
H+
which are the two main inhib NTs of CNS?
- which one is dom in brain? [1]
- which one is dom in spinal cord? [1]
which are the two main inhib NTs of CNS?
- which one is dom in brain: GABA
- which one is dom in spinal cord: glycine
describe reciprocal antagonist inhibition that occurs when bicep flexes
muscle spindle in bicep: activates skeletal muscle contraction (excitatory)
but also: 1a afferent activates inhibitory interneuron: antagonsitic inhibition (release of glycine) of triceps !!
both E & I together = reciprocal antagonist inhibition !
how quickly do:
- neurotransmitters
- neuromodulator
- neurotrophic factors
release / cause change?
**NT: fast !
neuromodulater (s-mins):**
activates GPCRs
neutrophic factor (mins - hours):
neuromodulators typically bind to which type of receptors?
ion activated channels
GPCRs
enzyme linked channels
nucleus binding rs
neuromodulators typically bind to which type of receptors?
ion activated channels
GPCRs
enzyme linked channels
nucleus binding rs
which of the following applies to Glutamate?
- neurotransmitters only
- neuromodulator only
- neurotrophic factor only
- neurotransmitters & neuromodulator
- neurotransmitters, neuromodulator & neurotrophic factor
which of the following applies to Glutamate?
- neurotransmitters only
- neuromodulator only
- neurotrophic factor only
- *- neurotransmitters & neuromodulator**
- neurotransmitters, neuromodulator & neurotrophic factor
how does neuromodulation occur?
- NT binds to GPCR
- this dissocaites the G protein
- the dissciated G protein binds to secondary molecule and activates it
- this then works on something else (e.g. a channel - to open)
- where does Ach bind to ACh R (specifics !!)
- describe structure of Ach R
what happens when Ach binds to ACHR?
structure: α2βγð subunits; spans across inside of cell, cell membrane and outside of cell (where the binding sites are)
when 2 Ach binds to AchR: change in hydrophobic interactions in alpha helical structure = creates an ion pore
binding occurs of Ach occurs at C loops (of cysteine-cysteine bond)
muscle AP recorded by electrical stimulatin of P nerve.
what is a
M wave?
H-reflex?
F-wave?
m wave: direct activation of motor units by electrical stimulation
H reflex: electrical equivelent to stretch reflex
f-wave: antidromic motor nerve action potentials bouncing off the a-motorneurons
