Neuronal Responses Flashcards
where are synapses located (6)
- axosecretory: axon -> blood stream
- axoaxonic: axon -> axon (esp. axon hillock)
- axodendritic: pre - post synaptic cleft (majority)
- axoextracellular: axon -> no connection, into extracellular fluid (e.g. to adrenal gland)
- axosomatic and axosynaptic: axon -> soma OR another exon terminal
describe syanpse of neuromuscular junction
Neuromuscular junction (between motor neuron and muscle)
(- perirphery NS)
- NT: acetylcholine.
- Ach binds to receptor: nicotinic acetylcholine receptor (nAChR), Na+ enters muscle cell = depolarisation
- purely excitatory inputs: one NT, one receptor: always causes an AP.
= muscle contraction
why are synapses more complicated than neuromuscular junctions?
- most synpases have both excitatory and inhibitory inputs
- most synpases have different / lots of NTs
(generation of AP depends on sum of all inputs to depolarise neurone above threshold)
what is the receptor used for Ach synapse at neuromuscular junction?
Nictotinic ACh receptor
how do inhibitory post synpatic potentials work?
- K+ permeability increased
OR
- increased Cl- perm.
give an example of direct and indirect inhibitory post synaptic pontetial
indirect: Muscarinic ACh receptor:
- G-protein activated
- acts via 2nd messenger
- indirectly opens K+ channel
direct: GABAA receptor:
- opens Cl- channel
BOTH: = hyperpolarisation
describe the relationship (in terms of frequency) between NT and receptor types
have few NT (energy saving), but many use multiple receptor types: NT have different roles depending on which receptor use
e.g. ACh uses nicotonic and muscarinic receptors
what and describe are the two classes of cell surface receptor types for synapses?
ligand gate ion channels:
- opens pore for ions
- very fast
- aka ionotropic
G-protein coupled receptors (GPCR)
- activated receptor activates G proteins that affects enzymes
- metabotropic
- slow
- can have bigger effect
which ACh receptor is ionotropic and which is metabotropic?
iontropic ACh receptor: nicotonic receptors. (PNS, bit in CNS)
metabotropic ACh receptor: muscarinic receptor
which is the main excitatory NT in CNS?
use one or both type of receptors?
how can the ionotropic receptors be classified?
- glutamate
- both ionotropic and metabatropic receptores
- 3 ionotropic receptors classified as:
a) NMDA
b) Non-NMDA
i) AMPA
ii) Kainate
what is main inhibitory CNS NT?
how work (basic)?
GABA: calming effect
- allows Cl- into cell: hyperpolarisation
what class of drugs binds to GABAa receptor?
cause a conformational change: channel stays open for longer, more Cl- enter cause more hyperpolirastion: induces sleep
- *- Benzodiazepines** bind to GABAA receptor, causing structural change
- Allows more Clto move through the channel into neuron & hyperpolarises the neuron
- Sedative, sleep-inducing, anxiolytic
g-protein receptor:
why do they give more diverse response c.f. ionotropic receptors?
(what is structure like?)
- gives a more diverse response depending on what G-protein is linked to
- (structure:
a) 7 transmembrane segments
b) lots of different ligands
c) over 700 GPCR)
describe basic overview of glutamate G-protein coupled receptor response?
G-protein coupled receptor –> G protein comple (intracellular) –> enzyme (+/-) –> 2nd messenger
its the second messenger which causes varied responses:
- e.g. cAMP released: inhibitory
- IP3 or DAG released: excitatory
describe the sequence of events that could happen with G-protein coupled receptor
- NT is released - binds to G-protein coupled receptor
- Activates G-protein complex
- Enzyme from G-protein complex could cause ATP -> cAMP
- cAMP could cause the opening of another channel (e.g. a Na+ / Ca2+ channel)
- Na+ / Ca2+ can trigger opening of Cl - (turns off the system)
what could happen in GPCR if there is too much ligand?
might use Ca2+ to open Cl- channel to rebalance and regain resting membrane potential -> switches excitatory signal off
why do you need less GPCRs to make a respnse (c.f. ionotropic receptors)?
which out of ionotropic or metabotropic, needs more to make a response on post-synaptic cleft?
need more ionotropic
GPRC: secondary messengers amplify signals to downstream target molecules - can need just one ligand binding to one GPCR
what are the three main type of 2nd messengers of GPCR?
- hydrophilic water soluble (IP33, cAMP, Ca2+)
- hydrophobic water insoluble (DAG and PIP3)
- gases (NO, CO and ROS)
how do you strengthen new synapses?
strengthen synpases:
- sleep!
a) shrink spines that are not being used to allow for more new spines to form
b) strengthens synapses after learning
how does receptor modulation by NTs occour?
receptor modulation by other NTs:
- NTs influence accumulation of opposite NTs on post-synaptic membrane
_e.g. ionotropic glutamate receptor fires excitatory response BUT also feedback to GABA receptor and causes to disperse (_and vice versa)
causes a balance of inhib and excitatory systems.
how does modulation of signals occur (adaptation)?
- if important sensory information: no adaptation. stimulus maintained all the time
-
less important sensory information: decay magnitude of the generator potential
a) slow adaptation (e.g. olfactory system)
b) rapid adaptation - declines over a more narrow window (c.f. slow)
give skin sensory receptors example that do
rapidly adapting
slowly adapting
rapidly adapting: Meissner corpuscles (light touch), Pacinian corpsucles (vibration)
slowly adapting: Merkel cells (pressure, texture), Ruffini endings (stretching of skin)
fun info
bc of refractory period, only have a set speed of generation AP
but CAN change the frequency of AP - increase transmission rate.
neurones have specific function -> go to one area of brain: encode one type of information (pressing eyeball)
how do reflexes work?
goes to the spinal cord, dont go to brain for reflex to occur: prevents overloading occuring of brain
