Neurotransmitters & Pharmacology Flashcards
4 features of Synaptic Transmission
Rapid timescale
Diversity
Plasticity
Learning and memory
what are protien molecules called on dendrites
spine
function of cell body/soma
Information reception
then integration of the information
lastly
Rapid transfer (action potential)
function of spine
increase the surface area of recipet of information recipt
what sort of trasmition happen in an action potential
electrical (AP)
chemical(nuerotrasmiter)
Electrical (AP)
can nuerotrasmition happen anywhere else other than synapse
nope
what are the post synaptic clefts
dendrite or soma
Synaptic transmission: 3 stages
- Biosynthesis, packaging and release of neurotransmitter (●)
- Receptor action( bind to receptor on postsynaptic receptor)
- Inactivation(happens on the postsynaptic region)
3 types of nuerotrasnmitter
Amino acids
Amines
Neuropeptides
Recap: synaptic transmission – essential features
Restricted to specialised structures - the synapses
Calcium is essential - transmitter release requires an increase in intracellular Ca2+ (200 M)
Transmission is fast - within ms
Synaptic vesicles (SVs) provide the source of neurotransmitter (4,000-10,000 molecules per SV)
transduction
is the transmission of molecular signals from a cell’s exterior to its interior
where are the synaptic vesciles docked
synaptic zone
how do nuerotransmitter enter vescicles
they have protien pumps
after being docked onto the pre synaptic membrane what happens
theyre primed
to release the nt
then fuse
what do the Special proteins on the vesicle and presynaptic membrane enable
enable fusion & exocytosis
what are they called on vesicles
vesicular protien
mediate the action of exocytosis of nt
improtnant in docking
Vesicular proteins are targets for
neurotoxins
what is Alpha latrotoxin
from black widow spider
function
stimulates transmitter release to depletion of presynaptic termial
what do the victims suffer from
muscular paralysis
function of Zn2+-dependent endopeptidases
inhibit transmitter release
example using tetanus toxin
causes spasms & paralysis
by inhibiting GABA and glycine release
another example using BOTULINUM TOXIN
causes flaccid paralysis
paralyisis due to muscle relaxation
structure of BOTULINUM TOXIN
bi chain (2 chain)
how does it work
first part binds to nerve terminal (cholernergic)
2nd chain penetrates the cholonergic nerve terminal and intercats with vesicular proteins
cleaves peptide bond thus inactivating them
so you no longer get docking
fusion or relase of transmiter
how is vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis enabled
Protein complex formation between vesicle, membrane and cytoplasmic proteins
is the transmitter release require energy
yes
Ion channel-linked receptors
mediate what sort of trasnmittion
FAST response (msecs) Mediate all fast excitatory and inhibitory transmission
exitotory signal is produced by what
opening of sodium ion channel (glutamate receptors)
leads to depolarisation of post synaptic terminal
and ihnibitory
chlorine( GABA) leads to hyperpolarisation of postsynaptic terminal
G-protein-coupled receptors
mediate what action
SLOW response (secs/mins)
what are the effectors
enzymes or channels
what happens upon binding to the gpc receptor
g protien binds to a receptor inside the cell (adenyl cyclase) produces sencond messenger like cAMP ehich causes effect to enzymes or channel
examples of Ion channel-linked receptors
CNS- Glutamate,GABA
NMJ-ACh at nicotinic receptors (nuermo muscular junction)
G-protein-coupled receptors
examples
CNS and PNS: ACh at muscarinic receptors
dopamine
noradrenaline
serotonin
Ion channel-linked receptors have how many subunits
and what do they allow
5
→ distinct functional properties
what does a excitatory nurotranssmitter receptor cause
an excitory postsynaptic potential
EPSP
what does an Inhibitory neurotransmitter receptor
cause
inhibitory postsynaptic potential (IPSP)
what is the main Excitatory trasmitter in brain
Glutamate
and Inhibitory t in brain
GABA
2 examples of Glutamate receptors
AMPA RECEPTORS
NMDA RECEPTORS
AMPA RECEPTORS mediate
Majority of FAST excitatory synapses
Rapid onset, offset and desensitisation
permeable to na
NMDA RECEPTORS
mediate
Slow component of excitatory transmission
Serve as coincidence detectors which underlie learning mechanisms
NMDA RECEPTORS permeable to
na and ca
how is glutamate synthesised
from glucose via TCA cycle & transamination
what happens once glutamate is exocyotsed
Glutamate reversibly binds postsynaptic receptors
how is it inactivated
Rapid uptake of glutamate
reloaded in vesicles and used again
how are they uptaken in glial cell and where are they
glial cell surround synapses
3. Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)
what happens in the glial cell
- Glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells
by what enzyme
glutamine sythesase
what happens to the glutamine
in is pumped into presynaptic teminal and used to make more glutamate
what is the process called
glutamate glutimine cycle
what happens when too (uncintrolled) much glutamate release
spiking in the Electroencephalography (EEG) (measures electrical activity in the brain)
what happens if too much glutumate in synapse
Abnormal cell firing leads to seizures associated with excess GLUTAMATE in the synapse
what happens as the glutamate is comming bac =k down to normal level
converted to glutamine but takes lomger to come back down to normal level
