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Flashcards in Neurotransmission And Drug Mechanisms Deck (16)

Dendrite to dendrite communication

No neurotransmitter
Via gap junctions-> connexion a


Neurotransmitter features

Change membrane potential
Alter neurotransmitter release
Major excitatory transmitter-> glut amine-> depolarisation
Major inhibitory transmitter-> GABA-> hyper polarisation
Either stored in vesicles or synthesised on demand
Released via Ca dependent exocytosis
Termination via high affinity uptake or metabolism


Glutamate life cycle

Taken up in to glial cells-> converted to glutamine -> returned to neurone
If it is released as glutamate it has further excitatory effects


Low capacitance channels

Don't let much ion through


Types of CNS neurotransmitter

Amines and amino acids (glutamate)-> small organic molecules containing at least one N-> stored and released in synaptic vesicles
Peptides-> large molecules-> stored and released from secretory granules
Can have a mixture of both at one axon


Ligand gated ion channels

Membrane spanning
Four-five subunits that come together to form a pore
Neurotransmitter binds to various sites on extracellular region-> conformational change-> pore opens
Less specific -> Ach channels are permeable to Na and K->
Net effect to depolarise the post synaptic cell towards the threshold -> excitatory -> glutamate, nicotinic Ach, 5-HT3 -> Na or Ca channels
Net effect to hyperpolarise-> Cl channels -> GABA
Fast transmission


Excitatory post synaptic potential

Transient post synaptic membrane depolarisation caused by pre synaptic release of neurotransmitter
Eg Ach and glutamate gated


Inhibitory post synaptic potential

Transient hyperpolarisation of the post synaptic membrane potential cause by pre synaptic release of neurotransmitter eg GABA


G protien coupled receptors

Slower and longer lasting with much more diverse post synaptic action
Activate other G protiens or second messengers
-> activate additional enzymes that regulate ion channel function and alter cellular metabolism
Wide spread effects-> metabotrophic


Auto receptors

Presynaptic receptors on the presynaptic axon that are sensitive to neurotransmitter-> commonly inhibit neurotransmitter release-> self regulation


Neurotransmitter reuptake transporters

May happen by simple diffusion
Reuptake via pre synaptic receptors->swap neurotransmitter for Na and Cl ->
May be enzymatically destroyed or relocated in to synaptic vesicles
Also exit in to glial cells
Or enzymatic destruction in cleft



a2 autoreceptor function
a2 agonist-> clonidine -> inhibits noradrenaline neuronal firing via a2 receptors in locus coerulus and terminal noradrenaline release
Noradrenaline-> regulation of arousal, mood pain
Agonists-> sedation, reduced anxiety
Antagonists-> increased vigilance, antidepressant, antixiognic
B-adrenoceptors-> increase cAMP formation


Drugs that act on ligand gated ion channels

Barbituates-> GABA modulators
Phencyclidine-> NMDA antagonist
Adenstertron-> 5-HT3 antagonist
Nicotine-> nicotine agonist


Glutamate gated channels

3 subtypes-> AMPA, NMDA, kainate
AMPA, NMDA-> bulk of excitatory synaptic transmission
AMPA-> permeable to Na and K-> rapid and large depolarisation -> excitatory
AMPA and NMDA co exist at many synapses
NMDA-> permeable to Na and Ca -> widespread, lasting changes
-> voltage dependent -> at normal resting potential channel is blocked by Mg -> moves when membrane is depolarised


GABA gated ion channels

Mediates most synaptic inhibition
a subunits bind transmitter
Several other binding sites-> benzodiazepines, barbituates, steroids (outside), picrotoxin (inside)
Only cause effect when GABA is also bound
Benzodiazpines-> increase frequency of channel opening
Barbituates-> increase duration of channel opening
The more Cl let in the more inhibitory effects


Neurotransmitters and psychiatric disorders

Alziehmers-> Ach
Schizophrenia-> dopamine, 5-HT
Depression-> NA, 5-HT
Anxiety/OCD-> GABA, NA, 5-HT
Bipolar-> post receptor