Receptors & Transmitters Flashcards

Question

Describe the glutamate-glutamine cycle

Answer 1

Releases L-glutamate = most important excitatory transmitter in the brain 1. Glutamine from the synapse is taken back up by the glutamine transporter and converted back into glutamate 2. Astrocytes remove glutamate from the area around the neurons and metabolise glutamate into glutamine 3. A transporter is used to send glutamine out of the astrocyte 4. Back to step 1 EAAT = excitatory amino acid transporter that recycles the glutamate

Answer 2

1. Current flow induced by AMPA activation leading to local depolarisation (small depolarisation) 2. Transmits to soma? (May not be big enough to transmit) 3. Local depolarisation deinactivates NMDA = greatly increased depolarisation & influx of Ca2+ 4. Transmits to soma 5. mGluR1 activation = slow/long depolarisation —> can also lift Mg2+ block = more depolarisation 6. Synapse may become strengthened with repeated use = LTP (long-term depolarisation)

Answer 3

Produce inhibitory response GABA a/c - ligand gated chloride channel - fast - pentamers - many different subunits GABA b - family C GPCRs (operate as dimers) - slower - one subunit specialised for binding GABA - other subunit responsible for interaction with G protein

Answer 4

Ligand gated chloride channel - GABA binds to GABA A receptor - Increase in chloride permeability = produces inhibition - ECl (reverse potential for Cl) is often close to RMP so tends to stabilise MP close to ECl - Leads to hyperpolarisation & inhibition

Answer 5

Found pre or post synaptically 2 subunits = GABA B1 and GABA B2

Answer 6

- soluble protein regulator of neuronal nicotinic receptors - important in brain development - in hollow fanged snakes, proteins related to Lynx 1 have evolved to become toxins - target muscle nicotinic ACh receptors - e.g. alpha-cobra toxin and alpha-bungarotoxin (from the cobra and Taiwanese banded krait)

Answer 7

- striatum contains high concentration of dopaminergic synapses - deficit in dopaminergic transmission = associated with Parkinson’s disease and excess of dopamine = associated with symptoms of Sz - release of dopamine in striatum is increased by presynaptic nicotinic ACh receptors acting as heteroreceptors (Ionotropic receptors gated by ACh) - these are more permeable to Ca2+ and have 2 mechanisms to increase dopamine release - when activated, the presynaptic nerve terminal becomes more depolarised so there’s a greater influx of Ca2+ through voltage gated channels - a secondary mechanism is that Ca2+ enters the nerve terminal through the nicotinic receptor itself

Answer 8

A sensor on the nerve terminal that gets signals from a different type of neurotransmitter than the one the cell normally releases = helps control how the cell responds by either increasing or decreasing its activity Nicotinic ACh receptors = most important type of heteroreceptors in the CNS as nearly every neurotransmitter has its release regulated by these

Answer 9

- noradrenaline released by sympathetic neurons acts on beta adrenal receptors on cardiac muscle to increase heart rate & the force of contraction - alpha 2 type adrenoreceptors on presynaptic nerve terminals act as autoreceptors and regulate noradrenaline release. These are GPCRs which interact with the G protein Gi - main effect of Gi is to decrease Adenylate cyclase activity (turns ATP into cAMP) - so activation of alpha 2 receptors decreases concentration of cAMP in the nerve terminal - cAMP increases activation of voltage gated calcium channels & thus noradrenaline release - so activation of alpha 2 receptors results in decreased noradrenaline release **Antidepressant Mirtazipine is an antagonist of alpha 2 receptors = increases noradrenaline and serotonin release**

Answer 10

Sensors on nerve terminals that help control how much of a chemical the cell releases (acts as a stop signal)