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Physiology > 9. 10. Postsynaptic membrane receptors: ionotropic and metabotropic receptors. Postsynaptic potentials. > Flashcards

9. 10. Postsynaptic membrane receptors: ionotropic and metabotropic receptors. Postsynaptic potentials. Flashcards

1
Q

Types of postsynaptic receptors ( depending on permeability affected directly or indirectly)

A

Ionotropic

Metabotropic

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2
Q

Properties of ionotropic receptors

A

When a mediator binds, it leads to DIRECT changes in permeability of given ion channel

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3
Q

Properties of metabotropic receptors

A

Binding of mediator leads to INDIRECT change in permeability of ion channel, change direction of biochemical reaction, change gene expression

Facilitated by G PROTEINS AND SECOND MESSENGERS which activates KINASES

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4
Q

Mechanism of metabotropic receptors

A

• specific mediator binding to receptor activates G proteins

• G protein= alpha, beta, gamma subunits

• activates effector protein, adénylate Cyclase

• that generates secind messenger cAMP which generates protein kinase

• kinase changes permeability of channel by PHOSPHORYLATION of amino acid sites on channel

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5
Q

What are the 4 classes of G proteins

A

Ga s - stimulates production of adenylate cyclase

Ga i- inhibits production of adenylate cyclase

Ga q- stimulates production of PLC

Ga 12/13 - involved in Rho family GTPase signalling

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6
Q

Types of mediators in terms of their synthesis

A

Low molecular weight compounds

Neuropeptides

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7
Q

Low molecular weight compound synthesis and examples

A

In presynaptic terminals- they hv rapid effect on postsynaptic membrane

Classical neurotransmitters: Ach, norepinephrine, dopamine, serotonin

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8
Q

Neuropeptide synthesis and examples

A

In cell body of presynaotic neuron
- axonal transport takes them there

Causes long term changes in permeability of postSM

They change amount of membrane receptors

Gastrin, somatostatin, encephalins, endorphins

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9
Q

Ach synthesis

A

In the presynaptic endings from acetyl-coenzyme A and choline catalysed by choline acetyl transferase

Secreted by preganglionic nerve fibres of sympathetic and parasympathetic nerve system

Secreted by large pyramidal cells in motor cortex

Secreted from spinal motor neurons innervating skeletal muscles

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10
Q

How is AcH degraded

A

Degraded in synaptic cleft to acetate and choline by cholineesterase

Can be used by presynaotic ending to make new AcH

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11
Q

What are the types of AcH receptors

A

Nicotine sensitive N CHOLINORECEPTORS

muscarine sensitive M-CHOLINORECEPTORS

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12
Q

What type of receptors are N-cholineoreceotors

A

Ionotropic ( so function like ion channels)

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13
Q

Where are N-cholinoreceptors located and how’s it activated

A

Im autonomic ganglia, neuromuscular junctions, CNS pathways

Binding leads to the entry of Na+ ions and k+ release- leads to excitatory EPSP

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14
Q

What type of receptors are M-cholinoreceptors

A

Metabotropic (g protein coupled)

The ion channel they regulate is distant from the receptor

M1-5

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15
Q

Effects and location of M1 cholinireceptors

A

Parietal cells of gastric glands, salivary glands, CNS, sympathetic ganglia

Causes closure of K+ when phospholipase(plc) and IP3 and DAG ( second messengers) bind

Leads to depolarisation- EPSP

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16
Q

Effects and location of M2- cholinoreceptors

A

In SA node

Causes opening of k+ channels which is directly mediated by class Gi G proteins via beta and gamma subunits

Hyoerpilsrizstion- IPSP

These slow down heart rate caused by parasympathetic nerve system

17
Q

Effects and location of M3 cholinoreceptord

A

Bronchial and salivary glands, pupillary constriction and broncho constriction

Lead to depolarisation- EPSP

18
Q

Effects and location of M5 cholinoreceptors

A

CNS

clinucal implications not fully explored

19
Q

Effects and location of M4

A

CNS

work via Gi and inhibit cAMP

Causes decreased loca motion

20
Q

Which muscarinuc receptors use Gq that up regulate PLC, IP3 and intracellur Ca2+

Which uses Gi

A

• M1 M3 M5

• M2 M4

21
Q

What is the most excitatory mediator in brain
What is most inhibitory mediator in brain

A

Glutamate

GABA

22
Q

How is glutamate and GABA synthesised

A

Glutamate: in kerbs cycle amination of a-ketoglutsrate

GABA- decarboxylation of glutamate ( glutamate y-aminobutyric acid)

23
Q

What are the type of glutamate recpetors

A

Ionotropic= NMDA and AMPA

Metabotropic= group 1,2,3

24
Q

How are NMDA and AMPA activated by glutamate

A
  • The glutamate released by presynaptic ending binds to both receptors
  • It ACTIVATES AMPA so depolarization-Na enter K exit
  • Depolarization reaches NMDA and causes release of Mg2+ (before it blocked channel) which ACTIVATES NMDA leading to influx of Na+ and Ca 2+ and K+ exit
  • Therefore for NMDA binding of glutamate required AND depolarization of membrane required
25
Q

Difference between Metabotropic glutamate receptors and ionotropic

A
  • Slower synaptic transmossion
  • BUT can amplify repeated weak signals due to cascade responses
  • Both receptors involved in learning and memory
  • in pre- and post-synaptic
    neurons of the hippocampus, cerebellum, and the cerebral cortex,
26
Q

What does GABA stand for and synthesis

A

γ-aminobutyric acid

decarboxylation of glutamate in Krebs cycle

Major inhibitory neurotransmitter in brain

27
Q

Tyoes of GABA receptors

A

GABA a GABAc = ionotropic

GABAb = metabotropic

28
Q

GABAa characteristics

A

Selective for Cl- ion and causes inhibitory post synaptic potential

Benzodiazepines and barbiturates facilitate this receptor and act as anticonvulsants and sedatives

29
Q

GABAc characteristics

A

Also a Cl- channel BUT doesnt have drug binding site like a

Leads to IPSP

30
Q

GABAb characteristics

A

Opens K+ channels

Activated by G protein Gi via b and y subunits

Leads to IPSP

31
Q

What are the function of the GABA receptors

A
  • reduce neuronal excitability by inhibition of neuron to
    neuron transmission.
  • If GABA binds to many neurons, this causes sedation
  • GABAergic neurons are present in hippocampus, thalamus, basal ganglia,
    hypothalamus, and brainstem.
32
Q

What are some biogenic amine neurotransmitter

A

Catecholamines ( dopamine, epinephrine, norepinephrine

Serotonin

33
Q

If damaged which neurons cause parkinsons disease

A

Dopamine neurons

34
Q

What does serotonin regulate and what happens if theres too much

A

Mood apetite sleep rhythms, digestion, blood clotting

shivering and diarrhea to
severe like, muscle rigidity, fever and seizures.

35
Q

What are the mechanisms of termination of neurotransmitter action?

A

Diffusion out of synaptic cleft.

Enzymatic degradation into synaptic cleft.

Going back to the presynaptic end.

36
Q

Examples of second messengers

A

cAMP, cGMP, IP3 , DAG

Physiology (20 decks)

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