CNS questions MCQ

Which Ion primarily enters Presynaptic terminal to trigger Neurotransmitter release

Calcium ions (Ca2+) enter the presynaptic terminal upon Depolarisation (less negative) triggering the release of neurotransmitters into the synaptic cleft.

Give an example of a ligand gated ion channel + G protein coupled channel targeted by CNS drugs

1) NMDA receptor

2) D2 receptor,

How do SSRI’s enhance neurotransmission in Depression ?

Selective Serotonin Reuptake Inhibitors (SSRIs) enhance neurotransmission in depression by blocking the reuptake of serotonin (5-HT) in the synaptic cleft, thereby increasing its availability in the brain.

How do Benzodiazepines enhance GABAergic transmission ?

Allosterically bind to GABA-A receptors which INCREASES the frequency of Chloride channels opening. More Hyperpolarisation (more negative) Hence MORE inhibition.

What is an example of use dependence in drug action ?

Lidocaine. Blocks Sodium channels EVEN more in rapidly firing Neurons.

If a drug exhibits Use dependence on Sodium channels what does that mean ?

The drug’s effectiveness increases with the frequency of Neuronal firing

SAQ :Outline the key steps involved in neurotransmission at a chemical synapse, from neurotransmitter synthesis to termination of its action and briefly explain how dysfunction at any one step might contribute to cns disorders

. NT’s are synthesised in the presynaptic neuron/terminal

. After being synthesised they are PACKAGED in synaptic vesicles to prepare for release

. An ACTION POTENTIAL will reach the presynaptic neurone, DEPOLARISING the membrane

. Depolarisation causes opening of CA 2+ Channels allowing calcium to enter the Neuron

.Increased Calcium ions triggers VESICLE FUSION with presynaptic membrane, and releases NT into synaptic cleft

. NT’s diffuse across synapse cleft and bind to RECEPTORS on POSTSYNAPTIC neurone.

. Depending on the receptor, the postsynaptic cell may depolarise (excitation) or hyperpolarise (inhibition).

. NT action is terminated

by; Reuptake into presynaptic neurone. Also by enzymatic breakdown ( AcH by acetylcholinesterase)

How does Cocaine affect brain reward pathway ?

Inhibits Dopamine reuptake by blocking Dopamine transporter

How do Opioids affect brain reward pathway ?

Bind to mu-opioid receptors reducing GABA’s inhibition. Causing more Dopamine to be released into the synaptic cleft, enhancing the feeling of pleasure and reward.

Which brain structure is primarily responsible for detecting and processing rewarding stimuli via dopamine release?

Nucleus accembus

What effect does prolonged agonist binding have ?

Causes conformational change in the receptor, making it LESS responsive even while bound to drug

SAQ: "Describe the pharmacological treatment options for anxiety disorders, including drug classes, examples, and brief mechanisms of action."

SSRI’s (first line) - E.g Sertraline work by inhibitng reuptake of Serotonin at synaptic cleft, increasing serotonin levels in brain improving MOOD.

SNRI’s - e.g Venlafaxine Act similarly but also increase NORADRENALINE levels. Effective alternative when SSRIs not tolerated

Benzodiazepines - Act by binding to GABA-A receptors, increasing Cl- influx hence increasing Inhibition. mainly for ACUTE SHORT TERM USE

Beta blockers- e.g Propanolol Used to relieve PHYSICAL symptoms like tremor, tachycardia. Peformance anxiety.

TCAs - Block reuptake of Serotonin + Noradrenaline but MORE side effects

MOAI’s - Inhibit enzyme Monoamine oxidase, prevent breakdown of Serotonin, NA and dopamine. Leaves more available in brain.