Neuroscience An extra bit. Dr Sasha Gartside Institute of Neuroscience Newcastle University
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1 Neuroscience An extra bit Dr Sasha Gartside Institute of Neuroscience Newcastle University
2 Drugs, receptors, and transporters Most psychoactive drugs interfere with neurotransmission The main targets are enzymes, transporters and receptors
3 How does understanding neuroscience and psychopharmacology help? An example: The pharmacotherapy of depression
4 The pharmacotherapy of depression Reserpine causes depressive symptoms reserpine inhibits monoamine storage Iproniazid (MAOI) and imipramine (5-HT/NA uptake inhibitor) effective antidepressants both increase monoamine neurotransmitters The Monoamine theory (1950s) Shildkraut
5 The pharmacotherapy of depression Many tricyclic analogues synthesised and used to treat depression One TCA (clomipramine) found to be selective 5-HT uptake inhibitor Clinically, clomipramine as effective as imipramine. The 5-HT theory of depression (1960s) Rational design of SSRIs- fluoxetine, paroxetine, fluvoxamine, sertraline.
6 The 5-HT theory of depression Deficit in 5-HT neurotransmission Increase 5-HT, relieve depression! Drugs which block 5-HT reuptake or metabolism are antidepressant But Delay in onset of therapeutic effect
7 Theories of antidepressant action Explaining the delay Postsynaptic receptor adaptation Autoreceptor desensitization
8 Adaptation of postsynaptic receptors? 5-HT Antidepressants raise 5-HT and NA Postsynaptic 5-HT 2 and receptors down regulated by antidepressants (slowly) But.. 5-HT 2 and antagonists are not antidepressant ECT upregulates 5-HT 2 receptors
9 Desensitization of 5-HT autoreceptors? 5-HT 1A autoreceptor 5-HT 1B autoreceptor 5-HT release 5-HT uptake 5-HT 5-HT is released in both terminal and cell body regions...and is cleared by reuptake in both regions
10 5-HT autoreceptors restrain ability of ADs to increase terminal 5-HT 5-HT 1A autoreceptor 5-HT 1B autoreceptor 5-HT release 5-HT uptake X 5-HT X X X SSRIs block uptake in both regions 5-HT levels in raphe nuclei rise and activate autoreceptors Autoreceptors inhibit firing and terminal release
11 Desensitization of 5-HT autoreceptors 5-HT 1A autoreceptor 5-HT 1B autoreceptor 5-HT release 5-HT uptake X 5-HT X After several weeks autoreceptors desensitize Although 5-HT levels at the cell body remain high, firing is restored Release is restored and, because terminal reuptake is blocked, terminal 5-HT rises
12 The tap and plughole Normal situation- plug hole open tap on After acute SSRI plug in but tap off After chronic SSRI- plug in tap on again
13 Raising 5-HT is crucial for antidepressant effect Acute pharmacology and autoreceptor desensitization theory suggest increased 5-HT is crucial for AD efficacy How can we hasten the rise in 5-HT?
14 Hastening effect of AD on terminal 5-HT 5-HT 1A receptor antagonists to block autoreceptor activation Pindolol tested Mixed reuptake blocker 5-HT autoreceptor molecules in development
15 Hastening the onset of SSRI action: the problem with 5-HT 1A receptor antagonists. 5-HT 5-HT 1A autoreceptor antagonists will disinhibit firing Note: these will also block postsynaptic 5-HT 1A receptors
16 Increasing therapeutic efficacy ~ 70 % patients fail to respond fully to conventional AD treatment Can efficacy be improved by further increasing 5-HT? Can efficacy be improved by also increasing NA?
17 Adjuncts to antidepressants: increasing 5-HT α 2 antagonists to increase drive α 1 agonists to increase firing α 2 adrenoceptor antagonist to disinhibit release (mirtazepine) 5-HT 5-HT 1A autoreceptor antagonists to disinhibit firing 5-HT 1B autoreceptor antagonists to disinhibit release
18 Do we need to raise 5-HT and NA? 5-HT NA TCAs, MAOIs, SNRIs, mirtazepine all increase both
19 Understanding something of the neurophysiology and psychopharmacology could lead to development of improved treatments
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