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Mental Health
Ketamine: A tale of two enantiomers
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<blockquote data-quote="madman" data-source="post: 198082" data-attributes="member: 13851"><p><strong>Figure 4. Hypothesised monoamine and opioid mechanisms and potential convergences with signalling pathways implicated in the antidepressant actions of ketamine. (a) (R,S)-ketamine inhibits lateral habenula (LHb) bursting via actions on N-Methyl-D-Aspartate (NMDA)/low voltage-sensitive t-type channels (T-VSCC)/mu-opioid receptors (MOR). This results in disinhibition of monoamine release via γ-aminobutyric acid (GABA)-ergic interneurons in the dorsal raphe nucleus (DRN) and ventral tegmental area (VTA) to projections including the medial prefrontal cortex (mPFC) and nucleus accumbens (NAcc). The action of (R,S)-ketamine on NMDA/MOR on GABAergic interneurons in the DRN and VTA may be a further mechanism of disinhibition of 5-HT and dopamine release. 5-HT release in mPFC may also occur via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor stimulation in DRN for (R,S)-ketamine and (S)-ketamine but might not be as relevant for (R)-ketamine. (b) Stimulation of postsynaptic 5-HT1A receptors via 5-HT in mPFC results in activation of Akt/mammalian target of rapamycin complex 1 (mTORC1) and potentially ERK signalling. Stimulation of postsynaptic D1 receptor via dopamine may result in activation of mTORC1/ERK and inactivation of eukaryotic elongation factor 2 (eEF2) kinase. Postsynaptic MOR activation may also potentiate the ERK signalling pathway.</strong></p><p>[ATTACH=full]13468[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 198082, member: 13851"] [B]Figure 4. Hypothesised monoamine and opioid mechanisms and potential convergences with signalling pathways implicated in the antidepressant actions of ketamine. (a) (R,S)-ketamine inhibits lateral habenula (LHb) bursting via actions on N-Methyl-D-Aspartate (NMDA)/low voltage-sensitive t-type channels (T-VSCC)/mu-opioid receptors (MOR). This results in disinhibition of monoamine release via γ-aminobutyric acid (GABA)-ergic interneurons in the dorsal raphe nucleus (DRN) and ventral tegmental area (VTA) to projections including the medial prefrontal cortex (mPFC) and nucleus accumbens (NAcc). The action of (R,S)-ketamine on NMDA/MOR on GABAergic interneurons in the DRN and VTA may be a further mechanism of disinhibition of 5-HT and dopamine release. 5-HT release in mPFC may also occur via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor stimulation in DRN for (R,S)-ketamine and (S)-ketamine but might not be as relevant for (R)-ketamine. (b) Stimulation of postsynaptic 5-HT1A receptors via 5-HT in mPFC results in activation of Akt/mammalian target of rapamycin complex 1 (mTORC1) and potentially ERK signalling. Stimulation of postsynaptic D1 receptor via dopamine may result in activation of mTORC1/ERK and inactivation of eukaryotic elongation factor 2 (eEF2) kinase. Postsynaptic MOR activation may also potentiate the ERK signalling pathway.[/B] [ATTACH type="full"]13468[/ATTACH] [/QUOTE]
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Mental Health
Ketamine: A tale of two enantiomers
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