There is increasing evidence for efficacy, tolerability, and safety of neurostimulation treatments. rTMS is now a first-line recommendation for patients with MDD who have failed at least 1 antidepressant. ECT remains a second-line treatment for patients with treatment-resistant depression, although in some situations, it may be considered first line. Third-line recommendations include tDCS and VNS. MST and DBS are still considered investigational treatments.
Though overlapping in distribution within the posterior hypothalamus, neurons containing orexin (Orx) and melanin concentrating hormone (MCH) may play different roles in the regulation of behavioural state. In the present study in rats, we tested whether they express c-Fos differently after total sleep deprivation (SD) vs. sleep recovery (SR). Whereas c-Fos expression was increased in Orx neurons after SD, it was increased in MCH neurons after SR. We reasoned that Orx and MCH neurons could be differently modulated by noradrenaline (NA) and accordingly bear different adrenergic receptors (ARs). Of all Orx neurons (estimated at approximately 6700), substantial numbers were immunostained for the alpha1A-AR, including cells expressing c-Fos after SD. Yet, substantial numbers were also immunostained for the alpha2A-AR, also including cells expressing c-Fos after SD. Of all MCH neurons (estimated at approximately 12,300), rare neurons were immunostained for the alpha1A-AR, whereas significant numbers were immunostained for the alpha2A-AR, including cells expressing c-Fos after SR. We conclude that Orx neurons may act to sustain waking during sleep deprivation, whereas MCH neurons may act to promote sleep following sustained waking. Some Orx neurons would participate in the maintenance of waking during deprivation when excited by NA through alpha1-ARs, whereas MCH neurons would participate in sleep recovery after deprivation when released from inhibition by NA through alpha2-ARs. On the other hand, under certain conditions, Orx neurons may also be submitted to an inhibitory influence by NA through alpha2-ARs.
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