Mechanisms of antihistamine-induced sedation in the human brain: H1 receptor activation reduces a background leakage potassium current
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Antipsychotics: Mechanisms underlying clinical response and side-effects and novel treatment approaches based on pathophysiology
2020, NeuropharmacologyCitation Excerpt :Sedation is a common complaint of patients taking antipsychotics (Arvanitis and Miller, 1997; Beasley et al., 1996; Kane et al., 1988; Marder and Meibach, 1994). Histamine H1 antagonism is a major contributor to sedation (Reiner and Kamondi, 1994). As shown in Fig. 2 clozapine, quetiapine, olanzapine and chlorpromazine, have the highest histamine H1 receptor affinity relative to their dopamine D2 receptor affinity, and these are the antipsychotics most associated with sedation, whereas drugs such as amisulpride, which have little affinity for H1 receptors (Fig. 1), are not associated with sedation (Leucht et al., 2013).
Sedative effect of Clozapine is a function of 5-HT<inf>2A</inf> and environmental novelty
2017, European NeuropsychopharmacologyAnalyses of rapid estrogen actions on rat ventromedial hypothalamic neurons
2016, SteroidsCitation Excerpt :It appears, therefore, HA induces depolarization by inhibiting K+ channels, i.e., reducing their numbers or average conductance. Our conclusion is consistent with reports by others that HA induces depolarization by inhibiting Kca channels [40–47], a leak current [38,48–51], M-current [52], voltage-gated [53], inward rectified [54] and some unspecified K+ currents [55,56]. No further pharmacological analysis was carried out on NMDA actions.