Neurotransmitters in Anxiety

Effects of non‐sedative anxiolytic drugs on responses to GABA and on diazepam‐induced enhancement of these responses on mouse neurones in cell culture

“…While PK 9084 is poorly established as an anxioselective agent, buspirone has been shown to be efficaceous in several clinical trials (Goldberg & Finnerty, 1979;Goldberg & Finnerty, 1982;Rickels et al, 1982). These results are consistent with the conclusion that anxiety can be treated by modification of non-GABAergic neurotransmission, possibly including 5-hydroxytryptaminergic, noradrenergic and dopaminergic systems (for review, see: Hoehn-Saric, 1982;Braestrup, 1982).…”

The Ability of Perindopril of Modulate Behavioural,Neuroendocrinal and Testicular Profiles in Stressed Rats

“…For example, increased displaceII)ent has been linked to increased ACTH; as currently observed and more so, for its parent CRH, as has been reported [33,34]. This is believed to be mediated via monaminergic transmission particularly dopaminergic through stimulation of D2 receptor subsets, [35.36] and may even be through adrenergic or serotonergic [34,36,37], Currently speaking, the brain content of the former two transmitters was found presently elevated, and the increase in their activities were also reported to be associated with anxiety [38,39] while 5HT content in the current work was significantly altered which could be viewed to coincide with the anxiogenic predominance in this stress modality studied and as confirmed in other reports emphasizing a role for serotonergic ag- The increase in environmental temperature encountered in H&L-S could have been an added factor to booster avoidance displacemento But this is rather questionable, as increased temperature was reported to markedly enhanced the activity of serotonergic neurons [7.41] and to induce generalized responses to ACTH; [42] to profile that was not totally fulfilled in the current study and that is debated by recent reports arguing a possible role for serotonin in thermo-regulation [37]. Furthermore, it is relevant to add, that sleep depravation as a component of the H&L modality studied was reported per se by some not to playa major role in eliciting any neuroendocrine response [43]0 ..…”

Anxiolytic-like Effects and Quantitative EEG Profile of Palmitone Induces Responses Like Buspirone Rather Than Diazepam as Clinical Drugs

“…Anxiolytic-like effect of A. cherimolia was previously reported due to the presence of palmitone as one bioactive metabolite and a GABA/BDZs receptor modulation [20]. As previously mentioned, GABA is the main neurotransmitter system influenced by potential anxiolytic drugs such as BDZs [32,35]. Anxiolytic-like response of several drugs modulating GABA A receptor has been blocked in the presence of PTX but not by flumazenil or bicuculine, suggesting that GABA A modulation is more efficiently prevented by obstruction of the chloride channel [9,11,36].…”

“…This effect was associated with serotonin neurotransmission since the 5-HT 1A metabolite was increased by 33% in the amygdala 24 h after palmitic acid treatment [31]. Fatty acids are also precursors of prostaglandins such as PGE2, and to a lesser degree, PGE1, which are reported to inhibit the hormones released under stress, mainly catecholamines but also histamine, gastrin, and serotonin [32,33]. Anxiolytic-like effects of fatty acids (C 6 -C 18 ) have also been associated with GABAergic neurotransmission in rats [11].…”