Effects of B-HT 920 in the tail-suspension test

Ferrari, Francesca; Cassinadri, Mariateresa; Tartoni, Pier Luigi; Tampieri, Auro

doi:10.1016/1043-6618(91)90067-8

Cited by 13 publications

(3 citation statements)

References 15 publications

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“…The contradiction (i.e. similar effects after ~2 adrenoceptor agonists and antagonists) seems to be reproducible, since clonidine and yohimbine have shown similar effects in a variety of behavioral investigations (Ferrari et al 1991;Matsumoto et al 1991;Cutler 1993;Kacsoh et al 1993).…”

Section: Discussionmentioning

confidence: 81%

The effect of α2 adrenoceptor blockers on aggressive behavior in mice: implications for the actions of adrenoceptor agents

1996

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The effects of three alpha 2 adrenoceptor blockers (idazoxan, yohimbine and CH-38083) on isolation-induced aggressive behavior was studied in male mice. The three drugs produced different behavioral profiles. Idazoxan reduced aggressiveness dose-dependently by decreasing the duration of offensive/aggressive interactions and increasing the duration of defensive behaviors. The other two drugs produced only parts of the dual action of idazoxan: yohimbine affected mainly defensive behaviors, while CH-38083 affected only the time spent with fighting. Saline injections per se also influenced behavior and, in contrast to alpha 2 adrenoceptor blockers, induced an increase in aggressiveness. These results are different from those previously obtained in rats, which show bell-shaped dose-response curves in response to alpha 2 adrenoceptor blockers (small doses increased, while large doses decreased aggression). It is postulated that the strong behavioral reaction of mice to the injection per se may mask the aggression-heightening effects of small doses of alpha 2 adrenoceptor blockers in this species. A theory is also presented regarding the complexity of adrenoceptor interactions when both pre-, and postsynaptic alpha 2 adrenoceptors are blocked.

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Section: Discussionmentioning

confidence: 81%

The effect of α2 adrenoceptor blockers on aggressive behavior in mice: implications for the actions of adrenoceptor agents

1996

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“…In contrast to these potentially therapeutic properties of clonidine, it has also been suggested that this drug can promote depression-like behavior in rodents (Kitada et al, 1983 ; Parale and Kulkarni, 1986 ; Ferrari et al, 1991 ; Rénéric et al, 2002 ), or under some circumstances has no substantial effect either alone or when co-administered with other putative antidepressants (Kitada et al, 1983 ; Evangelista et al, 1987 ; Antkiewicz-Michaluk et al, 2017 ).…”

Section: Alpha2 Agonistsmentioning

confidence: 99%

Are Noradrenergic Transmission Reducing Drugs Antidepressants?

Fitzgerald

2021

Front. Behav. Neurosci.

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Major depressive disorder (MDD) remains a significant public health problem worldwide, and revised treatment strategies are therefore urgently needed, including the creation of novel antidepressant compounds or using existing molecular entities in new ways. Etiologic theories of MDD from decades ago have suggested that synaptic deficiencies of monoaminergic neurotransmitters play a causative role in this neuropsychiatric disorder, and that boosting monoamines with drugs such as SSRIs, SNRIs, TCAs, and MAOIs has antidepressant effects and in some individuals can even induce hypomania or mania. While other factors, such as various intracellular molecular pathways and hippocampal neurogenesis, undoubtedly also play a role in MDD, monoaminergic boosting drugs nonetheless have clearly demonstrated antidepressant properties. There is also, however, a body of studies in the preclinical literature suggesting that monoaminergic transmission reducing drugs, including noradrenergic ones, also have antidepressant-like behavioral properties in rodents. Given that there is increasing evidence that the monoamines have u-shaped or Janus-faced dose-response properties, in which a mid-range value is “optimal” in a variety of behavioral and physiological processes, it is plausible that either too much or too little synaptic norepinephrine in key circuits may exacerbate MDD in some individuals. Here we briefly review rodent depression-related behavioral data, focusing on the forced swim test, from three major classes of noradrenergic transmission reducing drugs (alpha2 agonists, beta blockers, alpha1 antagonists), and find much support for the hypothesis that they have antidepressant-like properties. Whether these drugs are antidepressants in human subjects remains to be determined.

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“…While it is tempting to see the tail-suspension test as a more sensitive version of the forced swim test, there are subtle differences between them, which are not at present understood but involve significant mediation by a noradrenergic-receptor-mediated mechanism(s) (Ferrari et al, 1991). In particular, 5HT 1A receptor agonists are active in the forced swim test, but are ineffective in the tailsuspension test (Porsolt et al, 1991), whereas the mixed 5-HT 1A/1B receptor agonist RU 24969 was active in the latter.…”

Section: Tail-suspension Testmentioning

confidence: 99%