European Journal of Pharmacology: Molecular Pharmacology
Regular paperExpression of Fos-like immunoreactivity by yohimbine and clonidine in the rat brain
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Nucleus incertus Orexin<inf>2</inf> receptors mediate alcohol seeking in rats
2016, NeuropharmacologyCitation Excerpt :Interestingly yohimbine (1 mg/kg i.p.) itself did not evoke Fos-IR in OX neurons. Previous studies have shown variable impact of yohimbine (5 mg/kg i.p) on Fos activation, Singewald et al. (2003) observed an increase of Fos in the LH, but Tsujino et al. (1992) observed no change (Singewald et al., 2003; Tsujino et al., 1992). Footshock increases OX Fos in the DMH, PeF or rats (Harris et al., 2005) and DMH, PeF and LH of mice (Watanabe et al., 2005).
Modulation of cannabinoid signaling by amygdala α<inf>2</inf>-adrenergic system in fear conditioning
2016, Behavioural Brain ResearchCitation Excerpt :Yohimbine is specific in its antagonism of the α2 “inhibitory” subtype, and is used clinically as a probe to identify abnormal physiological and affective responses to increased noradrenergic signaling. Although yohimbine has been suggested or reported to interact with receptors for other monoamines [33], the α2 receptor agonist clonidine reverses yohimbine-induced anxiety, and the ability of yohimbine to increase cFos expression and establishment of long-term memory formation in the cortex, amygdala, and other brain regions in rats is attenuated or blocked by pretreatment with clonidine or propranolol, a post-synaptic β-adrenergic receptor antagonist [34–36]. Yohimbine increases neurotransmitter release from noradrenergic axon terminals by blocking presynaptic feedback inhibition of release, and simultaneously reduces the ability of NE to exert inhibitory post-synaptic effects while leaving the excitatory effects of NE at postsynaptic α1 and β receptors unopposed [37].
Yohimbine anxiogenesis in the elevated plus maze is disrupted by bilaterally disconnecting the bed nucleus of the stria terminalis from the central nucleus of the amygdala
2012, NeuroscienceCitation Excerpt :Among adrenergic receptors, YO is specific in its antagonism of the α2 “inhibitory” subtype, and was used in this study as an experimental tool to increase excitatory NA receptor signaling. Although YO has been suggested or reported to interact with receptors for other monoamines (Johnston and File, 1989; Winter and Rabin, 1992; Millan et al., 2000), the α2 receptor agonist clonidine reverses YO-induced anxiety, and the ability of YO to increase cFos expression in the cortex, amygdala, and other brain regions in rats is attenuated or blocked by pretreatment with clonidine or propranolol, a post-synaptic β-adrenergic receptor antagonist (Charney et al., 1983; Gubits et al., 1989; Johnston and File, 1989; Bing et al., 1992; Tsujino et al., 1992). Nevertheless, interpretation of our results does not depend on whether or not YO’s actions are limited to increased transmitter release from NA terminals and increased post-synaptic adrenergic receptor signaling.
Xylazine activates oxytocinergic but not vasopressinergic hypothalamic neurons under normal and hyperosmotic conditions in rats
2005, Neurochemistry International