• Ennio Avolio, Raffaella Alò, Antonio Carelli, and Marcello Canonaco.
• Comparative Neuroanatomy Laboratory of Ecology Department, University of Calabria, Ponte Pietro Bucci 4b, 87030 Arcavacata di Rende, Cosenza, Italy.
• Behav. Brain Res. 2011 Apr 15; 218 (2): 288-95.

AbstractAt present neurobiological interests are directing more attention towards the major role of the amygdalar GABA(A) receptor on orexin-dependent behaviors. This telencephalic region has been widely studied especially in view of its control on various psychiatric disorders such as anxiety and depression. Recently, cross-talking relationships between these two specific neuroreceptor systems of the central-cortical amygdalar complex has been considered an important element for anxiety type of behaviors. In the present study, we investigated the effects of central amygdalar infusions with orexin-A, orexin-B±GABA(A) receptor α₂ subunit agonist (flunitrazepam) on elevated plus-maze and light-dark explorative behaviors of the facultative hibernating Syrian hamster. In a first case, it seemed that doses of orexin administered directly into the central nucleus were responsible for greater anxiogenic type of effects as shown by more time being spent both in the dark compartment and the closed arm of the elevated plus-maze, whereas, these effects were suppressed in the presence of flunitrazepam. At the cellular level, the effects of orexin accounted for evident argyrophilic reactions (neurodegeneration phenomena) including altered cell membrane and loss of cytoplasmic architecture in most amygdalar and hippocampal neuronal fields, while in the presence of flunitrazepam these reactions resulted to either be unappreciable or absent. Overall the actions of α₂-dependent inhibitory signals tend to corroborate, for the first time, a neuroprotective role against the over-excitatory orexinergic neurodegeneration reactions and thus its abnormal anxiety-like indications may prove to be therapeutically useful for orexin-dependent sleeping disorders.Published by Elsevier B.V.

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