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Distribution of Alpha 2-adrenergic Binding Sites in the Parabrachial Complex of the Rat

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Date 1995 Dec 1
PMID 8751108
Citations 8
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Abstract

The present study describes the distribution of alpha 2-adrenoceptors in the parabrachial and Kölliker-Fuse nucleus of the rat by employing the tritium-labeled alpha 2-receptor antagonist rauwolscine ([3H]-RAUW) as a ligand. The [3H]-RAUW binding was densitometrically quantified in five nuclei of the parabrachial (PB) complex in serial coronal sections. We found that cytoarchitectonically and anatomically distinct nuclei of the PB complex exhibit different numbers of [3H]-RAUW-binding sites. The largest number of binding sites was observed over the external lateral PB and caudally over the waist area of the PB. Lower numbers of binding sites were found in the remaining lateral PB nuclei, followed by the medial PB and the Kölliker-Fuse nucleus. In addition we disclosed that the internal lateral PB contains a very low number of binding sites while the external medial PB is marked by dense [3H]-RAUW binding. Also, the affinities of the binding sites differed between the PB areas. High affinities were observed in the external lateral PB, the remaining lateral PB nuclei and in the waist area of the PB, while the medial PB and the Kölliker-Fuse nucleus exhibited only low affinities for the ligand. Furthermore, saturation curves demonstrated non-linear profiles, indicating the presence of more than one population of binding sites in the PB nuclei for the radioligand. Our data demonstrate that the PB exhibits a distinct distribution of alpha 2-adrenergic binding sites. These correlate well with the cytoarchitectonically defined nuclei of the PB complex and with the pattern of ascending axons from the medial nucleus of the solitary tract and the area postrema terminating in the PB. Since a large number of these projection neurons utilize adrenaline or noradrenaline as their transmitters, we conclude that solitary-parabrachial neurotransmission to the forebrain is, at least in part, mediated via alpha 2-adrenoceptors.

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