Hostname: page-component-848d4c4894-pjpqr Total loading time: 0 Render date: 2024-06-17T23:23:14.050Z Has data issue: false hasContentIssue false

Modulation of neurons in the paraventricular thalamic nucleus by α2 adrenoceptor agonists: evidence for physiological and morphological heterogeneity

Published online by Cambridge University Press:  11 June 2007

Urs Heilbronner
Affiliation:
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany
Gabriele Flügge
Affiliation:
Clinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany

Abstract

The paraventricular thalamic nucleus (PVT) receives dense noradrenergic input, but little is known about α2 adrenoceptors (ARs) in this nucleus. We have investigated effects of the agonist α-methyl-norepinephrine (m-NE) on PVT neurons in vitro. Based on their physiological and morphological characteristics, three distinct classes of PVT neurons have been identified. The first class exhibits membrane hyperpolarization on stimulation with m-NE (0.05–25 µM). This hyperpolarizing effect is observed in the presence of tetrodotoxin (TTX; 0.5–1 µM), blocked by yohimbine (1 µM) and mimicked by clonidine (10 µM), which indicates that it is mediated by postsynaptic α2 ARs. Further experiments indicate that it is mediated through an increase in G protein-coupled K+ conductance. In a second class of neurons, m-NE (0.05–25 µM) induces a slow membrane depolarization that is mimicked by phenylephrine (5 µM) and blocked by prazosin (75 nM), which indicates the involvement of α1 ARs. The third class of neurons is insensitive to m-NE (5–25 µM), and has a lower input resistance and a larger dendritic tree compared to the two other classes. The three types of neurons differ in their resting properties, and their firing patterns are changed by m-NE. These findings indicate anatomical and functional specialization of PVT neurons.

Type
Research Article
Copyright
© 2007 Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)