Disinhibition of the rostral ventral medulla increases blood pressure and Fos expression in bulbospinal neurons
RIS ID
109349
Abstract
The GABA agonist muscimol, injected into the depressor area of the caudal ventrolateral medulla, increased blood pressure and increased the expression of the immediate early gene c-fos in the rostral ventral medulla (RVM) of the rat. The number of Fos-immunoreactive (Fos-IR) neurons seen in the RVM was increased 3-fold after muscimol compared to Fos-IR after vehicle treatment. In the rostral aspect of the RVM approximately half of the Fos-IR neurons were identified as spinally projecting after the injection of the retrograde tracer cholera toxin B subunit into the upper thoracic spinal cord. These bulbospinal Fos-IR neurons were identified in the lateral aspects of the RVM, in the area where baroreceptor-sensitive neurons have been identified in electrophysiological studies, and alos in more medial areas of the RVM. Fos-IR neurons were also identified in the intermediolateral cell column of the thoracic spinal cord after muscimol injection, but were rarely observed in this area after vehicle treatment. This study demonstrates the functional connectivity of the caudal and rostral areas of the medulla oblongata and the spinal cord, supporting the view that the caudal ventrolateral medulla contains neurons that provide a tonic inhibitory control over neurons in the RVM and that, in turn, the spinally projecting neurons in the RVM provide an excitatory input to the spinal cord sympathetic preganglionic neurons. The results show that the withdrawal of an inhibitory input is a sufficient stimulus to increase the expression of c-fos and increase neuronal activity in the RVM. c-fos expression also increases in the neurons that receive an excitatory input from these RVM neurons.
Publication Details
Minson, J. B., Llewellyn-Smith, I. J., Arnolda, L. F., Pilowsky, P. M., Oliver, J. R. & Chalmers, J. P. (1994). Disinhibition of the rostral ventral medulla increases blood pressure and Fos expression in bulbospinal neurons. Brain Research, 646 (1), 44-52.