Cookies

We use cookies to ensure that we give you the best experience on our website. You can change your cookie settings at any time. Otherwise, we'll assume you're OK to continue.

Durham University

Department of Biosciences

Academic Staff

Publication details for Dr S Pyner

Watkins, ND., Cork, SC. & Pyner, S. (2009). An immunohistochemical investigation of the relationship between neuronal nitric oxide synthase, GABA and presympathetic paraventricular neurons in the hypothalamus. Neuroscience 159(3): 1079-1088.

Author(s) from Durham

Abstract

Functional studies suggest that nitric oxide (NO) modulates sympathetic outflow by enhancing synaptic GABAergic function. Furthermore, the paraventricular nucleus of the hypothalamus (PVN), an important site for autonomic and endocrine homeostasis constitutes an important center mediating NO actions on sympathetic outflow. However, the exact anatomical organization of GABA and NO releasing neurons with the PVN neurons that regulate autonomic activity is poorly understood. The present study addressed this by identifying PVN-presympathetic neurons in the rat with the retrograde tracer Fluorogold injected into T2 segment of the spinal cord or herpes simplex virus injected into the adrenal medulla (AM). GABAergic or nitric oxide cell bodies were identified by antibodies directed towards GABA or glutamate decarboxylase (GAD67) enzyme or neuronal nitric oxide synthase. This revealed a population of GABAergic neurons to be synaptically associated with a chain of pre-sympathetic neurons targeting the AM. Furthermore, this GABAergic population is not a cellular source of NO. Within the PVN, the majority of cellular nitric oxide was localized to non-spinally projecting neurons while for the PVN-spinally projecting neuronal pool only a minority of neuron were immunopositive for neuronal nitric oxide synthase. In summary, nitrergic and GABAergic neurons are associated with a hierarchical chain of neurons that regulate autonomic outflow. This anatomical arrangement supports the known function role of a NO-GABA modulation of sympathetic outflow.