Publication

Influence of intraventricular application of baclofen on arterial blood pressure and neurotransmitter concentrations in the hypothalamic paraventricular nucleus of rats

Journal Paper/Review - Oct 9, 2011

Units
PubMed
Doi

Citation
Czell D, Efe T, Preuss M, Schofer M, Becker R. Influence of intraventricular application of baclofen on arterial blood pressure and neurotransmitter concentrations in the hypothalamic paraventricular nucleus of rats. Neurochem Res 2011; 37:381-6.
Type
Journal Paper/Review (English)
Journal
Neurochem Res 2011; 37
Publication Date
Oct 9, 2011
Issn Electronic
1573-6903
Pages
381-6
Brief description/objective

The hypothalamic paraventricular nucleus (PVN) is a key site for regulating neuroendocrine functions in the magnocellular part and autonomic activities in the parvocellular part. Its anatomical proximity to the third ventricle could be a good target for intrathecal injection of baclofen. We investigated the correlation of intrathecal application of baclofen (a specific GABAB receptor agonist) and the release of epinephrine, norepinephrine, dopac, homovanillinic acid (HVA), glutamate and aspartate from the PVN. The decomposition products HVA, dopa and dopac of norepinephrine, epinephrine and dopamine, respectively, were used as parameters for the secretion of dopamine. We implanted a microdialysis probe in the PVN of 25 Wistar rats. In 13 rats, 1.5 μg baclofen was injected in the lateral ventricle and the equivalent quantity of Ringer's lactate solution injected in the remaining 12 rats as a control group. Neurotransmitters and amino acids were quantified by high-performance liquid chromatography. There was a conspicuous but not significant effect of baclofen concerning the secretion of epinephrine, norepinephrine, dopac, glutamate and aspartate from the PVN. A significant increase in HVA concentration was observed only in rats treated with baclofen compared with the control group. These findings suggest that baclofen influences the secretion of neurotransmitters and amino acids involved in autonomic activities mediated by GABAB receptors.