Proceedings of The Physiological Society
University of Leeds (2002) J Physiol 544P, S006
Projections from the central nucleus of amygdala to brainstem neurones that are activated by alteration of blood pressure
Sikha Saha, Mark J. Drinkhill, Jonathan P. Moore and Trevor F.C. Batten
Institute for Cardiovascular Research, School of Medicine, University of Leeds, Leeds LS2 9JT, UK
The central nucleus of amygdala (CeA) is a forebrain nucleus involved in the integration of cardiovascular functions during stress and anxiety (Iwata et al. 1987). Anatomical and physiological studies indicate that the CeA sends projections to several brainstem nuclei, including the nucleus of the solitary tract (NTS). We have recently shown that axons projecting from the CeA to the NTS contain λ-aminobutyric acid (GABA) and the vesicular GABA transporter (Saha et al. 2000). Some CeA terminals in the NTS were also immunopositive for somatostatin, and apposed dendrites displaying immuno-reactivity for the sst2A receptor subunit (Saha et al. 2002).
Here we have used the expression of the immediate early gene c-fos to identify NTS neurones that are activated following infusion of either a hypertensive agent, phenylephrine (PE) or a hypotensive agent, sodium nitroprusside (NP). Adult rats were anaesthetized with pentobarbitone (40 mg kg-1, I.P.) and infused for 1 h with either PE (1 mg ml-1 in saline, n = 8) or NP (1 mg ml-1 in saline, n = 6), at a rate sufficient to maintain mean arterial pressure at least 25 % above or below the resting level, respectively. Control rats (n = 4) were infused with saline for the same length of time. Axons originating from the CeA were identified in the same animals by microinjection of biotin dextran amine (BDA, 0.2 ml of 10 %) in the CeA 12-15 days earlier, under the same conditions of anaesthesia. At the end of the infusion period, the rats were humanely killed by perfusion with aldehyde fixative, and vibratome sections of the brainstem were processed for Fos-protein immunohistochemistry. PE-induced hypertension resulted in c-fos expression in neurones mainly restricted to the dorsomedial subnucleus of the NTS. On the other hand, NP-induced hypotension produced more widespread c-fos expression in the NTS which was most concentrated in the medial and ventral subnuclei. Following microinjection of BDA into the CeA, anterogradely labelled varicose fibres were observed in close apposition with Fos-immunoreactive neurones in the dorsomedial NTS.
The results suggest that the CeA may directly influence the activity of NTS neurones that are involved in regulation of blood pressure in response to stressful conditions. Further electron microscopic studies are needed to confirm that the terminals derived from the CeA axons form synapses with the activated neurones in the NTS.
All procedures accord with current UK legislation.
Where applicable, experiments conform with Society ethical requirements