EFFECT OF MICROINJECTION OF MUSCIMOL INTO THE DORSOMEDIAL OR PARAVENTRICULAR HYPOTHALAMIC NUCLEUS ON AIR STRESS-INDUCED NEUROENDOCRINE AND CARDIOVASCULAR CHANGES IN RATS

The paraventricular nucleus (PVN) contains neurons that release cortic otrophin-releasing factor (CRH) and thus provide the stimulus for the release of adrenocorticotrophic hormone (ACTH), the neuroendocrine hal lmark of the response to stress. However, inhibition of neuronal activ ity in the nearby dorsomedial hypothalamic nucleus (DMH) by microinjec tion of the GABA(A) receptor agonist muscimol suppresses cardiovascula r changes seen in air stress in conscious rats, while similar treatmen t in the PVN has no effect. Because the DMH projects to the PVN and al so contains CRH neurons, we decided to investigate the role of neurona l activity in the DMH in the neuroendocrine response to stress. In con trol rats or after microinjection of saline vehicle into either the PV N or the DMH, air stress resulted in equivalent increases in plasma le vels of ACTH, heart rate, and arterial pressure. Bilateral microinject ion of muscimol 80 pmol/100 nl/side into either the PVN or the DMH pri or to air stress reduced the associated increases in plasma ACTH (-37% and -71%, respectively), while only injection into the DMH attenuated the accompanying tachycardia (-62%) and presser (-83%) effects. Thus, neurons in the DMH, but not in the PVN, play a role in both the cardi ovascular and neuroendocrine response to air stress.