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Cardiovascular alterations seen after microinjection of bicuculline methiodide (BMI) or excitory amino acid (EAA) into the medial hypothalamus is due to activity in the dorsomedial hypothalamic nucleus (DMH) and not from activity in the paraventricalar hypothalamic nucleus (PVN). In concious rats microinjection of 10 pmol BMI, 0.5 pmol kainic acid, or 5 pmol N-methyl-D-aspartate into the DMH remarkably enhances heart rate and there is mildly increased arterial pressure but injections into other areas led to changes which increasingly reduced in magnitude with increasing distance from the nucleus.

Injection of muscimol in dorsomedial hypothalamus and stress-induced Fos expression in paraventricular nucleus. Am J Physiol Regulatory Integrative Comp Physiol 280: R1276-R1284, 2001.--Prior microinjection of the [GABA.sub.A]-receptor agonist muscimol into the dorsomedial hypothalamus (DMH) in conscious rats attenuates the increases in heart rate, blood pressure, and circulating adrenocorticotrophic hormone seen in air stress. Here, we examined the effect of similar treatment on air stress- or hemorrhage-induced Fos expression in the paraventricular nucleus (PVN). Muscimol (80 pmol/100 nl per side) or saline (100 nl per side) was microinjected bilaterally into the DMH in conscious rats before either air stress, an emotional or neurogenic stressor, or graded hemorrhage, a physiological stressor. Each stressor evoked a characteristic pattern of Fos expression in the parvocellular and magnocellular PVN after saline. Injection of muscimol into the DMH suppressed Fos expression in the PVN associated with air stress but not with hemorrhage. Injection of muscimol at sites anterior to the DMH and closer to the PVN had no effect on Fos expression in the PVN after air stress. Thus activation of neurons in the DMH is necessary for excitation of neurons in the PVN during air stress but not during hemorrhage. adrenocorticotrophic hormone; hemorrhage; heart rate; [Gamma]-aminobutyric acid