Injection of muscimol in dorsomedial hypothalamus and stress-induced Fos expression in paraventricular nucleus.

Prior microinjection of the GABA(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.

Dysautonomia in fatal familial insomnia as an indicator of the potential role of the thalamus in autonomic control.

Fatal familial insomnia (FFI) is characterized by insomnia, dysautonomia, disruption of circadian rhythms, and motor dysfunction. The typical neuropathological findings in FFI are severe neuronal depletion in the mediodorsal (MD) and anteroventral nuclei of the thalamus. The interaction between the thalamus and central autonomic control mechanisms is poorly understood.

Removal of GABAergic inhibition in the mediodorsal nucleus of the rat thalamus leads to increases in heart rate and blood pressure.

The mediodorsal nucleus of the thalamus (MD) has connections with central autonomic centers involved in cardiovascular control and undergoes severe degeneration in fatal familial insomnia, a human disease characterized by progressive dysautonomia. Microinjections of the GABAA antagonist bicuculline methiodide (BMI) into the medial and central portion of the MD lead to significant, dose-dependent increases in both heart rate and blood pressure. Similar injections into surrounding regions elicited little to no change.

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 corticotrophin-releasing factor (CRH) and thus provide the stimulus for the release of adrenocorticotrophic hormone (ACTH), the neuroendocrine hallmark of the response to stress. However, inhibition of neuronal activity in the nearby dorsomedial hypothalamic nucleus (DMH) by microinjection of the GABA(A) receptor agonist muscimol suppresses cardiovascular changes seen in air stress in conscious rats, while similar treatment in the PVN has no effect. Because the DMH projects to the PVN and also contains CRH neurons, we decided to investigate the role of neuronal activity in the DMH in the neuroendocrine response to stress.

Role of the dorsomedial hypothalamus in the cardiovascular response to stress.

1. Disinhibition of the dorsomedial hypothalamus (DMH) in rats by local microinjection of GABAA receptor antagonists evokes behavioural and physiological changes resembling those seen in acute experimental stress. 2.