Distribution of PNMT and Epinephrine in the medulla oblongata of normotensive and spontaneous hypertensive rats

Summary The distribution of the Epinephrine forming enzyme (PNMT) activity and Epinephrine (E) levels was investigated in the medulla oblongata of spontaneous hypertensive rats (SH-rats) and in two normotensive strains, namely Wistar Kyoto rats (WK-rats) and Wistar rats. The PNMT activity increases progressively from the caudal to rostral parts in the C₁ and C₂ regions of the medulla oblongata.The enzyme activity and the E levels are in all parts of the C₁ and C₂ regions higher in Wistar rats than in WK-rats. The PNMT activity in all parts of the C₂ region (with the exception of the caudal region), and in the middle part of the C₁ region is higher in SH-rats than in WK-rats. The E levels in the SH-rats are higher than in WK-rats in the mediocaudal parts of the C₂ and C₁ regions.Supported by NIMH and NSF grants.     

Genetic epidemiology of an institutionalized cohort of mental retardates

By criterion scaling and principal component analysis of performance, social class, symptoms, institutionalization, and medical history, a cohort of mental defectives has been divided into medical, biological, and sociofamilial categories. This division, corresponding to differences in etiology and severity, reveals changing patterns of admission and provides evidence that male excess is not primarily due to sex linkage. The incidence of mental retardation increases about 5% with first-cousin marriage, in agreement with other studies. The decline of IQ with inbreeding appears to be due entirely to rare recessive genes, not to dominance deviations of polygenes.     

Catecholamine-stimulated cyclic AMP formation in phenylethanolamine n-methyltransferase containing brain stem nuclei of normal rats and of rats with spontaneous genetic hypertension

Stimultaion of cyclic AMP formation by epinephrine and norepinephrine has been studied in discrete areas of rat brain that include the epinephrine-containing brain stem nuclei C-1 and C-2. In the C-1 area, epinephrine-stimulated cyclic AMP formation was partially reversed by 100 microM phentolamine and by 10--100 microM propranolol or alprenolol and hence appeared to involve activation of a mixture of both alpha- and beta-adrenergic receptors as has been reported for other rat brain areas such as the cerebral cortex. However, in the C-2-area, the epinephrine and norepinephrine stimulated cyclic AMP formation involved the activation of a single receptor type which was alpha-like in character. Stimulation of cyclic AMP formation by epinephrine in the C-2 area was antagonized by nanomolar concentrations of both phentolamine and yohimbine. The epinephrine-stimulated formation of cyclic AMP in the C-2 but not in the C-1 area was augmented in a strains of rats which exhibit spontaneous genetic hypertension (SHR) vs. Wistar-Kyoto controls. It is suggested that the enhanced epinephrine-stimulated cyclic AMP formation in the C-2 area of SHR rats could be a physiological compensatory response to some other hypertension-causing lesion which, for example, results in chronically reduced epinephrine release or in ruduced availability of epinephrine at its postsynaptic receptor thereby leading to receptor supersensitivity. Supporting this possibility was the finding that treatment of SHRs and control animals and reserpine resulted in enhancement of epinephrine-stimulated cyclic AMP formation in the C-2 area of control rats, essentially obliterating the difference between control and SHR. The findings are also interepreted as supporting the involvement of epinephrine neurons in central vaso-depressor mechanisms.