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M C Bohn

Publications and source records attributed to M C Bohn.

81 records · Page 5Linked to original sources
PubMed1981

Substance P in principal sympathetic neurons: regulation by impulse activity.

Regulation of the putative peptide neurotransmitter substance P was examined in the superior cervical sympathetic ganglion of the neonatal rat. Surgical decentralization (denervation) of the superior cervical ganglion increased ganglion substance P content. In cultured ganglia, the amount of substance P increased more than 50-fold after 48 hours, and this rise was dependent on protein and RNA synthesis. Veratridine prevented the increase in substance P in vitro, and tetrodotoxin blocked the veratridine effect; this suggests that sodium influx and membrane depolarization prevent substance P elevation. Immunohistochemical analysis of cultured ganglia indicated that substance P was present in the perikarya of principal sympathetic neurons and in ganglionic nerve processes. Transsynaptic impulses, through the mediation of postsynaptic sodium influx, may decrease substance P in sympathetic neurons.

Ganglia, Sympathetic↗
PubMed1981

Transmitter phenotypic expression in the embryo.

The initial appearance and development of noradrenergic and adrenergic phenotypic characters was studied in the rat embryo by immunocytochemical methods. Tyrosine hydroxylase and dopamine-beta-hydroxylase (noradrenergic enzymes) appeared at 11.5 days of gestation (Day E 11.5; 27-30 somites) in sympathetic ganglion primordia and in cells of the gut. While tyrosine hydroxylase and dopamine beta-hydroxylase immunoreactivity increased progressively in ganglion primordia, the enzymes disappeared in the gut cells after E 13.5. However, the gut cells themselves persisted, as indicated by the high-affinity uptake of noradrenaline (norepinephrine). Consequently, initial appearance of noradrenergic characters does not ensure persistence and subsequent development, indicating that early phenotypic expression is a mutable process. This contention was supported by the observations that pharmacological stress of pregnant rats in the form of reserpine, or treatment with glucocorticoids, prolonged the appearance of catecholamines in the gut cells. Thus, maternal-embryonic relations in general, and maternal glucocorticoids in particular, may influence embryonic phenotypic expression. Treatment of embryos with nerve growth factor also prolonged the appearance of noradrenergic characters in the gut cells. Expression of the adrenergic phenotype was apparently regulated differently from noradrenergic expression, since phenylethanolamine-N-methyltransferase (PNMT), the adrenaline-(epinephrine)-synthesizing enzyme, was undetectable in ganglion primordia and gut cells. PNMT initially appeared at E 17.5 in cells which had migrated to be adrenal anlage. Extensive studies suggest that the initial appearance of PNMT occurs independently of glucocorticoid regulation, while subsequent development is dependent on corticoids.

Animals↗
PubMed1980

Maternal glucocorticoid hormones influence neurotransmitter phenotypic expression in embryos.

Treatment of pregnant rats with reserpine prevented the normal disappearance of catecholamine fluorescence in presumptive neuroblasts of the embryonic gut. These cells normally express the noradrenergic phenotype transiently during embryonic development. The effect of reserpine was reproduced by treating mothers with hydrocortisone acetate. Moreover, the reserpine effect was blocked by treatment with dexamethasone, which inhibits the stress-induced increase in plasma glucocorticoids, and by mitotone, which causes adrenocortical cytolysis. It is concluded that reserpine, through the mediation of maternal glucocorticoid hormones, alters the phenotypic expression of these embryonic neuroblasts.

Animals↗
PubMed1980

Cerebellar granule cell genesis in the hydrocortisone-treated rats.

The development of the cerebellar cortex was studied by quantitative light microscopic methods in rats treated with hydrocortisone on postnatal days 7-18. This treatment resulted in a decreased number of cells in the external granular layer (EGL) and an early disappearance of the EGL. In the adult cerebellum of these neonatally treated animals, the total number of granule cells in lobule VIII was decreased by 41% and that of molecular layer microneurons by 28%. Autoradiographic determinations of the 'birthdays' (time of origin) of cerebellar microneurons showed that the peaks of cell formation in the internal granular and molecular layers occurred at earlier ages than in controls. In the granule cell population, this observation was the result of both decreased cell proliferation during the treatment and premature cessation of division in granule cell precursors in the EGL. The morphological effects of 'late' hydrocortisone treatment on the cerebellum observed in this study are compared with those of 'early' hydrocortisone treatment on days 1-4 and those of thyroid hormone from previous studies. It is suggested that endogenous levels of both thyroid and glucocorticoid hormones during the neonatal period may influence the rate of neurogenesis in the postnatal rat cerebellum.

Animals↗
PubMedDate not supplied

Ontogeny of adrenergic fibers in rat spinal cord in relationship to adrenal preganglionic neurons.

Adrenergic neurons in the C1 cell group in the rostral ventrolateral medulla oblongata contain epinephrine, as well as its biosynthetic enzyme, phenylethanolamine N-methyltransferase (PNMT). These neurons send axons to regions of the central nervous system known to regulate autonomic function, including the sympathetic preganglionic nuclei of thoracic and upper lumbar spinal cord. Previous studies have shown that PNMT is expressed in neurons located in the medulla oblongata on embryonic day 14; however, the development of the projections from these cells has not been studied. With the aid of high-performance liquid chromatography (HPLC) to determine levels of catecholamines and immunocytochemistry to demonstrate PNMT, the ontogeny of the adrenergic bulbospinal pathway in the embryonic, postnatal, and adult rat has been studied. In addition, the relationship between PNMT-immunoreactive (IR) fibers and retrogradely labeled sympathetic preganglionic neurons projecting to adrenal medulla are described. PNMT-IR fibers were first observed in the caudal medulla oblongata and lateral funiculus of spinal cord on gestational day 15(E15). On E16, PNMT-IR fibers in the thoracic spinal cord were observed in the intermediate gray matter at the level of the lateral horn. Epinephrine was measureable in spinal cord on E20. Both the density of PNMT-IR fibers and the levels of epinephrine increased to a maximum during the second postnatal week and then declined to adult levels. These observations suggest that a period of adrenergic hyperinnervation of spinal sympathetic nuclei occurs during the neonatal period. PNMT-IR terminals in spinal cord were observed, primarily, although not exclusively, in sympathetic nuclei of thoracic cord and parasympathetic nuclei of upper sacral cord. Adrenergic fibers in the intermediolateral nucleus (IML) and the central autonomic nucleus (CAN) dorsal to the central canal were particularly dense during the second postnatal week in both midthoracic and upper sacral segments. In the neonate, a "ladder-like" pattern of PNMT-IR fiber staining was observed which represented transverse fiber bundles connecting IML with CAN and extensive longitundinal fiber bundles along the border of the funiculus in IML. At all spinal levels, adrenergic fibers were also observed adjacent to the ependyma dorsal or lateral to the central canal. The relationship between adrenal preganglionic neurons and PNMT-IR fibers in IML was examined on postnatal days 4, 15, and 60. With retrograde labeling from adrenal medulla, it was demonstrated that PNMT-IR fibers are associated with adrenal preganglionic neurons throughout postnatal development.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Glands↗
PubMedDate not supplied

Expression of phenylethanolamine N-methyltransferase (PNMT) and neuropeptide Y (NPY) in embryonic rat medulla oblongata grown in Oculo.

Expression and development of specific markers of the adrenergic phenotype were studied in central neurons grown in transplant system. Medulla oblongata from embryonic day 12.5 (E12.5) or E18 rat was grafted into the anterior chamber of the eye of adult rat hosts. After two months, grafts were examined for the presence of immunoreactivity (IR) and catalytic activity to the epinephrine-synthesizing enzyme, phenylethanolamine N-methyltransferase (PNMT, E.C. 2.1.1.28), a specific adrenergic marker. In addition, grafts were examined for immunoreactivity to neuropeptide Y (NPY) and tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. In E12.5 grafts, PNMT was expressed de novo, enzyme activity developed to levels similar to those in adult rat brainstem and PNMT-IR neurons were observed. TH-IR and NPY-IR neurons were also observed. In contrast, PNMT-IR was not observed in E18 grafts even though these already contained PNMT-IR neurons at the time of grafting. This was not due to poor growth of E18 grafts, in general, since TH-IR neurons were present and the protein content of the grafts was similar to that of E12.5 grafts. These studies suggest that adrenergic neurons survive well in oculo if they are transplanted prior to the age when neuroblasts have initially expressed the adrenergic phenotype, migrated to their final positions and elaborated processes. In addition, these studies establish a transplant system in which factors required for the development of central adrenergic neurons can be more easily studied than in situ.

Animals↗