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W W Blessing

Publications and source records attributed to W W Blessing.

At least 127 records · Page 7Linked to original sources

Arterial pressure and plasma vasopressin: regulation by neurons in the caudal ventrolateral medulla of the rabbit.

Experiments in the anesthetized rabbit have demonstrated that the caudal ventrolateral medulla oblongata contains tonically active vasodepressor neurons which are themselves inhibited by GABAergic and glycine-like inputs. Alteration of neuronal function in this region also elevates plasma vasopressin levels, contributing to, but not completely accounting for, the hypertension and pulmonary edema observed after destruction of neurons in the region.

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Synaptic interaction of vagal afferents and catecholaminergic neurons in the rat nucleus tractus solitarius.

Combined radioautography and immunocytochemistry were used to define the ultrastructure and synaptic relations between vagal sensory afferents and catecholaminergic (CA) neurons of the A2 group located within the nucleus tractus solitarius (NTS) of rat brain. The vagal afferents were radioautographically labeled by tritiated amino acids anterogradely transported from the nodose ganglion. Immunocytochemical labeling for tyrosine hydroxylase (TH) served for the identification of catecholaminergic neurons. The radiographically labeled axons seen by light microscopy were widely distributed throughout the more caudal NTS. The reduced silver grains were more densely distributed within the NTS located homolateral to the injected nodose ganglion. The radioautographically labeled processes were localized in regions containing catecholaminergic neurons as indicated by immunoreactivity for TH. Electron microscopic analysis of the medial NTS at the level of the obex demonstrated that the reduced silver grains were localized within axon terminals. The radioautographically labeled terminals were 2-3 microns in diameter, contained numerous small, clear and a few large, dense vesicles, and formed predominately axodendritic synapses. Many of the recipient dendrites contained immunoreactivity for TH. In rare instances, vagal afferents formed synaptic appositions with both TH-labeled and unlabeled axon terminals and neuronal soma. This study provides the first ultrastructural evidence that the catecholaminergic neurons within the NTS receive direct synapses from sensory neurons in the nodose ganglion.

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Evidence that GABA and glycine-like inputs inhibit vasodepressor neurons in the caudal ventrolateral medulla of the rabbit.

Local microinjections of muscimol and glycine into the caudal ventrolateral medulla of the rabbit, caused an acute increase in arterial blood pressure. Bicuculline and strychnine, antagonists of these agents, acutely decreased arterial pressure when microinjected into the same region. Control injections placed 1.5 mm medially did not affect arterial pressure. The pressure changes were independent of heart rate changes and were prevented by prior cervical cord transection. Results suggest that vasodepressor neurons in the caudal ventrolateral medulla are themselves inhibited by GABA and glycine-like inputs.

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Inhibitory cardiovascular function of neurons in the caudal ventrolateral medulla of the rabbit: relationship to the area containing A1 noradrenergic cells.

Experiments were performed to test the hypothesis that A1 noradrenergic neurons, in the caudal ventrolateral medulla, have an inhibitory cardiovascular function. The lateral portion of the caudal medulla was systematically explored, using focal electrical stimulation, in anesthetized, paralyzed rabbits and arterial pressure and heart rate responses were recorded. Since electrical stimulation activates fibers of passage as well as neuronal cell bodies, we also determined cardiovascular responses to microinjections of L-glutamate, a neuroexcitatory amino acid with minimum effects on fibers of passage. Histological studies of stimulation sites were combined with catecholamine fluorescence histochemical studies to localize the A1 cells. A decrease in arterial pressure and heart rate, restricted to the region containing A1 cells, was observed with low frequency stimulation and with microinjections of L-glutamate. In contrast, when GABA, an inhibitory amino acid, was microinjected into the A1 region, we observed an increase in arterial pressure and heart rate. L-Glutamate and GABA responses were dose-related. The fall in pressure was independent of the fall in heart rate. Results support our hypothesis, providing evidence that neurons in the A1 area tonically inhibit sympathetic vasomotor tone.

Adrenergic Fibers↗

Destruction of noradrenergic neurons in rabbit brainstem elevates plasma vasopressin, causing hypertension.

When A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbits are destroyed electrolytically or by local injection of the neurotoxin kainic acid, the concentration of vasopressin in plasma increases, causing hypertension. The A1 neurons may tonically inhibit the activity of vasopressin-secreting neuroendocrine cells through a direct hypothalamic projection.

Adrenergic Fibers↗

Cell groups in the lower brain stem of the rabbit projecting to the spinal cord, with special reference to catecholamine-containing neurons.

Two groups of experiments were carried out in rabbits. In the first groups, the distribution of cell bodies within the pons and medulla projecting ipsilaterally and contralaterally to the thoracic or lumbar spinal cord was studied using the horseradish peroxidase (HRP)/tetramethylbenzidine (TMB) procedure. In the second group, both a previously described double-labeling technique and a new modification of it were used to determine the location of catecholamine (CA)-fluorescent pontomedullary cells projecting to the spinal cord. The results demonstrate that the catecholamine (probably norepinephrine)-containing neurons which innervate the thoracic spinal cord are confirmed almost exclusively to the pons where they were found within the A5, A7 and subcoeruleus groups, as well as the ventral portion of the principal part of the locus coeruleus and the more caudal locus coeruleus, including the A4 cell group. Within the medulla oblongata no doubly labeled A2 cells were observed and the few double labeled A1 cells which were observed were confined to the rostral portion of this group. A dense group of HRP-positive but non-fluorescent cells was found rostral to the A1 area in the ventrolateral reticular formation. These cells, which correspond in position to PNMT-containing cells in the rat, appear to project to both thoracic and lumbar segments of the spinal cord. In contrast, spinally projecting neurons within the nucleus tractus solitarius originated from different subnuclei according to their segmental destination. New information about the organization of medial reticulospinal and vestibulospinal pathways was also obtained.

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Projection of ventrolateral medullary (A1) catecholamine neurons toward nucleus tractus solitarii.

The distribution and interconnections of brainstem catecholamine cell groups thought to be important in cardiovascular control were studied using histochemical and ultrastructural techniques in the rabbit. Lesions and microinjections of horseradish peroxidase (HRP) were made in the nucleus tractus solitarii in the dorsomedial medulla, and in the ventrolateral medulla. After lesions of the dorsomedial medulla the fluorescence intensity of the A1-group of catecholamine neurons was increased, and swollen axons could be seen coursing from the ventrolateral medulla toward the lesions on the same side, but not the opposite side. Most of these axons ran in a band about 2 mm in width, centered at the level of the obex. Electron microscopically, specific cells, identified as A1-catecholamine neurons, showed evidence of chromatolysis after the dorsomedial lesions. Following injection of HRP into the nucleus tractus solitarii. A1-catecholamine cells in the ventrolateral medulla on the same side contained the reaction product. Lesions of the ventrolateral medulla did not produce evidence of a reciprocal projection of A2-catecholamine neurons toward the ventrolateral medulla. Thus axons of the A1-group of catecholamine neurons in the ventrolateral medulla project toward the ipsilateral nucleus tractus solitarii in a relatively compact band at the level of the obex. On the other hand, the A2-group of catecholamine neurons in the dorsomedial medulla does not appear to send projections toward the A1-group.

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Importance of new catecholamine pathways in control of blood pressure.

The first comprehensive maps of central catecholamine pathways referred to both noradrenaline and dopamine neurons. They described the catecholamine neurons as having their cell bodies in the brainstem with spinal axons descending mainly from two medullary cell groups (A1 and A2) and with ascending axons arising mainly from more rostral groups (A3-A13). More recent work utilising immunohistochemistry has established the presence of adrenaline neurons in the brain, in two medullary cell groups (C1 and C2). While these were originally thought to lie within the rostral part of the A1 and A2 cell groups, work from this laboratory has now established that the adrenaline neurons are topographically distinct from the A1 and A2 cells, do not fluoresce with standard methods, and are collected into three groups, the third group (C3) lying in the midline of the rostral medulla. Work in this laboratory using a combination of histochemical fluorescence and retrograde transport of horseradish peroxidase has demonstrated that existence of a descending dopaminergic projection from the hypothalamus to the spinal cord, indicating that descending pathways can arise well above the medulla. Recent studies on the A1 neurons have established the presence of projections from the A1 cells to the median eminence of the hypothalamus and towards the nucleus tractus solitarius in the medulla. Other experiments have demonstrated that most of the descending catecholamine axons do not arise from the A1 and A2 cell groups in the caudal medulla, but higher up in the brainstem especially from the A5 and A7 cell groups. These new descriptions of central catecholamine neurons will necessarily modify the interpretation of many experiments on the central regulation of arterial pressure.

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Catecholamine cell groups of the cat medulla oblongata.

The distribution of catecholamine-containing cells within the cat medulla oblongata has been studied using formaldehyde-glutaraldehyde fluorescence histochemistry. The diffuse ventrolateral cells (A1) were scattered around but not within the lateral reticular nucleus and no cells were found dorsal to the inferior olivary nucleus. The dorsomedial (A2) cells were scattered within the nucleus tractus solitarius with an occasional cell within the dorsal motor nucleus of the vagus. No A2 cells were found within or ventral to the hypoglossal nucleus. This description contrasts in several respects with a recently published atlas of the catecholamine-containing neurons in the cat medulla.

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Immune lesions of central noradrenergic neurons produced by antibodies to dopamine-beta-hydroxylase.

(1) Intraventricular injection of antibodies to dopamine-beta-hydroxylase (DBH) caused degeneration of central noradrenergic nerve terminals in rats and guinea-pigs. In rats it was necessary to infuse exogenous complement in the form of guinea-pig serum together with the anti-DBH, whereas in guinea-pigs the anti-DBH was effective on its own. Control animals were infused with equivalent amounts of non-immune serum and complement and showed no signs of degeneration other than in the region of the needle tract. (2) There was a loss of varicosities in most terminal fields of the noradrenergic projections and swollen distorted axons were seen in both ascending and descending noradrenergic pathways. Noradrenergic cell bodies in the locus coeruleus and subcoeruleus appeared unaffected. No histochemical changes were observed in dopaminergic neurons. (3) The ultrastructural changes in degenerating axons that were first identifided by fluorescence histochemistry included swelling, vacuolation, accumulation of dense cored vesicles, lysosome-like bodies and smooth membranous sacs. The surrounding neuropil appeared normal. (4) There was a significant depletion of noradrenaline in all regions of the rat brain ranging from 20% in the hypothalamus to 80% in the neocortex. Dopamine concentrations were unaffected. (5) These observations provide a new approach to the production of selective lesions in specific neurotransmitter pathways that could be extended to non-adrenergic neurones. They may also be useful as a model for the study of autoimmune diseases of the nervous system.

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Direct projection of catecholamine (presumably dopamine)-containing neurons from hypothalamus to spinal cord.

A procedure for combining catecholamine (CA) and horseradish peroxidase (HRP) histochemistry was used to demonstrate that some of the catecholamine-containing cells in the rabbit dorsal hypothalamus project directly to the thoracic spinal cord. These cells, which are probably dopaminergic, may be involved in the integration of pituitary hormonal secretion and peripheral autonomic nervous regulation.

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