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Biomedical subjects

W W Blessing

Publications and source records attributed to W W Blessing.

At least 109 records · Page 6Linked to original sources
PubMed1987

Origin of serotonin innervation of the arcuate and ventromedial hypothalamic region.

Combined fluorescence serotonin immunohistochemistry and retrograde transport labelling with Fast blue and Fluoro-gold were used to identify serotonin-immunoreactive neurons in the midbrain and pons which project to the region of the arcuate and ventrome-dial hypothalamic nuclei. Approximately 90% of doubly labelled neurons were located in the 3 major mesencephalic serotonin-containing cell groups: dorsal raphe (38%), median raphe (21%) and medial lemniscus group (29%). Within these groups, there were numerous non-retrogradely labelled serotonin-immunoreactive neurons as well as numerous non-serotonin-immunoreactive retrogradely labelled neurons. No doubly labelled neurons were observed caudal to raphe pontis although non-serotonin-immunoreactive neurons were retrogradely labelled in the more caudal raphe nuclei.

Amidines↗
PubMed1987

Neuropeptide Y injected into the supraoptic nucleus causes secretion of vasopressin in the unanesthetized rat.

Injection of neuropeptide Y (NPY, 0.01-1.0 nmol in 0.25 microliter vehicle) into the supraoptic nucleus of unanesthetized rats increased plasma vasopressin, measured by radioimmunoassay, to a maximum of 90 +/- 18 ng/liter. Injections of vehicle or somatostatin did not increase plasma vasopressin, nor did injections of NPY into the amygdala. Double-labelling immunohistochemical studies demonstrated that fibers containing NPY-like immunoreactivity form a close association with vasopressin immunoreactive perikarya in the supraoptic nucleus. It appears that NPY may directly excite vasopressin-containing neurons causing secretion of vasopressin.

Animals↗
PubMed1987

Neurons (presumably A1-cells) projecting from the caudal ventrolateral medulla to the region of the supraoptic nucleus respond to baroreceptor inputs in the rabbit.

Extracellular recordings were made in the caudal ventrolateral medulla from 29 neurons that could be antidromically activated from the region of the supraoptic nucleus in the rabbit. The median axonal conduction velocity was 0.8 m/s. Of 15 cells tested only one did not respond to some form of baroreceptor input. Fourteen were inhibited by experimentally increasing arterial pressure and 8 were excited by decreasing arterial pressure. Stimulation of the aortic depressor nerve decreased the discharge rate of 8 out of 12 cells tested. The location and projections of these neurons suggest that they were A1 noradrenaline-synthesizing cells.

Action Potentials↗
PubMed1987

Neuropeptide Y-like immunoreactive C1 neurons in the rostral ventrolateral medulla of the rabbit project to sympathetic preganglionic neurons in the spinal cord.

After injection into the thoracic spinal cord of the rabbit, gold particles coupled to concanavalin A were found in the rostral ventrolateral medulla in neurons which contained neuropeptide Y-like immunoreactivity. These cells have previously been shown to belong to the C1 catecholamine (presumably adrenaline)- synthesizing group. Nerve terminals in the intermediolateral column contained both tyrosine hydroxylase and neuropeptide Y-like immunoreactivity. When fast blue was injected into the adrenal gland the retrogradely labeled preganglionic neurons were shown to be surrounded by nerve terminals containing neuropeptide Y-like immunoreactivity. Our results indicate that at least some of these terminals derive from C1 neurons which also synthesize neuropeptide Y.

Animals↗
PubMed1987

Depressor neurons in rabbit caudal medulla do not transmit the baroreceptor-vasomotor reflex.

Experiments to determine whether depressor neurons in the caudal ventrolateral medulla form an integral part of the central pathway transmitting the baroreceptor-vasomotor reflex were performed on rabbits anesthetized with urethan. The function of the depressor neurons was altered by intramedullary injections of agents that stimulate or block receptors for gamma-aminobutyric acid and by electrolytic lesions in the caudal ventrolateral medulla. Muscimol abolished both the depressor response and the inhibition of renal nerve activity normally observed after stimulation of the aortic depressor nerve and caused a paradoxical reversal of the depressor response. However, muscimol only partially impaired the inhibition of renal nerve activity produced by experimental elevation of arterial pressure, and it did not affect the increase in renal nerve activity normally produced by decreasing arterial pressure. Bicuculline methiodide amplified the depressor response and the inhibition of renal nerve activity and also restored baroreceptor-vasomotor reflexes abolished by muscimol. Bilateral electrolytic lesions did not alter any component of the baroreceptor-vasomotor reflex. Results indicate that the depressor neurons in the caudal ventrolateral medulla do not form an integral part of the central pathway mediating the baroreceptor-vasomotor reflex. However, output from the depressor neurons appears to inhibit sympathoexcitatory neurons, which also receive baroreceptor-derived inhibitory inputs.

Animals↗
PubMed1987

Noradrenaline, by activation of alpha-1-adrenoceptors in the region of the supraoptic nucleus, causes secretion of vasopressin in the unanaesthetized rat.

In unanaesthetized rats chronically prepared with venous and intracerebral cannulae, noradrenaline injected into the region of the supraoptic nuclei caused a dose-dependent increase in plasma vasopressin, measured by radioimmunoassay. A similar response was obtained with phenylephrine, but not with either clonidine or isoprenaline. The secretion of vasopressin was not secondary to change in arterial pressure, since similar injections of noradrenaline resulted in a small increase in arterial pressure, measured in the anaesthetized rat. These results suggest that noradrenaline stimulates alpha-1-adrenoceptors, presumably located on vasopressin-secreting neurones, thereby causing these cells to secrete vasopressin into the circulation. Tyramine injections also resulted in a prompt elevation in plasma vasopressin, indicating that endogenous noradrenaline is capable of releasing vasopressin.

Animals↗
PubMed1987

Ultrastructural evidence for gamma aminobutyric acid-immunoreactive synapses on somatostatin-immunoreactive perikarya in the periventricular anterior hypothalamus.

Somatostatin-immunoreactive perikarya in the periventricular anterior hypothalamus were demonstrated to be surrounded by gamma aminobutyric acid GABA-immunoreactive nerve terminals, by combining pre-embedding immunocytochemistry for somatostatin and gold labelling post-embedding immunocytochemistry for GABA. Ultrastructural studies revealed that in each 100-nm section, cells immunoreactive for somatostatin (n = 62) were contacted by a mean of 7.6 +/- 0.4 terminal profiles of which 3.0 +/- 0.3 (40%) were GABA-immunoreactive. Most GABA-immunoreactive terminals contained clear rounded vesicles and, where synaptic specializations were well demonstrated, appeared to be symmetric. The finding provides evidence that there is a significant GABA input to somatostatin neurons, an observation strengthening the hypothesis that GABA may inhibit somatostatin neurons, thereby causing increased secretion of growth hormone.

Animals↗
PubMed1986

Distribution of tyrosine hydroxylase and neuropeptide Y-like immunoreactive neurons in rabbit medulla oblongata, with attention to colocalization studies, presumptive adrenaline-synthesizing perikarya, and vagal preganglionic cells.

We studied the distribution, within the rabbit medulla oblongata, of neuronal cell bodies containing either tyrosine hydroxylase or neuropeptide Y-like immunoreactivity. Both avidin-biotin and immunofluorescence procedures were used. Because the two primary antibodies were raised in different species it was possible to perform simultaneous colocalization studies with the immunofluorescence procedure. Tyrosine hydroxylase-containing neurons in the rostral medulla were demonstrated to contain a catecholamine by the colchicine-enhanced FAGLU (formaldehyde-glutaraldehyde) fluorescence histochemical procedure. These neurons are presumably adrenergic, corresponding to the C1 and C2 groups described in the rat. No C3 group was found in the rabbit. The distribution of tyrosine hydroxylase-containing neurons in the caudal medulla was in accordance with previous descriptions of the A1 and A2 groups based on the unenhanced FAGLU procedure. Neuropeptide Y-like immunoreactivity was observed in cell groups corresponding to those already described in the rat, but additional groups were discovered in the rabbit. Some neurons containing neuropeptide Y-like immunoreactivity were observed in nucleus raphe pallidus and these also contained serotonin (5-HT). In the nearby nucleus reticularis gigantocellularis there were occasional neurons that contained neuropeptide Y-like immunoreactivity without any colocalized 5-HT. Neuropeptide Y-like immunoreactivity was also observed in the dorsal motor nucleus of the vagus, rostral to the obex, and these neurons were demonstrated to be true vagal preganglionic cells by colocalization of neuropeptide Y-like immunoreactivity and Fast Blue retrogradely transported from the cervical vagus. We found that neuropeptide Y-like immunoreactivity was colocalized in approximately 75% of the tyrosine hydroxylase-containing neurons in the rostral medulla (C1 and C2 cells). A smaller proportion of the A1 cells also contained this peptide but it was absent from both the most caudal A1 cells and from the A2 cells. Some tyrosine hydroxylase-containing neurons occur in direct apposition to vagal preganglionic cells in both the dorsal motor nucleus of the vagus and the nucleus ambiguous. However, colocalization studies revealed that none of these neurons contained Fast Blue when this dye was retrogradely transported from the cervical vagus. Medullary catecholamine-synthesizing neurons apparently do not contribute axons to the vagus nerve. This finding is consistent with our own studies in the rat but is in contrast to studies in this species published by other workers.

Animals↗
PubMed1986

Activation of GABA receptors in the hypothalamus stimulates secretion of growth hormone and prolactin.

Localized intracerebral microinjections of GABA, muscimol, picrotoxin and bicuculline were made in the anterior and basal hypothalamus to determine possible sites of action of GABA in the regulation of prolactin and growth hormone (GH) secretion. Studies were carried out in unanesthetized male rats with chronic indwelling atrial cannulae and intracerebral guide cannulae which permitted stress free blood sampling and intrahypothalamic injections, respectively. Preoptic/anterior hypothalamic area. (PO/AHA) injection of muscimol (0.16 nmol) stimulated both prolactin and GH secretion. GABA (1600 nmol) stimulated prolactin. Bicuculline (0.016 and 0.16 nmol) inhibited GH secretion. Medial basal hypothalamic (MBH) injection of muscimol (0.1 and 1.0 nmol) and GABA (1000 nmol) stimulated prolactin but had no effect on GH secretion. Picrotoxin and bicuculline did not stimulate GH. These findings indicate that activation of PO/AHA GABAergic receptors facilitates secretion of GH and prolactin and activation of MBH GABAergic receptors stimulates secretion of prolactin. It is proposed that GABA inhibits somatostatin neurons in the PO/AHA to facilitate GH and inhibits tuberoinfundibular dopamine or GABA neurons in the MBH to stimulate prolactin.

Animals↗
PubMed1986

Adrenoceptors in the preoptic-anterior hypothalamic area stimulate secretion of prolactin but not growth hormone in the male rat.

Plasma growth hormone (GH) and prolactin concentrations were measured by radioimmunoassay in unanesthetized male rats after stereotaxic microinjection of adrenergic agents and 6-hydroxydopamine into the preoptic-anterior hypothalamic area (PO/AHA). Norepinephrine, epinephrine, isoprenaline and clonidine failed to stimulate GH, moreover, 16 nanomoles norepinephrine produced a decrease. However, these agents stimulated prolactin secretion and the mixed alpha antagonist phentolamine, administered systemically, inhibited the stimulatory action of epinephrine on prolactin secretion. GH and prolactin secretory patterns were not affected by 6-hydroxydopamine disruption of catecholamine terminals in the PO/AHA. GH responses to adrenergic agonists and the failure of 6-hydroxydopamine to affect GH secretory patterns indicate that PO/AHA norepinephrine afferents do not facilitate GH secretion. Taken in conjunction with previous studies, the results suggest that there must be an extra-hypothalamic site at which norepinephrine is stimulatory for GH. Prolactin responses suggest that alpha adrenoceptors in the PO/AHA may participate in prolactin secretion.

Animals↗
PubMed1985

Evidence that catecholamine-synthesizing perikarya in rat medulla oblongata do not contribute axons to the vagus nerve.

We attempted to confirm reports that medullary catecholamine-synthesizing neurons in the rat contribute axons to the vagus nerve. Vagal preganglionic neurons in the medulla were identified by the retrograde intra-axonal transport of Fast Blue from the cervical vagus. Catecholamine-synthesizing neurons were identified using a specific antibody against tyrosine hydroxylase. A rhodamine-labelled second antibody was used to ensure that Fast Blue and tyrosine hydroxylase could be viewed entirely independently. We did not find any medullary neurons which contained both tyrosine hydroxylase and Fast Blue. Although further investigations by other laboratories are necessary, we believe that previous studies, using punctate versus diffuse horseradish peroxidase staining to doubly label neurons may have produced false positive results.

Amidines↗
PubMed1985

Tetrodotoxin elevates arterial pressure but not plasma vasopressin when injected into the caudal ventrolateral medulla of the rabbit.

When tetrodotoxin (TTS) is microinjected into the caudal ventrolateral medulla it elevates arterial pressure. This is consistent with previous microinjection experiments which show that the injected region contains neurons whose activity inhibits peripheral sympathetic vasomotor tone. However, TTX does not alter plasma vasopressin and this suggests that increases in plasma vasopressin which follow electrolytic lesions may result from excitatory effects of the lesions.

Animals↗
PubMed1985

Caudal ventrolateral medulla can alter vasopressin and arterial pressure.

The effects of specific treatments of the caudal ventrolateral medulla (CVLM) on vasopressin (AVP) release and arterial pressure (AP) were examined in urethane-anesthetized rabbits. Electrical stimulation of the CVLM for 5 minutes did not increase plasma AVP; it did however elicit an acute fall in arterial pressure. Similarly, stimulation of cells in the CVLM by microinjection of L-glutamate caused an acute decrease in AP but no change in plasma AVP. Muscimol injected into the CVLM increased AP but not AVP. On the other hand, bicuculline decreased AP and markedly increased plasma AVP, and the increase in AVP following bicuculline injection was not secondary to the fall in AP. These results demonstrate that the CVLM is involved in the regulation of AVP release. Furthermore, taken together with previous findings, these studies indicate that AVP and AP respond differently to treatments of the CVLM, suggesting that different cells in the CVLM are involved in the regulation of AVP release and AP.

Animals↗
PubMed1985

Inhibiting the rabbit caudal ventrolateral medulla prevents baroreceptor-initiated secretion of vasopressin.

The A 1 noradrenergic neurones are known to project from the caudal ventrolateral medulla to the vasopressin-secreting neuroendocrine cells in the hypothalamus. They therefore represent a possible central pathway from the medulla to the hypothalamus for baroreceptor-initiated secretion of vasopressin. We tested this hypothesis in the anaesthetized rabbit. Muscimol, a gamma-aminobutyric-acid-receptor agonist, was injected into the caudal ventrolateral medulla to inhibit the A 1 noradrenergic neurones. Secretion of vasopressin, measured by radioimmunoassay, was initiated either by arterial haemorrhage or by constriction of the inferior vena cava. After injection of vehicle into the caudal ventrolateral medulla, or after injection of muscimol into nearby control areas, both haemorrhage and constriction of the inferior vena cava produced the expected elevation in plasma vasopressin. After injection of muscimol into the caudal ventrolateral medulla, secretion of vasopressin in response to haemorrhage and to constriction of the inferior vena cava, was completely abolished. The A 1 noradrenergic neurones may be the sole pathway transmitting the reflex for baroreceptor-initiated secretion of vasopressin from the medulla to the hypothalamus.

Adrenergic Fibers↗
PubMed1985

Release of antidiuretic hormone in quadriplegic subjects in response to head-up tilt.

Plasma antidiuretic hormone (ADH) levels during head-up tilt were measured in quadriplegic patients and normal healthy subjects. In normal subjects, neither rapid tilt (from horizontal to 70 degrees head-up in 20 seconds and remaining head-up for 5 minutes) nor gradual tilt (from horizontal to 70 degrees head-up over 15 minutes) significantly changed the plasma ADH level. In contrast, rapid tilt elevated plasma ADH levels approximately fourfold in quadriplegic subjects. A less dramatic elevation in plasma ADH levels followed gradual tilt in quadriplegic subjects. These data, along with the possibility that the pressor potency of ADH is enhanced in quadriplegic subjects, suggest that ADH is involved in the maintenance of blood pressure in quadriplegics in a head-up position.

Adult↗
PubMed1984

Visualisation of catecholamine-fluorescent nerve cell bodies in the rat brain after colchicine treatment.

Central administration of colchicine causes accumulation of catecholamines in nerve cell bodies and enhances their visualisation in the rat brain by the formaldehyde-glutaraldehyde (FAGLU) histofluorescence method. The detection of catecholamine-containing nerve cells by the FAGLU method was considerably improved in rats pretreated with colchicine, and adrenaline-synthesising nerve cells, which are not normally detected by the FAGLU method, could be readily localized after colchicine. The identity of the FAGLU-fluorescent nerve cells was confirmed by simultaneous immunofluorescent detection of catecholamine-synthesising enzymes in sections of the medulla oblongata. The FAGLU method applied to colchicine-treated animals could provide a simple means of detecting central adrenaline nerve cells in other species.

Animals↗