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D J Reis

Publications and source records attributed to D J Reis.

At least 289 records · Page 16Linked to original sources
PubMed1984

Rostral ventrolateral medulla: selective projections to the thoracic autonomic cell column from the region containing C1 adrenaline neurons.

Anterograde, retrograde, and combined axonal transport methods were used to describe the descending efferent projections of a region of rostral ventrolateral medullary reticular formation important in cardiovascular control. We have termed this region, which contains C1 adrenaline-synthesizing neurons, the nucleus reticularis rostroventrolateralis (RVL). Efferent projections from the RVL innervate all segmental levels of the thoracic intermediolateral and intermediomedial columns as shown using retrograde transport of lectin-conjugated horseradish peroxidase (HRP) or fast blue dye, and anterograde transport of either HRP or labeled amino acids. The projection is highly specific in that there are no projections to thoracic dorsal or ventral horns. This innervation corresponds to the distribution of preganglionic sympathetic neurons in the intermediolateral column. In particular, terminals surround neurons projecting to the adrenal medulla, as demonstrated by combined anterograde and retrograde transport methods at the light level. Terminals containing phenylethanolamine-N-methyl transferase (PNMT) were mapped using immunocytochemical techniques. PNMT-labeled terminals were present at all levels of thoracic intermediolateral column, in a distribution similar to that of the descending projections from the RVL. We have previously shown using double label techniques (Ross et al., '81-'83), that many of the spinal projections of the RVL originate from C1 neurons. These data support our suggestion that certain bulbospinal neurons within the RVL, in particular the C1 neurons, are crucial for tonic vasomotor control.

Animals↗
PubMed1984

A new group of neurons in hypothalamus containing phenylethanolamine N-methyltransferase (PNMT) but not tyrosine hydroxylase.

Intraventricular injection of colchicine in rat results in the appearance within hypothalamus of numerous neurons containing the adrenaline-synthesizing enzyme, phenylethanolamine N-methyltransferase, but not the other catecholamine biosynthetic enzymes. Increased PNMT staining in hypothalamus was paralleled by an increase in PNMT activity measured in micropunch preparations. Immunotitration demonstrated that this increase was due to accumulation of specific enzyme protein. The finding that hypothalamic neurons express PNMT without tyrosine hydroxylase suggests that such neurons may produce methylated amines other than adrenaline.

Animals↗
PubMed1984

Modulation of cardiovascular and electrocortical activity through serotonergic mechanisms in the nucleus tractus solitarius of the rat.

The nucleus tractus solitarius (NTS) is an integral part of the baroreceptor reflex arc. Thus, stimulation of the NTS elicits changes in arterial pressure and heart rate as well as in numerous other physiologic parameters including electrocortical activity. Serotonin (5-HT), which has been implicated in cardiovascular and electrocortical control, is present in nerve terminals within the NTS. Therefore, this study was designed to determine whether 5-HT may effect that control within the NTS. Serotonin injected into the NTS of anesthetized rats produced marked changes in the EEG, arterial pressure, and heart rate. EEG activity changed from irregular 1-5 Hz, 350-500 microV waves with an overlying 13-15 Hz, low voltage rhythm to a regular, 5 Hz, 250-300 microV rhythm. The dose-dependent cardiovascular changes were maximal at a dose of 400 pmol which produced a fall of mean arterial pressure of 48 +/- 2 mm Hg from a baseline of 96 +/- 4 mm Hg and of heart rate of 90 +/- 9 bpm from a baseline of 400 +/- 18 bpm (n = 6; P less than 0.001). Both the cardiovascular and EEG effects of 5-HT injected into the NTS were blocked by the prior injection of the 5-HT antagonist metergoline at the same site. However, the bilateral microinjection of metergoline into the NTS did not affect the baroreceptor reflex. Thus, although serotonergic mechanisms in the NTS may be involved in the modulation of electrocortical and cardiovascular activity, they are not integral to the baroreceptor reflex arc.

Animals↗
PubMed1984

Dopamine synthesis in inbred mouse strains which differ in numbers of dopamine neurons.

BALB/cJ and CBA/J mice have been shown to have different numbers of dopamine (DA) neurons in the central nervous system, with BALB/cJ mice having 20-50% more DA neurons in each dopaminergic cell group which is reflected in a difference in tyrosine hydroxylase activity in these cell groups. The present study compared the levels of DA and the rate of DA synthesis between these two inbred mouse strains. Three measures were used to reflect the rate of DA synthesis: the levels of DA metabolites (DOPAC and HVA) in the striatum, the rate of disappearance of DA following inhibition of tyrosine hydroxylase with alpha-methyl-P-tyrosine, and the rate of accumulation of DOPA following inhibition of aromatic amino acid decarboxylase with NSD-1015. Striatal DA levels were slightly higher in CBA/J mice than BALB/cJ mice. The rate of DA synthesis in the striatum, as estimated from the accumulation of DOPA following NSD-1015 injection or from the decline of DA levels following alpha-methyl-p-tyrosine injection, was from 30-50% greater in the BALB/cJ mice compared to the CBA/J mice. In striatum, DOPAC levels were higher, HVA levels lower, and DOPAC plus HVA levels equal in CBA/J mice compared to BALB/cJ mice. The results show that BALB/cJ mice, with more DA neurons than CBA mice, also synthesize more DA. In addition, the data suggest that DA levels do not necessarily reflect numbers of DA neurons, and that catecholamine metabolite levels are not a good measure for comparing catecholamine synthesis between inbred animal strains.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Strain difference in fear between spontaneously hypertensive and normotensive rats is mediated by adrenal cortical hormones.

In the present study we sought to determine whether the strain difference in fear reactivity between spontaneously hypertensive rats (SHR) and strain-matched WKY controls might be related to adrenocortical function. SHR and WKY were subjected to adrenalectomy prior to classical fear conditioning. Adrenal cortical steroids were replaced in some animals. Adrenalectomy produced comparable effects on conditioned fear reactivity in SHR and WKY and steroid replacement reversed the effects of adrenalectomy in both strains. However, a larger dose was required to compensate for adrenalectomy in SHR. These date implicate functions related, directly or indirectly, to the adrenal cortex, in the maintenance of the strain difference in fear reactivity.

Adrenal Cortex Hormones↗
PubMed1984

Distribution of catecholamine neurons in the hypothalamus and preoptic region of mouse.

The distribution and morphology of cells containing tyrosine hydroxylase (TH) were mapped by using the immunoperoxidase technique in the hypothalamus and preoptic area in two strains of mouse, CBA/J and BALB/cJ. On the basis of rostral-caudal contiguities between cell aggregates, hypothalamic preoptic neurons were subdivided into three arbitrary groups: (1) dorsal, (2) intermediate, and (3) ventral. New or more prominent collections of TH cells were observed, and in some regions, cells were more complexly organized than originally described. In the dorsal group, a rostral collection of small ovoid cells, previously not described, were located in the anterior preoptic nucleus (APN) of Loo ('31) and extended rostrally and ventrally into the preoptic periventricular gray. The next constituent occupied the paraventricular nucleus (PVN), and was composed of two classes of cells: (1) a small ovoid cell within anterior and medial parvocellular PVN in contiguity rostrally with a similar cell in APN and (2) a larger, angular cell within and adjacent to the lateral PVN in contiguity caudally with cells in the zona incerta (ZI). Further caudally, a larger and more pleomorphic collection of TH neurons was localized in the medial ZI, particularly at midtuberal levels. These cells were not scattered, as previously reported, but were differentiated into two clear-cut densities, a larger medial island and a more elongated lateral island. Cells of ZI, both large and small, extended caudally into the dorsal hypothalamic and subparafascicular nuclei and periventricular gray. In contrast to previous descriptions, no cells were seen in the nucleus reuniens. In the intermediate group, the most rostral constituent occupied the preoptic periventricular gray, extended as far as the lamina terminalis, and merged dorsocaudally with cells in APN. While the variably shaped cells of the hypothalamic periventricular gray (PVG) were still present in the retrochiasmatic region, a striking absence of these cells was noted at midtuberal levels between the dorsomedial and arcuate hypothalamic nuclei. At this level, a new group of small-round TH cells, resembling those of the arcuate nucleus, was identified in the dorsomedial hypothalamic nucleus (DMN). At caudal tuberal levels, similar neurons were found in the posterior hypothalamic nucleus (PH). These neurons overflowed medially into the PVG and caudoventrally into the arcuate nucleus. In the ventral group, the most rostral constituent, composed of both small and ovoid cells in the retrochiasmatic area, appeared to represent the rostral commissural portion of the arcuate nucleus (Arc).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Catecholamine-synthesizing enzymes in paraganglia of aged Fischer-344 rats. Immunohistochemistry and fluorescence microscopy.

The catecholamine-synthesizing enzymes, tyrosine hydroxylase, dopamine-beta-hydroxylase and phenylethanolamine-N-methyltransferase were examined by immunohistochemistry in hypertrophied paraganglia of aged male Fischer-344 rats. All paraganglionic cells reacted with antibodies against tyrosine hydroxylase. Dopamine beta-hydroxylase was identified in most paraganglionic cells, indicating that they synthesized norepinephrine. A variable number of paraganglia were positive for phenylethanolamine-N-methyltransferase, which suggested that they synthesized epinephrine. The formaldehyde-induced fluorescence method demonstrated greenish-yellow fluorescence or yellowish-brown fluorescence. The intensity of the fluorescence was in the same range as in adrenal medullary cells. The observations indicate that paraganglia are capable of synthesizing epinephrine.

Animals↗
PubMed1984

Olfactory bulb dopamine neurons survive deafferentation-induced loss of tyrosine hydroxylase.

Peripheral deafferentation of the rodent olfactory bulb results in loss of dopamine content, tyrosine hydroxylase activity and immunocytochemical staining for tyrosine hydroxylase in juxtaglomerular dopamine neurons. Reinnervation of the bulb by afferent neurons results in the return of all parameters to control levels suggesting that the dopamine neurons did not degenerate but that the expression of tyrosine hydroxylase enzyme was transneuronally regulated in a static population of juxtaglomerular cells. To evaluate this possibility, we determined the activity and immunocytochemical localization of the second enzyme in the dopamine biosynthetic pathway, DOPA decarboxylase. At a time when tyrosine hydroxylase activity was reduced to 25% of control values, DOPA decarboxylase activity in the lesioned bulb was maintained at about 65% of that in the unlesioned bulb. Immunocytochemical staining with antibodies to both enzymes, performed sequentially in the same sections, demonstrated that in the unlesioned bulb tyrosine hydroxylase and DOPA decarboxylase are co-localized in the same population of juxtaglomerular neurons. Similar results were obtained in adjacent sections each stained with one of the two antibodies. In contrast, in the deafferented bulb, about three times as many neurons were stained with DOPA decarboxylase as with tyrosine hydroxylase antibodies. The DOPA decarboxylase activity measurements and immunocytochemistry argue for the continued presence, in the lesioned olfactory bulb, of a population of tyrosine hydroxylase deficient dopamine neurons. The data suggest that olfactory receptor cell innervation transneuronally regulates the expression of tyrosine hydroxylase by mechanisms separate from those controlling the levels of DOPA decarboxylase.

Afferent Pathways↗
PubMed1984

Aromatic L-amino acid decarboxylase in the rat brain: immunocytochemical localization in neurons of the brain stem.

Neurons containing the enzyme aromatic L-amino acid decarboxylase were immunocytochemically localized in the brain stem of the rat. The enzyme occurred as expected in previously well characterized monoaminergic cell groups, and in addition in some nuclei with unknown neurotransmitters. Major aggregates of neurons that were immunoreactive for aromatic L-amino acid decarboxylase but contained neither tyrosine hydroxylase nor serotonin, were found in the pretectal nuclei, the lateral parabrachial nucleus, and the dorsolateral subdivision of the nucleus tractus solitarius. Aromatic L-amino acid decarboxylase was also present in serotonin neurons and the majority of catecholamine cell groups. Dopamine, noradrenaline, and adrenaline cells exhibited characteristic staining intensities to anti-aromatic L-amino acid decarboxylase reflective of relative enzyme levels in the different groups. Some cells in the dorsal motor nucleus of the vagus that were previously classified as dopaminergic lacked immunoreactivity to aromatic L-amino acid decarboxylase.

Animals↗
PubMed1984

In vivo release by vagal stimulation of L-[3H] glutamic acid in the nucleus tractus solitarius preloaded with L-[3H] glutamine.

In anesthetized and paralyzed rats, using a push-pull perfusion technique, we examined the effect of bilateral vagal stimulation on the release of L-[3H] glutamic acid (L- [3H] Glu) from the nucleus tractus solitarius (NTS), after preloading the tissue either with L-[3H] Glu or L-[3H] glutamine (L- [3H] Gln). Vagal stimulation sufficient to produce a maximum fall of arterial pressure (AP) evoked release of L- [3H] Glu from the NTS when the tissue was preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] aspartic acid (D-[3H] Asp) when this stable Glu analogue was used to preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] precursor L-Gln is a good marker of the releasable pool of L-Glu in vivo and are consistent with the hypothesis that L-[3H] Glu is a neurotransmitter in the NTS, mediating the vasodepressor response from cardiopulmonary mechanoreceptors.

Afferent Pathways↗
PubMed1984

Inhibitory influences from arterial baroreceptors on vasopressin release elicited by fastigial stimulation in rats.

Electrical stimulation of the fastigial nucleus in anesthetized, paralyzed, and artificially ventilated rats for 10 seconds (50 Hz) induced a stimulus-locked elevation of arterial pressure (the fastigial pressor response) and increased plasma vasopressin. Cervical spinal cord transection abolished the stimulus-locked fastigial pressor response and augmented the vasopressin response to a 10-fold increase (19 +/- 1 to 188 +/- 58 pg/ml, P less than 0.05; n = 8). Grading the pressor elevations occurring during the fastigial nucleus stimulus changed the amounts of vasopressin released in the same animal: acute adrenalectomy and chemosympathectomy by guanethidine reduced the magnitude of the fastigial pressor response and facilitated the vasopressin release to fastigial nucleus stimulation (intact: 52 +/- 11 pg/ml; after adrenalectomy and chemosympathectomy, 254 +/- 73 pg/ml, P less than 0.05, n = 6). Subsequent intravenous administration of a bolus of phenylephrine to increase mean arterial pressure during fastigial nucleus stimulus, as in intact situation, reduced the vasopressin release (47 +/- 9 pg/ml). After sinoaortic denervation plus vagotomy, the fastigial pressor response was preserved; however, vasopressin still increased 11-fold (from 11 +/- 1 to 126 +/- 23 pg/ml, P less than 0.01, n = 8). Vagotomy alone did not affect the vasopressin resting level nor the 4-fold increase in response to fastigial nucleus stimulation. Therefore, stimulus-locked elevations of arterial pressure oppose, by reflex mechanisms mediated through baroreceptors, but do not prevent the release of vasopressin elicited by stimulation of the fastigial nucleus.

Animals↗
PubMed1984

Biochemistry and molecular biology of catecholamine neurons: a single gene or gene family hypothesis.

We postulate that the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH), dopamine B-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) are coded for by similar gene coding sequence(s). This is based on the following observations: (1) proteolytic digestion of these enzymes produces similar peptides whose amino acid composition is nearly identical; (2) antibodies to each enzyme coprecipitate more than one of these enzymes from in vitro poly(A)mRNA translation products; (3) using hybrid selection analysis to positively identify the cDNA clones, we discovered that DBH cDNA clones cross-hybridize with PNMT mRNA, and PNMT cDNA cross-hybridize with DBH mRNA; (4) DNA hybridization analysis demonstrated that DBH and PNMT cDNA probes hybridized to several common restriction fragments of total cellular DNA. The evidence suggests that these enzymes are coded for by a single gene or linked genes coding for all catecholamine enzymes.

Amino Acid Sequence↗
PubMed1984

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.

Animals↗
PubMed1984

Role of adrenaline neurons of ventrolateral medulla (the C1 group) in the tonic and phasic control of arterial pressure.

We have sought to determine if adrenaline neurons of the C1 group are responsible for cardiovascular functions heretofore attributed to neurons in the rostral ventrolateral medulla. C1 neurons were identified in rat with antibodies to the adrenaline synthesizing enzyme, PNMT. These project to spinal cord wherein they selectively innervate the sympathetic columns. C1 neurons are also innervated by projections, mostly unilateral, from the nucleus tractus solitarii (NTS). Stimulation of the C1 area electrically, by local injection of the excitatory amino acid, L-glutamate, or with the GABA antagonist bicuculline, elevates arterial pressure (AP). Bilateral electrolytic lesions, microinjection of GABA, or administration of tetrodotoxin, in contrast, collapses AP to levels comparable to that of spinal cord transection. After lesions of one NTS, a lesion of the contralateral C1 area abolishes all reflex activity elicited by electrical or natural stimulation of baroreceptors on the side of C1 lesion without modifying resting AP. Lesions of axon bundles of PNMT neurons in the medulla also abolish baroreflexes after unilateral NTS lesions. C1 neurons appear to be the neurons mediating cardiovascular effects of application of drugs or cold to rostral portions of the ventrolateral medulla. We conclude adrenaline neurons of the C1 area represent the purportedly tonic vasomotor neurons of the rostral ventrolateral medulla and mediate the vasodepressor limb of reflexes arising from arterial baroreceptors and other cardiopulmonary afferents. Whether the tonic vasomotor response to stimulation of C1 neurons is dependent upon the release of adrenaline is not yet certain.

Animals↗
PubMed1984

Glutamatergic mechanisms in the nucleus tractus solitarius in blood pressure control.

The nucleus tractus solitarius (NTS), the site of termination of visceral afferents of the ninth and tenth cranial nerves, mediates and integrates the reflex cardiovascular and noncardiovascular responses to stimulation of cardiopulmonary and other visceral afferents. On injection into the NTS, the amino acid L-glutamate (L-Glu) and its excitatory analogs produce dose-dependent hypotension and bradycardia, a baroreceptor reflex-like response. The L-Glu antagonist glutamate diethyl ester blocks the response both to L-Glu and to baroreceptor reflex activation. Electrical stimulation of vagal c-fibers selectively releases 3H into a push-pull cannula after preloading of the NTS with L-[3H]Glu or D-[3H]aspartate. The NTS contains a high-affinity uptake system for inactivation of L-Glu. Like L-Glu, acetylcholine and serotonin, which are also found in the NTS, both elicit a baroreceptor reflex-like response when microinjected into the NTS. However, cholinergic and serotonergic antagonists do not block the baroreceptor reflex. A glutamatergic neuron (or neurons) projecting into NTS appears to be an integral part of the baroreceptor reflex arc.

Acetylcholine↗
PubMed1984

The brain and hypertension: reflections on 35 years of inquiry into the neurobiology of the circulation.

In 1948 knowledge of the role of the central nervous system in controlling blood pressure was rudimentary and the possibility that the brain could contribute to hypertension was barely acknowledged. Over the past 35 years the development of new technologies, particularly those of the neurosciences, and their application to cardiovascular medicine have markedly increased our understanding of how the brain governs the circulation. Notable has been the increase in knowledge of the neuroanatomy, neurochemistry, and physiology of the representation, within the brain, of the pathways critical in governing blood pressure, particularly those involved in tonic and baroreflex control of the circulation. The observation that perturbations in these networks can lead to the development of hypertension or the reversal of established hypertension and the demonstration that some of these networks are targets of drugs used in the clinical treatment of hypertension provide obvious clinical relevance to the discoveries. In the future, it is expected that more will be discovered about the biochemical neuroanatomy, and hopefully the molecular biology, of these neuronal networks. Such advances will permit more rigorous testing of the proposition that defects in these systems may underlie the disorder of hypertension in human beings.

Blood Pressure↗
PubMed1984

Fastigial nucleus stimulation and concurrent activation of cardiovascular receptors; differentiate effects on arterial pressure, heart rate and vasopressin release.

The integrated effects of stimulation of fastigial nucleus (FN) and of concurrent activation of baroreceptors on arterial pressure (AP), heart rate (HR) and vasopressin (VP) release in anaesthetized, paralysed, artificially ventilated rats were investigated. Stimulation of FN blocked the fall in AP and HR elicited by afferent vagal stimulation. It also abolished the atropine-sensitive bradycardia occurring at the peak of the stimulus-elicited pressor elevation in 6-hydroxydopamine treated rats. Sinoaortic denervation plus vagotomy left the cardiovascular responses to FN stimulus unmodified but facilitated FN elicited VP secretion. Vagotomy alone was ineffective. After high spinal cord transection more VP than in the intact condition was secreted after FN stimulation: simultaneous afferent vagal stimulation did not affect the facilitated VP release. Therefore FN stimulation can inhibit the reflex effects on AP and HR from baroreceptors, while the high-(but not the low-) pressure receptors can partly inhibit the VP release elicited by FN stimulation.

Animals↗