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D J Reis

Publications and source records attributed to D J Reis.

At least 253 records · Page 14Linked to original sources
PubMed1986

Somatostatin and cholecystokinin octapeptide differentially modulate the release of [3H]acetylcholine from caudate nucleus but not cerebral cortex: role of dopamine receptor activation.

The effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-induced release of acetylcholine (ACh) were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Potassium (5-55 mM) produced a concentration-dependent increase in the release of [3H]ACh in the presence of extracellular Ca2+. SOM (1 microM), CCK-8 (1 microM) and the dopamine (DA) receptor agonist, apomorphine (APO, 30 microM) inhibited the K+-induced (35 mM) release of [3H]ACh by 26-32% from CN, but did not affect ACh release from CX. Other peptides (1 microM), such as Met-enkephalin, vasoactive intestinal peptide, thyrotropin-releasing hormone and substance P, had no effect on release of [3H]ACh in CN or CX. Sulpiride (SULP), a dopamine receptor antagonist, prevented the effects of APO and SOM, but not CCK-8, to inhibit [3H]ACh release. The results indicate that: (1) SOM and CCK-8 inhibit the release of [3H]ACh in CN, but not CX; and (2) the inhibitory effect of SOM, but not CCK-8, on [3H]ACh release is mediated by dopaminergic mechanisms.

Acetylcholine↗
PubMed1986

Met-enkephalin selectively increases the spontaneous release of amino acid neurotransmitters from rat striatal slices.

Met-enkephalin (1 microM) increased the spontaneous release of endogenous glutamate (+155%), taurine (+80%) and glycine (+50%) from rat striatal slices, but was without effect in the cerebral cortex. This effect was calcium-dependent and significantly reduced in the presence of naloxone (1 microM). Naloxone alone had no effect on release of any substance. Release of aspartate, gamma-aminobutyric acid and [3H]acetylcholine was not significantly affected. Met-enkephalin did not affect potassium (35 mM)-evoked neurotransmitter release, nor did it affect the uptake of D-[3H]aspartate, [3H]taurine or [14C]glycine. The data indicate that opioid receptor activation selectively increases the spontaneous calcium-dependent release of putative amino acid neurotransmitters in the rat striatum.

Amino Acids↗
PubMed1986

Disruption of auditory but not visual learning by destruction of intrinsic neurons in the rat medial geniculate body.

The contribution of intrinsic neurons in the medial geniculate body (MG) of the rat to the classical conditioning of emotional responses to acoustic stimuli was examined. Injection of ibotenic acid, which destroys cell bodies but not axons of passage, into the MG disrupted the conditioned changes in mean arterial pressure and emotional behavior elicited by a tone previously associated with footshock. Unconditioned responses elicited by the tone and by the footshock were unaffected. Moreover, the same animals readily learned to associate a visual stimulus with footshock. Thus, destruction of intrinsic neurons in the MG selectively disrupts the conditioning of emotional responses to acoustic stimuli. The MG appears to be the afferent link in a modality specific emotional learning pathway.

Acoustic Stimulation↗
PubMed1986

A novel vasodepressor response elicited from the rat cerebellar fastigial nucleus: the fastigial depressor response.

We sought to determine by using kainic acid (KA), an agent stimulating neuronal cell bodies but not fibers, whether the elevations in arterial pressure (AP) and heart rate (HR) elicited by electrical stimulation of the cerebellar fastigial nucleus (FN) are due to excitation of local neurons in FN or fibers passing through the area. Rats were anesthetized (chloralose 40 mg/kg), paralyzed (tubocurarine) and artificially ventilated. Electrical stimulation of FN (50 Hz, 10-100 microA) increased AP and HR. In contrast restricted microinjections of KA (0.05-5 nmol/100 nl) in FN elicited a sustained, dose-dependent decrease in AP and HR. The response is not due to diffusion of KA to adjacent sites. Excitation by KA of neurons intrinsic to FN elicits a heretofore unrecognized vasodepressor response, the fastigial depressor response.

Animals↗
PubMed1986

An endogenous clonidine-displacing substance from bovine brain: receptor binding and hypotensive actions in the ventrolateral medulla.

A substance has been isolated from bovine brain which displaces 3H-clonidine binding to rat brain membranes (clonidine-displacing substance; CDS). To determine whether CDS is similar to the antihypertensive agent clonidine, the in vitro binding properties of partially-purified CDS and its physiological action in the rostral ventrolateral medulla were examined. Like clonidine, CDS potently inhibited 3H-para-aminoclonidine binding to receptors in bovine ventrolateral medulla membranes (clonidine, IC50 = 24 +/- 8nM; CDS, IC50 = 0.30 +/- .10 Units), with highest affinity for non-adrenergic sites (clonidine, IC50 = 6 +/- 1nM; CDS, IC50 = 0.12 +/- .07 Units). CDS had no effect at beta-adrenergic or muscarinic cholinergic receptors. Like clonidine, CDS elicited a potent, reversible (less than 10 min) dose-dependent fall in arterial pressure (AP) and heart rate when microinjected specifically into the C1 area of the rostral ventrolateral medulla in the rat (maximum delta AP, -65 +/- 7 mm Hg). CDS represents an as-yet-uncharacterized endogenous, physiologically-active agent in brain which may participate in cardiovascular control via non-adrenergic receptors in the rostral ventrolateral medulla.

Animals↗
PubMed1986

Muscarinic cholinergic receptors mediate the cerebrovasodilation elicited by stimulation of the cerebellar fastigial nucleus in rat.

We have investigated the effects of systemic administration of atropine sulfate on the global cerebrovascular vasodilation elicited by electrical stimulation of the cerebellar fastigial nucleus (FN) in chloralose-anesthetized rat. Atropine (0.3 mg/kg, i.v.) abolished the cerebrovasodilation elicited from FN but did not affect the concomitant elevation in arterial pressure and the EEG changes. We conclude that the cerebrovascular effect of FN stimulation, but not the peripheral cardiovascular or EEG changes, are mediated by cholinergic muscarinic receptors associated with cerebral vessels and/or intrinsic neural pathways.

Animals↗
PubMed1986

Destruction of intrinsic neurons in the lateral hypothalamus disrupts the classical conditioning of autonomic but not behavioral emotional responses in the rat.

The present study examined whether destruction of intrinsic neurons in the lateral hypothalamus of the rat would disrupt the acquisition of classically conditioned changes in arterial pressure. Ibotenic acid, a cellular toxin which spares axons of passage, was injected bilaterally in the hypothalamus either medial or lateral to the fornix. After 2 weeks the animals were subjected to classical fear conditioning trials involving the presentation of a tone in association with footshock. The next day changes in arterial pressure and emotional behavior elicited by the tone alone were measured. Destruction of intrinsic neurons in the lateral hypothalamus prevented the normal establishment of the arterial pressure conditioned response but did not affect the behavioral response. Unconditioned arterial pressure responses elicited by the tone and shock were not affected. Medial hypothalamic injections had no effect on any of the responses. The location of the lateral hypothalamic cell loss overlapped with the neurons projecting to the autonomic region of the spinal cord. Intrinsic neurons in the lateral hypothalamus therefore appear to be specifically involved in mediating learned cardiovascular adjustments.

Animals↗
PubMed1986

Strain-specific differences in levels of the mRNA for the epinephrine synthesizing enzyme phenylethanolamine N-methyltransferase.

The activity of the epinephrine biosynthetic enzyme phenylethanolamine N-methyltransferase (PNMT, EC 2.1.1.28) is 3- to 8-fold greater in rats of the Fischer 344 and Buffalo strains. The biochemical basis for the strain differences has been analyzed at the level of PNMT protein and messenger RNA production. Fischer rat adrenals possess approximately 5-fold more PNMT protein than those of the Buffalo rat as established by Western blotting and immunoprecipitation of adrenal gland homogenates. Poly(A)+ RNAs purified from adrenal glands of each strain were translated in a reticulocyte lysate system, immunoprecipitated with antibody to PNMT and fractionated by SDS-PAGE. A 35S-labelled protein of Mr = 34,000 was immunoprecipitated from adrenals of Fischer and Buffalo rats, indicating that the molecular weights of PNMT do not differ in these strains prior to post-translational processing. Hybridization of a 740 base pair (bp) cDNA for PNMT indicated that the mRNAs for PNMT are the same size in the adrenals of both strains. However, the adrenals of Fischer rats contain 2- to 4-fold more PNMT mRNA than Buffalo rats, as established by quantitative dot blot hybridization and Northern blot analysis. The medulla oblongata, the site of cell bodies of central adrenergic neurons, also contains approximately 2-fold more PNMT mRNA in Fischer rats. The strain specificity in the production of PNMT reflects differences in the expression of the gene for PNMT. Thus, an inherited capacity for PNMT expression may in fact provide the intrinsic determinants responsible for neurotransmitter production. These data provide a direct link between regulation of catecholamine enzyme biosynthesis at the genomic level and the availability of specific catecholamines for neurotransmitter and hormonal functions.

Adrenal Glands↗
PubMed1986

Interruption of projections from the medial geniculate body to an archi-neostriatal field disrupts the classical conditioning of emotional responses to acoustic stimuli.

We have previously found that the coupling of changes in autonomic activity and emotional behavior to acoustic stimuli through classical fear conditioning survives bilateral ablation of auditory cortex but is disrupted by bilateral lesions of the medial geniculate nucleus or inferior colliculus in rats. Auditory fear conditioning thus appears to be mediated by the relay of acoustic input from the medial geniculate nucleus to subcortical rather than cortical targets. Since the medial geniculate nucleus projects, in addition to auditory cortex, to a striatal field, involving portions of the posterior neostriatum and underlying archistriatum (amygdala), we have sought to determine whether interruption of connections linking the medial geniculate nucleus to this subcortical field also disrupts conditioning. The conditioned emotional response model studied included the measurement of increases in mean arterial pressure and heart rate and the suppression of exploratory activity and drinking by the acoustic conditioned stimulus following delayed classical conditioning, where the footshock unconditioned stimulus appeared at the end of the conditioned stimulus. The peak increase in arterial pressure and the duration of activity and drinking suppression were greater in unoperated animals subjected to delayed conditioning than in pseudoconditioned controls, where the footshock was randomly rather than systematically related to the acoustic stimulus. Increases in heart rate, however, did not differ in conditioned and pseudoconditioned groups. While the arterial pressure and behavioral responses therefore reflect associative conditioning, the heart rate response does not. Rats were prepared with bilateral lesions of the medial geniculate nucleus, bilateral lesions of the striatal field or asymmetrical unilateral lesions destroying the medial geniculate nucleus on one side and the striatal field on the contralateral side. The latter preparation leaves one medial geniculate nucleus and one striatal field intact but disconnected and thus produces a selective auditory deafferentation of the intact striatal field. Control groups included animals with unilateral lesion of the medial geniculate nucleus, with unilateral lesion of the medial geniculate nucleus combined with lesion of the ipsilateral striatal field, unilateral lesion of the medial geniculate combined with lesion of the contralateral anterior neostriatum (a striatal area outside of the medial geniculate nucleus projection field).(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1986

Anatomical evidence for interactions between catecholamine- and adrenocorticotropin-containing neurons.

Recent studies suggest that neurons containing adrenocorticotropin and catecholamines are localized to similar areas of the brain. In this immunocytochemical study, the distributions of neurons and terminals containing adrenocorticotropin and tyrosine hydroxylase, the first enzyme in the catecholamine biosynthetic pathway, were compared using the peroxidase-antiperoxidase technique. Neurons containing adrenocorticotropin and tyrosine hydroxylase formed overlapping hyperbolic lamina in the mediobasal hypothalamus. Although adrenocorticotropin and tyrosine hydroxylase containing neurons often formed small clusters, no double labeled cells were observed. Overlap also occurred between adrenocorticotropin and tyrosine hydroxylase terminal fields in several diencephalic nuclei including the periventricular hypothalamic gray and paraventricular thalamus. In contrast, other regions displayed striking compartmentalization of terminal fields; for example, in both the paraventricular hypothalamus and central nucleus of the amygdala, adrenocorticotropin was located in ventral and tyrosine hydroxylase in more dorsal aspects of the nuclei. Adjacent sections also showed a close correspondence between adrenocorticotropin terminals and tyrosine hydroxylase cell bodies in paraventricular, periventricular, dorsomedial and ventral hypothalamic nuclei. These data provide anatomical substrates for potential functional interactions between catecholamine and adrenocorticotropin systems in forebrain.

Adrenocorticotropic Hormone↗
PubMed1986

Lesions of nucleus tractus solitarii globally impair cerebrovascular autoregulation.

We studied the effects of acute bilateral electrolytic lesions of the nucleus tractus solitarii (NTS) on regional cerebral blood flow (rCBF) and its autoregulation in rats anesthetized (alpha-chloralose, 40 mg/kg), paralyzed (tubocurarine), and artificially ventilated. rCBF or regional cerebral glucose utilization (rCGU) was measured 30 min after NTS lesions, by the 14C-iodoantipyrine technique or 2-deoxyglucose method, respectively. Cerebrovascular autoregulation was assessed in groups of 4-5 rats at three levels of arterial pressure (AP): 90, 125, and 140 mmHg. AP was lowered by hemorrhage or elevated by intravenous infusion of phenylephrine. NTS lesions did not alter rCBF at 125 mmHg (P greater than 0.05) but resulted in loss of autoregulation (P less than 0.05, analysis of variance). In contrast, lesions of the cuneate nucleus or transection of the baroreceptor afferents did not alter autoregulation. NTS lesions did not affect the reactivity of the cerebrovascular bed to hypercarbia (PaCO2 57.4 +/- 1; n = 5) or hypocarbia (PaCO2 24.4 +/- 1; n = 5) nor the rCGU in any brain regions (P greater than 0.05; n = 5). We conclude that lesions of the NTS impair cerebrovascular autoregulation. The effect is not due to changes in metabolism, nonspecific effects of the lesions, vasoparalysis, or interruption of the baroreceptor reflex arch. Neural pathways originating in or passing through the NTS can regulate the cerebrovascular autoregulation of the entire brain.

Animals↗
PubMed1986

Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface.

We sought to establish whether neurons of the C1 area of the rostral ventrolateral medulla (RVL) mediate changes in arterial pressure and heart rate evoked by topical application of drugs to the ventral medullary surface of the rat. Animals were anesthetized, paralyzed, and ventilated. The ventral surface was mapped with L-glutamate, and a restricted zone was identified from which L-glutamate, as well as kainic acid, bicuculline, strychnine, carbachol, or physostigmine, increased arterial pressure and heart rate. The hypertensive effects of carbachol and physostigmine were blocked by previous local application of atropine but not hexamethonium. Application of gamma-aminobutyric acid (GABA) or glycine to this area produced hypotension and bradycardia. Located caudal to the trapezoid bodies and lateral to the pyramids, this area corresponded to points with lowest threshold for pressor responses evoked by electrical stimulation and overlapped the distribution of epinephrine-synthesizing cells of the RVL. Processes arising from these neurons were identified reaching and contacting the ventral surface. Unilateral lesions involving the C1 area or phenylethanolamine-N-methyltransferase-labeled descending axons derived from this area imparied by greater than 70% the response to ipsilateral application of L-glutamate, GABA, or glycine to the ventral surface. We suggest that neurons within the C1 area of RVL adjacent to or including epinephrine cells may mediate cardiovascular changes elicited from a restricted chemosensitive zone of the ventral medullary surface of the rat.

Animals↗
PubMed1986

Phenylethanolamine N-methyltransferase-containing neurons in rat retina: immunohistochemistry, immunochemistry, and molecular biology.

We sought to characterize in detail neurons in rat retina that contain phenylethanolamine N-methyltransferase (PNMT), the epinephrine biosynthetic enzyme. Cell bodies and processes of PNMT-containing neurons in retina were identified by immunohistochemistry. The coexistence of other catecholamine biosynthetic enzymes in the same cells was also investigated. Biochemical, molecular biological and immunochemical methods were applied to determine whether retinal PNMT is similar to the adrenal enzyme, since regulation of PNMT in retina and adrenal appears to be different. The results show that there are two types of PNMT-containing cells: those containing PNMT exclusively and those containing PNMT with two other catecholamine-synthesizing enzymes, tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC), but not dopamine beta-hydroxylase (DBH). PNMT-only cell bodies are localized in the inner nuclear layer (INL) and the ganglion cell layer (GCL). Their processes are observed in outer and inner strata of the inner plexiform layer (IPL). Only a small fraction of PNMT neurons in INL also contain TH and AADC. These cells send their processes to the adjacent stratum of the IPL. Antibodies to bovine adrenal DBH, however, fail to localize DBH in any rat retinal cells. Immunochemical titration shows that PNMT from both retina and adrenal gland has the same immunoreactivity. Furthermore, a PNMT-cDNA probe hybridizes equally with PNMT-mRNA isolated from both the retina and the adrenal gland. These results indicate that PNMT is identical in these tissues.

Adrenal Glands↗
PubMed1985

Projections from the nucleus tractus solitarii to the rostral ventrolateral medulla.

Projections from the nucleus tractus solitarii (NTS) to autonomic control regions of the ventrolateral medulla, particularly the nucleus reticularis rostroventrolateralis (RVL), which serves as a tonic vasomotor center, were analyzed in rat by anterograde, retrograde, and combined axonal transport techniques. Autonomic portions of the NTS, including its commissural, dorsal, intermediate, interstitial, ventral, and ventrolateral subnuclei directly project to RVL as well as to other regions of the ventrolateral medulla. The projections are organized topographically. Rostrally, a small cluster of neurons in the intermediate third of NTS, the subnucleus centralis, and neurons in proximity to the solitary tract selectively innervate neurons in the retrofacial nucleus and nucleus ambiguus. Neurons generally located in more caudal and lateral sites in the NTS innervate the caudal ventrolateral medulla (CVL). The RVL, CVL, and nucleus retroambiguus are interconnected. A combined retrograde and anterograde transport technique was developed so as to prove that projections from the NTS to the ventrolateral medulla specifically innervate the region of RVL containing neurons projecting to the thoracic spinal cord or the region of the nucleus containing vagal preganglionic neurons. When the retrograde tracer, fast blue, was injected into the thoracic spinal cord, and wheat germ agglutinin-conjugate horseradish peroxidase (HRP) was injected into the NTS, anterogradely labeled terminals from the NTS surrounded the retrogradely labeled neurons in the RVL and in the nucleus retroambiguus in the caudal medulla. Among the bulbospinal neurons in the RVL innervated by the NTS were adrenaline-synthesizing neurons of the C1 group. When fast blue was applied to the cervical vagus, and HRP was injected into the NTS, anterogradely labeled terminals from the NTS surrounded retrogradely labeled neurons in the rostral dorsal motor nucleus of the vagus, the region of the nucleus ambiguus, the retrofacial nucleus, and the dorsal portion of the RVL, a region previously shown to contain cardiac vagal preganglionic neurons. This combined anterograde and retrograde transport technique provides a useful method for tracing disynaptic connections in the brain. These data suggest that the RVL is part of a complex of visceral output regions in the ventrolateral medulla, all of which receive afferent projections from autonomic portions of the NTS. Bulbospinal neurons in the RVL, in particular the C1 adrenaline neurons, may provide a portion of the anatomic substrate of the baroreceptor and other visceral reflexes.

Afferent Pathways↗
PubMed1985

Strain differences in pituitary prolactin content: relationship to number of hypothalamic dopamine neurons.

BALB/cJ mice have more tuberoinfundibular dopamine neurons, and thus greater tyrosine hydroxylase activity, than CBA/J mice. Strain differences in the synthesis and release of prolactin would also be predicted since dopamine released from the tuberoinfundibular neurons is the prolactin inhibitory factor which plays a role in the regulation of both prolactin synthesis and release. As expected, CBA/J mice, with fewer dopamine neurons, synthesized and released significantly more prolactin than BALB/cJ mice; that is, both pituitary and serum prolactin concentrations were greater in CBA/J mice. To determine if there were more cells containing prolactin or more prolactin per cell, pituitaries were stained with antibodies to prolactin and densitometric analysis made of both the average staining per unit area and total staining per pituitary. For both indices CBA/J mice had more staining than BALB/cJ mice. Using these criteria the difference in staining was attributed to more prolactin-stained lactotrophs in the CBA/J strain. Although no differences in the number of acidophils demonstrated by Pearse Trichrome method were observed, acidophils from BALB/cJ mice appeared smaller and contained less cytoplasm than those from CBA/J mice. We conclude that strain differences in the number of tuberoinfundibular dopamine neurons are inversely related to the number of immunocytochemically demonstrable prolactin-containing cells in the anterior pituitary.

Animals↗
PubMed1985

Projections to the subcortical forebrain from anatomically defined regions of the medial geniculate body in the rat.

Although the auditory cortex is believed to be the principal efferent target of the medial geniculate body (MG), our recent behavioral studies indicate that in rats the conditioned coupling of emotional responses to an acoustic stimulus is mediated by subcortical projections of the MG. In the present study we have therefore used WGA-HRP as an anterograde and retrograde axonal marker to (1) define the full range of subcortical efferent projections of the MG; (2) identify the cells of origin within the MG of each projection; and (3) determine whether the subregions of the MG that project to subcortical areas receive inputs from acoustic relay nuclei of the mid-brain, particularly the inferior colliculus. The rat MG was first parcelled into three major cytoarchitectural areas: the ventral, medial, and dorsal divisions. The suprageniculate nucleus, located within the body of the MG just dorsal to the medial division, was also identified. Efferent projections of the MG were determined by combined anterograde and retrograde tracing methods. Injections of WGA-HRP in the MG produced anterograde transport to cortex and several subcortical areas, including the posterior caudate-putamen and amygdala, the ventromedial nucleus of the hypothalamus, and the subparafascicular thalamic nucleus. The cells of origin of the subcortical projections were then mapped retrogradely after injections in the anterogradely labeled areas. Injections in the caudate-putamen or amygdala retrogradely labeled the medial division of the MG and the suprageniculate nucleus, as well as several adjacent areas of the posterior thalamus surrounding the MG. In contrast, injections in the ventromedial nucleus of the hypothalamus or the subparafascicular thalamic nucleus only produced labeling in the areas surrounding MG. Afferents to MG from the inferior colliculus were then identified. The central nucleus of the inferior colliculus, the main lemniscal acoustic relay nucleus in the midbrain, was found to project to the ventral and medial divisions of the MG. In contrast, the dorsal cortex and external nucleus of the inferior colliculus project to each division of the MG and to several additional nuclei in adjacent areas of the posterior thalamus. These data demonstrate that the medial division of MG, the suprageniculate nucleus, and immediately adjacent areas of the posterior thalamus provide a direct linkage between auditory neurons in the inferior colliculus and subcortical areas of the forebrain and thereby support the view that thalamic sensory nuclei relay afferent signals to subcortical as well as cortical areas.

Amygdala↗