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D J Reis

Publications and source records attributed to D J Reis.

At least 307 records · Page 17Linked to original sources
PubMed1984

Tonic vasomotor control by the rostral ventrolateral medulla: effect of electrical or chemical stimulation of the area containing C1 adrenaline neurons on arterial pressure, heart rate, and plasma catecholamines and vasopressin.

We have studied the responses to electrical and chemical stimulation of the ventrolateral medulla in the chloralose-anesthetized, paralyzed, artificially ventilated rat. Locations of most active pressor responses were compared to regions containing neurons labeled immunocytochemically for phenylethanolamine N-methyltransferase (PNMT), the enzyme catalyzing the synthesis of adrenaline. Elevations of arterial pressure (+81.6 +/- 2.5 mm Hg) and cardioacceleration (+73 +/- 13.6 bpm) were elicited with low current (5 times threshold of 9.5 +/- 1.1 microA) electrical stimulation in a region of rostral ventrolateral medullary reticular formation we have termed the nucleus reticularis rostroventrolateralis (RVL). Electrical stimulation of the RVL increased plasma catecholamines (16.8-fold for adrenaline, 5.3-fold for noradrenaline, and 1.9-fold for dopamine) and vasopressin (1.7-fold before spinal transection, 4.7-fold after). The location of the most active pressor region in the ventrolateral medulla corresponded closely with the location of C1 adrenaline-synthesizing (PNMT-containing) neurons. In addition, the location of the most active pressor region in the dorsomedial medulla corresponded with the location of a bundle of PNMT-containing axons. Unilateral injections into the RVL of the excitatory amino acid monosodium L-glutamate (50 pmol to 10 nmol), but not saline, caused transient dose-dependent and topographically specific elevations (maximum +71.6 +/- 4.9 mm Hg) of arterial blood pressure and tachycardia. Injections of the rigid structural analogue of glutamate, kainic acid, caused large, prolonged (at least 15 min) pressor responses and tachycardia. Unilateral injections of the inhibitory amino acid gamma-aminobutyric acid (GABA) into the RVL caused transient dose-dependent hypotension (maximum -40.8 +/- 6.6 mm Hg) and bradycardia, whereas the specific GABA antagonist bicuculline caused prolonged (10 to 20 min) elevations (+64.2 +/- 6.8 mm Hg) of arterial pressure and tachycardia. By contrast, injections of the glycine antagonist strychnine had no significant effect. Bilateral injections of the neurotoxin, tetrodotoxin, dropped arterial pressure to low levels (51.7 +/- 4.7) not changed by subsequent spinal cord transection at the first cervical segment (52.5 +/- 6.2). We propose the following. (1) Neurons within the RVL, most probably C1 adrenaline-synthesizing neurons, exert an excitatory influence on sympathetic vasomotor fibers, the adrenal medulla, and the posterior pituitary. (2) These neurons are tonically active and under tonic inhibitory control, in part via GABAergic mechanisms--perhaps via the nucleus of the solitary tract (NTS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗
PubMed1984

Subcortical efferent projections of the medial geniculate nucleus mediate emotional responses conditioned to acoustic stimuli.

The purpose of this study was to identify the afferent link in the neural pathway which mediates emotional responses coupled to auditory stimuli. We evaluated whether autonomic and behavioral responses elicited by acoustic conditioned emotional stimuli are based on afferent information derived from the auditory cortex or from the auditory thalamic relay station, the medial geniculate nucleus (MG), in rats. The rat auditory cortex was defined through anterograde neuroanatomical tracing studies involving the injection of HRP into MG. Lesions were then placed in the auditory cortex or in MG. After 10 to 20 days the rats were subjected to classical fear conditioning trials involving the pairing of a pure tone with electric footshock. Changes in mean arterial pressure and heart rate and the duration of immobilization ("freezing") and drink suppression elicited by presentation during extinction trials (no footshock) of the acoustic conditioned emotional stimulus were measured. Auditory cortex lesions did not affect the magnitude of the mean arterial pressure or heart rate conditioned responses nor the duration of freezing or drink suppression. In contrast, lesions of MG suppressed the magnitude of both the autonomic and somatomotor (behavioral) conditioned emotional responses but did not affect either autonomic or somatic responses elicited by the footshock unconditioned stimulus. Lesions of the inferior colliculus, the primary source of afferent input to MG, replicated the effects of MG lesions. These findings demonstrate that lesions of MG and lower auditory centers, but not lesions of the auditory cortex, block autonomic and behavioral conditioned emotional responses coupled to acoustic stimuli and indicate that subcortical rather than cortical efferents of MG sustain these responses. Our concurrent observation that MG projects to several subcortical areas (central and lateral amygdala; caudate-putamen; ventromedial hypothalamus) involved in emotional behavior and autonomic function suggests hypotheses concerning subsequent links in this emotional processing pathway.

Acoustic Stimulation↗
PubMed1983

Medullary catecholamine inputs to the anteroventral third ventricular cardiovascular regulatory region in the rat.

Lesions in the tissue at the anteroventral end of the third ventricle (AV3V area) prevent the development of a variety of forms of experimental hypertension. This region receives afferents from several cell groups which have been implicated in cardiovascular regulation, including the nucleus of the solitary tract and neurons in the ventrolateral medulla. About 70% of the nucleus of the solitary tract neurons which could be retrogradely labeled from the AV3V area stained immunohistochemically for tyrosine hydroxylase, but not phenylethanolamine-N-methyltransferase, and were therefore presumably noradrenergic. About half of the neurons in the rostral part of the ventrolateral medulla which innervated the AV3V area stained for both enzymes, and thus were apparently adrenergic. These medullary catecholaminergic inputs to the AV3V area may be of importance in explaining recent data concerning the roles of both regions in experimental hypertension.

Animals↗
PubMed1983

Lesions of the basal forebrain in rat selectively impair the cortical vasodilation elicited from cerebellar fastigial nucleus.

We sought to determine in rat, whether interruption of the major extrathalamic projections to the cerebral cortex originating in and projecting through the basal forebrain (BF), will impair the increase in regional cerebral blood flow (rCBF), but not metabolism, elicited in the cerebral cortex by electrical stimulation of the cerebellar fastigial nucleus (FN). Studies were conducted in anesthetized, paralyzed, ventilated rats, with blood gases controlled and AP maintained in the autoregulated range. Electrolytic lesions were placed unilaterally in the BF at the level of the lateral preoptic region lying in rostral portions of the medial forebrain bundle and resulted in a reduction of up to 47% of the choline acetyltransferase activity in the ipsilateral cerebral cortex. rCBF was measured in homogenates of 9 paired brain regions by the 14C-iodoantipyrine technique. In unlesioned rats, FN stimulation symmetrically and significantly (P less than 0.05) increased rCBF in all brain regions with the greatest increase (to 180%) in the frontal cortex. Two days following a unilateral BF lesion, FN stimulation failed to increase rCBF in the ipsilateral cerebral cortex distal to the BF lesion. In contrast, rCBF was increased to an almost comparable degree in the remainder of the brain. BF lesions alone resulted in a 18-23% reduction in cortical rCBF ipsilaterally (P less than 0.025). BF lesions did not alter the cerebrovascular vasodilation elicited by CO2 nor perturb autoregulation. The cortical vasodilation elicited by FN stimulation is mediated by intrinsic neuronal pathways and depends upon the integrity of neurons, possibly cholinergic, originating in, or passing through, the BF.

Animals↗
PubMed1983

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.

Animals↗
PubMed1983

Strain differences in fear between spontaneously hypertensive and normotensive rats.

The purpose of this study was to determine whether the reduced conditioned fear response in spontaneously hypertensive rats (SHRs) relative to Wistar-Kyoto controls (WKYs); (a) reflects a decrease in fear in SHRs or an increase in fear in WKYs, relative to other strains; (b) is secondary to strain differences in cardiovascular regulation; (c) represents a weaker conditioned response or a weaker memory trace; and (d) generalizes beyond tests of conditioned fear. SHRs, WKYs and Sprague-Dawley (SD) rats were subjected to classical fear conditioning (30 trials) involving the pairing of a tone conditioned emotional stimulus (CES: 800 Hz, 82 dB, 10 s) with an electric footshock unconditioned stimulus (US: 1.5 mA, 0.5 s). Cardiovascular responses elicited by the CES (without the US) were assessed through computer assisted techniques in chronically instrumented animals. Conditioned fear behavior was assessed as the proportion of time accounted for by crouching or freezing during a 300 s presentation of the CES without the US. Unconditioned fear reactivity was examined using the open field test. Conditioned fear reactivity (% freezing during 300 s CES) was reduced (P less than 0.01) in SHRs relative to both WKYs and SDs, which did not differ (SHR: 57% +/- 5; WKY 85% +/- 3; SD: 93% +/- 4). Young (7 week) and mature (14 week) animals within each strain differed in resting mean arterial pressure (MAP, in mm Hg) (WKY: young , 102 +/- 1; mature, 133 +/- 2; P less than 0.01; SHR: young, 124 +/- 3; mature, 153 +/- 5; P less than 0.01) but did not differ in conditioned fear reactivity (WKY: young, 91% +/- 3; mature, 93% +/- 3; SHR: young, 47% +/- 3; mature, 62% +/- 8.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Aromatic L-amino acid decarboxylase in the rat brain: coexistence with vasopressin in small neurons of the suprachiasmatic nucleus.

We demonstrated the coexistence of aromatic L-amino acid decarboxylase (AADC) and arginine-vasopressin in neurons of the hypothalamic suprachiasmatic nucleus of Sprague-Dawley rats. Neurons that lacked monoamines but expressed immunoreactivity to the enzyme AADC occupied the rostral and caudal poles of the suprachiasmatic nucleus and mediodorsal and dorsolateral positions along the entire extent of the nucleus. AADC was also localized in similar neurons of the suprachiasmatic nucleus of rats from other strains including the homozygous Brattleboro rat.

Animals↗
PubMed1983

Adrenaline synthesizing neurons in the rostral ventrolateral medulla: a possible role in tonic vasomotor control.

Adrenaline-containing neurons of the rostral ventrolateral medulla (the C1 group) project selectively to autonomic spinal neurons in rats. Stimulation of these neurons electrically or chemically elevates arterial pressure, while neuronal blockade by microinjection of tetrodotoxin bilaterally drops arterial pressure to levels comparable to those produced by spinal cord transection. Adrenaline neurons of the ventral medulla appear necessary for maintaining normal levels of blood pressure, and thus may constitute a tonic vasomotor center.

Animals↗
PubMed1983

Local cerebral blood flow increases during auditory and emotional processing in the conscious rat.

Local cerebral blood flow was measured in rats by the 14C-labeled iodoantipyrine technique with quantitative autoradiography during the processing of environmental stimuli. Presentation of a tone increased blood flow in the auditory but not the visual pathway. When the animal had previously been conditioned to fear the tone, blood flow additionally increased in the hypothalamus and amygdala. Local cerebral blood flow can thus be used to detect patterns of cerebral excitation associated with transient (30- to 40-second) mental events in experimental animals.

Acoustic Stimulation↗
PubMed1983

Global increase in cerebral metabolism and blood flow produced by focal electrical stimulation of dorsal medullary reticular formation in rat.

We sought to determine whether the increases in local cerebral blood flow (LCBF) elicited by focal electrical stimulation within the dorsal medullary reticular formation (DMRF), are secondary to or independent of, increased local cerebral glucose utilization (LCGU). Rats were anesthetized (chloralose), paralyzed, artificially ventilated and arterial pressure and blood gases controlled. LCBF and LCGU were determined in two separate groups of animals, using the autoradiographic [14C]iodoantipyrine and [14C]2-deoxyglucose methods, respectively. In unstimulated controls, LCBF (n = 5) and LCGU (n = 5) were linearly related (r = 0.780; P less than 0.001) in the 27 brain regions studied. During DMRF stimulation LCGU increased significantly in 21 of the 27 regions, including cerebral cortex (up to 168% of control), thalamic nuclei (up to 161%) and selected ponto-medullary regions (e.g. parabrachial complex: 212%; vestibular complex: 147%). Along with LCGU, LCBF rose significantly in 25 regions (sensory motor cortex: 163%; anterior thalamus: 161%; parabrachial complex: 186%). Correlation analysis demonstrated that, during DMRF stimulation, the close relationship between LCBF and LCGU is preserved (r = 0.845; P less than 0.001) and that, in addition, the increase in LCBF (delta LCBF) is proportional to the increase in LCGU (delta LCGU) (delta LCBF = 2.18 delta LCGU + 6.92; r = 0.7729; P less than 0.001). Excitation of neurons or fibers within DMRF increases brain metabolism globally and blood flow secondarily. The DMRF appears to modulate cerebral metabolism globally, by as yet undefined pathways.

Animals↗
PubMed1983

The effect of forebrain lesions in the neonatal rat: survival of midbrain dopaminergic neurons and the crossed nigrostriatal projection.

Lesions were placed in the striatum and the olfactory tubercle of 1-day-old rat pups. Control and experimental animals were raised to adulthood. Efferent projections of mesencephalic neurons were examined by injecting the retrograde tracers horseradish peroxidase or Fast Blue into the undamaged striata of some experimental animals. The survival of the mesencephalic dopaminergic neurons was monitored by using immunocytochemical localization of tyrosine hydroxylase. Small lesions in the caudate-putamen had no appreciable effect on the survival of tyrosine hydroxylase-containing neurons in the mesencephalon, but the density of dopaminergic terminals adjacent to the lesion increased in the remaining caudate-putamen. Striatal lesions that involved an estimated area of more than one-third resulted in loss of dopamine neurons of the substantia nigra compacta. Rostral lesions in the striatum affected mostly rostrally positioned neurons in the substantia nigra. Dorsal lesions of the caudate-putamen resulted in disappearance of dorsal A9 neurons. Reduction of the A10 and A8 dopamine neuron groups occurred if the neonatal lesions involved the olfactory tubercle and nucleus accumbens. Some tyrosine hydroxylase-containing neurons persisted even after the largest lesions. These dopaminergic neurons formed a crossed nigrostriatal pathway which was confirmed by retrogradely transported tracers. The density of this crossed projection in the adult appeared unaffected by the neonatal lesion. We concluded that dopaminergic neurons form topographically ordered projections with their targets in the newborn rat. Rearrangement of these fibers appeared limited, but compensatory increase of axon terminal density was evident in partially lesioned target areas.

Animals↗
PubMed1983

Ricin transport distinguishes between central and peripheral neurons.

Ricin conjugated to horseradish peroxidase was retrogradely transported by peripheral neurons of the nodose ganglion after microinjection into the nucleus tractus solitarius but was not transported by central neurons projecting to the nucleus tractus solitarius. Similarly, ricin was not transported by central neurons projecting to the caudate nucleus. Differences in labeling of central and peripheral neurons with ricin may reflect differences in surface glycoconjugates on processes of these neurons.

Animals↗
PubMed1983

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.

Animals↗
PubMed1983

Cholinergic mechanisms in the nucleus tractus solitarii and cardiovascular regulation in the rat.

To determine the role played by cholinergic neurons in cardiovascular regulation by the nucleus tractus solitarii (NTS), microinjections (0.1 microliter) of acetylcholine (ACh) or carbachol (C) were made into the NTS of rats, and the changes in arterial pressure and heart rate were recorded. The dose-dependent hypotension and bradycardia which resulted were mediated by the activation of muscarinic, but not nicotinic, receptors confined to the NTS. Blockade of muscarinic receptors bilaterally in the NTS resulted in mild hypertension and attenuated, but did not abolish, the baroreceptor reflex. Eserine, injected into the NTS, augmented and prolonged the action of acetylcholine and slightly increased the maximal baroreceptor reflex response. Thus, cholinergic mechanisms in the NTS tend tonically to lower arterial pressure and may modulate the baroreceptor reflex, without being an integral part of the reflex arc.

Acetylcholine↗
PubMed1983

Some neurons of the rat central nervous system contain aromatic-L-amino-acid decarboxylase but not monoamines.

Neurons containing the enzyme aromatic-L-amino-acid decarboxylase (AADC) but lacking either tyrosine hydroxylase or serotonin were found in the spinal cord of neonatal and adult rats by light and electron microscopic immunocytochemistry. The majority of these neurons localized to area X of Rexed contact ependyma. Thus, spinal AADC neurons have the enzymatic capacity to catalyze directly the conversion of the amino acids tyrosine, tryptophan, or phenylalanine to their respective amines tyramine, tryptamine, or phenylethylamine. These amines normally present in the central nervous system may be of potential clinical significance as endogenous psychotomimetics.

Animals↗
PubMed1983

Electrical stimulation of cerebellar fastigial nucleus increases cerebral cortical blood flow without change in local metabolism: evidence for an intrinsic system in brain for primary vasodilation.

We sought to determine whether the increase in regional cerebral blood flow (rCBF) elicited by electrical stimulation of the fastigial nucleus of the cerebellum (FN) is secondary to, or independent of, increased local cerebral metabolism (rGMR) in anesthetized (chloralose) paralyzed rats. rCBF and rGMR were determined autoradiographically in separate groups of animals with comparable blood gases and systemic pressure, by the [14C]iodoantipyrine and [14C]2-deoxyglucose methods respectively. In sham-operated controls, rCBF (n = 5) and rGMR (n = 5) were closely related in the 28 brain areas studied (r = 0.733; P less than 0.005). During FN stimulation, rCBF (n = 6) increased significantly in 24 of the 28 areas, the greatest increase being in the cerebral cortex (up to 215%). rGMR (n = 9) increased in only 15 areas, so that the correlation between rCBF and rGMR throughout the brain became weaker (r = 0.568; P less than 0.005). Where the rCBF increases were the greatest (particularly in the cerebral cortex), rGMR was unchanged. This suggests that the rCBF increase was not a consequence of the increased rGMR. We conclude that neurons originating in or passing through FN may influence local cerebral circulation through a primary cerebral vasodilatation not coupled to metabolism.

Animals↗