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D J Reis

Publications and source records attributed to D J Reis.

At least 271 records · Page 15Linked to original sources
PubMed1985

Distribution of neurons containing phenylethanolamine N-methyltransferase in medulla and hypothalamus of rat.

Neurons immunocytochemically labeled with the adrenaline-synthesizing enzyme phenylethanolamine N-methyltransferase were mapped in the brain of rat pretreated with colchicine. In medulla, immunoreactive cells in the C1 and C2 groups were distributed in a more complex manner than described previously. C1 neurons were identified in the reticular formation of ventrolateral medulla and were organized into two populations: (1) a cell column extending throughout the ventrolateral medulla, and lying ventral to the ambiguus cell group and either dorsal to the precerebellar lateral reticular nucleus or interposed between its two subdivisions; (2) a rostral cell cluster forming medial to the column at caudal levels and enlarging close to and in parallel with the ventral surface of the rostral ventrolateral medulla. A large proportion of cells and processes of the rostral cell group were oriented medially and ventromedially. processes of C1 neurons were traced dorsally toward the nucleus tractus solitarii, dorsal motor nucleus, and principal tegmental adrenergic bundle, ventrally toward the ventral surface, laterally toward the trigeminal complex, and medially or ventromedially toward the raphe. C2 neurons were located in the dorsomedial medulla and were subdivided into four distinct populations: (1) neurons in the rostral nucleus paragigantocellularis pars dorsalis (NGCd) and medial longitudinal fasciculus (MLF) were contiguous and similar in size and shape, with their long diameters oriented horizontally or diagonally along several axes; (2) neurons of the periventricular gray were located in a cytoarchitecturally undefined area dorsal to the MLF; these cells were ovoid, smaller, and organized more compactly than those in the NGCd-MLF; (3) a cell group in the rostromedial nucleus tractus solitarii (NTS) and dorsal motor nucleus overflowed caudally into the intermediate thirds of both structures; and (4) a parvicellular group in the NTS was compactly organized in the dorsolateral NTS and was best developed at the level of the area postrema. Processes of C2 neurons were generally directed sagitally, medially, and laterally along the ventricular floor and ventrally or medially toward the raphe; other fibers arborized and terminated within the NTS and dorsal motor nucleus. In the medulla, local processes were traced from C1 and C2 neurons directly into respective ventral and dorsal parts of the medullary raphe and surrounding intraparenchymal blood vessels. Fibers from these neurons were also followed, respectively, onto the ventral subpial surface and the floor of the fourth ventricle.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Widespread reductions in cerebral blood flow and metabolism elicited by electrical stimulation of the parabrachial nucleus in rat.

We have studied the effect of electrical stimulation of the parabrachial nucleus (PBN) and adjacent areas of dorsal pons on regional cerebral blood flow (rCBF) and glucose utilization (rCGU) in anesthetized (chloralose), paralyzed (tubocurarine) rats. rCBF and rCGU were measured in dissected tissue samples of 9 brain regions by the [14C]iodoantipyrine and [14C]2-deoxyglucose method, respectively. Electrical stimulation restricted to the medial parabrachial nucleus (PBNm, n = 5) elicited significant (P less than 0.05) reductions in rCBF in 7 out of 9 brain regions. Reductions were greatest in cerebral cortex (up to 35% in occipital cortex) and least in the white matter of the corpus callosum (23%). The effect on rCBF persisted after transection of the cervical sympathetic trunk (n = 5). In contrast, stimulation of the lateral portion of PBN (n = 5), periventricular gray (n = 5) and interestingly, the nucleus locus coeruleus (n = 5) failed to elicit similar changes in rCBF. PBNm stimulation also elicited decreases in rCGU (n = 4) in 5 out of 9 brain areas, most notably regions of cerebral cortex. The decreases in rCGU (delta rCGU) were linearly related to the decreases in rCBF (delta rCBF) according to the equation delta rCBF = 2.37 delta rCGU + 2.1 (r = 0.72; P less than 0.001). We conclude that excitation of neural pathways originating in, or passing through, PBNm elicits a widespread reduction in cerebral metabolism and secondarily in blood flow (secondary vasoconstriction). Since projections of the PBNm do not involve the entire cortex, it seems likely that the effect is mediated via inhibition of diffuse cortical projections through a subcortical site.

Animals↗
PubMed1985

Evidence for specific immunolysis of nerve terminals using antisera against choline acetyltransferase, glutamate decarboxylase and tyrosine hydroxylase.

Synaptosomes prepared from striatum or cerebral cortex of rat brain were incubated with antibodies raised against three neurotransmitter biosynthetic enzymes, choline acetyltransferase, glutamate decarboxylase and tyrosine hydroxylase in the presence or absence of complement. Immunolysis was first assessed by measuring the release of lactic dehydrogenase or reduction in potassium from synaptosomes, and lysis of neurochemically specific subpopulation of synaptosomes was detected by measuring release of either transmitters, their biosynthetic enzymes or by blockade of sodium-dependent uptake of transmitter or precursor. In both striatum and cortex, antibodies to choline acetyltransferase lysed only cholinergic while those against glutamate decarboxylase only lysed GABAergic nerve terminals. Antibodies against tyrosine hydroxylase lysed only the dopaminergic terminals in striatum but not noradrenergic terminals in cortex. The lysis occurred only in the presence of complement, and was never observed in the absence of complement. The studies indicate that antibodies to the neurotransmitter biosynthetic enzymes recognize antigens in the synaptosomal membrane specific only to neurons harboring the transmitters. The results suggest that the antibody-positive peptides in the membrane and neurotransmitter biosynthetic enzyme share common antigenic sites, probably common peptides.

Animals↗
PubMed1985

Newly identified GABAergic neurons in regions of the ventrolateral medulla which regulate blood pressure.

Glutamic acid decarboxylase (GAD), the enzyme which synthesizes the inhibitory transmitter gamma-aminobutyric acid (GABA), was localized immunocytochemically within cells and processes distributed throughout the ventrolateral medulla. In caudal regions, GAD-stained cells were adjacent to the 'precerebellar' lateral reticular nucleus and partially overlapped the A1 area of norepinephrine synthesizing neurons. The largest number of labeled neurons filled the rostral ventrolateral medulla (RVL), coinciding with and extending beyond the C1 adrenergic area. GAD-positive cells also occupied the nucleus reticularis parvocellularis, raphe magnus (RM) and lateral wings of RM in the region of the pararaphe. Intrinsic GAD-containing cells in the ventrolateral medulla may tonically inhibit sympathoinhibitory neurons in the caudal ventrolateral medulla (CVL) and sympathoexcitatory neurons in the RVL.

Animals↗
PubMed1985

Intrinsic gamma-aminobutyric acid neurons in the nucleus of the solitary tract and the rostral ventrolateral medulla of the rat: an immunocytochemical and biochemical study.

Sympathoexcitatory neurons in the C1 adrenergic area of the rostral ventrolateral medulla (RVL) are tonically inhibited by gamma-aminobutyric acid (GABA). To identify the source of this GABAergic input, the distribution of neurons containing glutamate decarboxylase (GAD) was determined immunocytochemically in rats treated with colchicine. Numerous GAD-stained neurons were located in the nucleus of the solitary tract (NTS) and in RVL. Unilateral lesions in NTS did not alter GABA content or GAD activity in RVL, indicating that the afferent projection from NTS to RVL is not GABAergic. Intrinsic GABAergic neurons in RVL may provide tonic inhibition of vasomotor neurons in the C1 area.

Animals↗
PubMed1985

Distribution of catecholamine-containing neurons in the normal human hypothalamus.

We have studied the distribution of catecholamine-containing neurons in the hypothalamus of 8 normal adult human brains, using Schmorl's stain for melanin and immunohistochemical staining for tyrosine hydroxylase (TH). TH immunoreactive perikarya were found in the wall of the third ventricle, in the areas in which dopaminergic neuroendocrine neurons are found in other primate species. Many of these neurons contained melanin pigment, and the percentage increased with age. Other melanin-pigmented neurons in the same distribution did not stain for TH, suggesting that postmortem TH immunostaining may not be sufficiently sensitive to visualize all catecholaminergic neurons. A separate group of larger TH-positive perikarya was seen in the lateral hypothalamic area. These may correspond to the incerto-hypothalamic dopamine neurons in other primate species. Only rare melanin-pigmented neurons were seen in this cell group, even at 66 years of age. Our data indicate that the hypothalamic neuroendocrine dopamine neurons in the human brain are distributed in a pattern similar to that in other primate species, and that both postmortem tyrosine hydroxylase and melanin staining provide an incomplete but representative sampling of the periventricular-arcuate cell group.

Adolescent↗
PubMed1985

Partial expression of catecholaminergic traits in cholinergic chick ciliary ganglia: studies in vivo and in vitro.

We have previously demonstrated that at embryonic Day (E) 8, some cells of the chick ciliary ganglion (CG) contain the catecholaminergic (CA) enzyme tyrosine hydroxylase (TH), but not phenylethanolamine-N-methyltransferase (PNMT); and that in culture essentially all cells express both enzymes. In the present study, we sought to determine, first, whether the expression of adrenergic traits in the CG in vivo is transient or permanent in the CG. To do so, CGs were removed from E5 to postnatal Day 5, fixed, and processed for the immunocytochemical localization of the CA enzymes: TH, L-amino acid decarboxylase (AADC), and PNMT. At all stages examined, some CG neurons expressed TH immunoreactivity (TH-IR) and all contained AADC-IR. However, none stained with PNMT antibodies, indicating that these cells stably express some, but not all, of the CA enzymes. Second, we examined whether CG neurons in culture expressed other CA markers. CG neurons did not contain detectable levels of TH enzyme activity nor did they transport and store exogenously supplied monoamines. These results indicate that some but not all traits necessary for adrenergic function are present in CG neurons in vitro. Third, we sought to establish whether CA expression in CG neurons is affected by modification in culture conditions. Cultures of CG neurons continued to express TH-IR even when grown in the presence of either 50% HCM or 20 mM KCl for 5 days. Finally, the expression of the cholinergic enzyme, choline acetyltransferase (CAT) was assessed in CG cultures by biochemical assay. CAT activity increased five-fold between 5 and 17 days in vitro, irrespective of the presence of TH-IR in 100% of the CG neurons of sister cultures. These data suggest that at least a subpopulation of CG neurons express both TH and CAT in culture. We conclude that the postmitotic neurons of the CG are able to express some but not all of the traits characteristic of a CA phenotype while maintaining cholinergic expression. These findings suggest that (1) the appearance of the full complement of adrenergic properties is not coordinated and may be regulated by different environmental cues and (2) parasympathetic neurons can express both adrenergic and cholinergic traits simultaneously.

Animals↗
PubMed1985

Sympathoinhibition by A1-noradrenergic neurons is mediated by neurons in the C1 area of the rostral medulla.

In anesthetized, paralyzed rats, bilateral microinjections of kainic acid (KA) into an area of caudal ventrolateral medulla containing A1 noradrenergic neurons of the A1 group (A1 area) first reduced and then elevated arterial pressure (AP), heart rate (HR) and sympathetic renal nerve activity. These effects are attributable to initial excitation and then paralysis of local neurons by KA. The microinjection of tetrodotoxin into an area of rostral ventrolateral medulla containing adrenaline neurons of the C1 group (C1 area) and which is innervated by neurons in A1 area abolished all the effects of KA. The pretreatment of the C1 area with 6-hydroxy-dopamine (6-OHDA) also abolished all the effects of KA. In contrast interruption of projections of the A1 area to the hypothalamus or nucleus tractus solitarii had no effects. The latency for response evoked in renal nerve by stimulation of A1 area was about 10 ms longer than that elicited from C1 area. Tyramine microinjected into the C1 area elicited a dose-dependent decrease in AP prevented by local application of desmethylimipramine. We conclude that neurons of the A1 area tonically inhibit sympathetic activity by inhibiting neurons of the C1 area probably by release of NA.

Adrenergic Fibers↗
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

Brain-stem mechanisms governing resting and reflex tone of precapillary vessels.

The sympathetic drive to the cardiovascular system depends on the integrity of neurons in the medulla oblongata. The adrenergic neurons of the C1-area of the cortical ventrolateral medulla are tonically active and provide the background excitation of the spinal preganglionic neurons, which relay to the postganglionic sympathetic neurons. The noradrenergic neurons of the A1-area of the caudal ventrolateral medulla act as tonic inhibitors of the sympathetic discharge; they mediate the depressor response to centrally acting alpha-adrenergic agonists such as clonidine. Imbalance between those two types of neuronal control systems leads to increased sympathetic discharge and hence elevated arterial blood pressure.

Animals↗
PubMed1985

Brain stem area with C1 epinephrine neurons mediates baroreflex vasodepressor responses.

In anesthetized, paralyzed rats, bilateral electrolytic lesions of rostral ventrolateral medulla (RVL) containing epinephrine neurons of the C1 group 1) abolished the reflex hypotension and bradycardia elicited by electrical stimulation of the left vagus nerve or stretch of the left carotid sinus and 2) reduced arterial pressure (AP) and heart rate (HR) to values comparable to spinal cord transection. Combined lesions of the right nucleus tractus solitarii (NTS) and left or right C1 area did not alter AP. However, lesions of right NTS combined with lesions or microinjection of kainic acid into the left, but not right, C1 area abolished vasodepressor reflexes. Vasodepressor reflexes were unchanged by midcollicular decerebration, bilateral lesions of the parabrachial complex of the pons, or (after right NTS lesions) by lesions of the raphe or other reticular areas of the left half of the medulla. We conclude that neurons of the RVL, possibly belonging to the C1 epinephrine group, mediate vasodepressor responses from arterial baro- and other cardiopulmonary receptors, the pathway may be via a direct NTS-RVL projection, neurons in the C1 area of RVL are necessary for maintaining resting levels of arterial pressure.

Animals↗
PubMed1985

Genetic effects and sexual dimorphism in tyrosine hydroxylase activity in two mouse strains and their reciprocal F1 hybrids.

This study further analyzed the environmental and genetic mechanisms underlying the previously reported strain differences in tyrosine hydroxylase (TH) activity in the nigrostriatal and hypothalamic dopamine system of the BALB/cJ (B) and CBA/J (C) inbred mouse strains and related behavioral processes using parental and reciprocal F1 hybrid generations. Significant strain differences were found in both sexes in all the measured characters. Comparing males and females, sexual dimorphisms were found in TH activity of substantia nigra (SN), corpus striatum (CS) and hypothalamus (H), and in exploratory behavior (IE). Presence of sexual dimorphism was genotype dependent, with the exception of TH activity in H. Major components of strain differences, maternal effects and additive gene effects, were separated by biometrical genetic methods. The analysis indicated that significant maternal effects were present in TH activity of TH and CS with a trend towards this phenomenon in the SN. Additive gene effects were significant in all characters and various degrees of dominance were expressed in the hybrids in TH activity of SN and CS, as well as in behavioral traits, IE and spontaneous locomotion (SL). All the biochemical and behavioral parameters were expressed at lower levels in CBA/J than in BALB/cJ mice and reciprocal F1 hybrids took intermediate positions between the two parental strains for all phenotypes examined, with the exception of IE, where complete dominance was found in (CXB)F1 females. These results are consistent with the hypothesis that some of the genes affecting TH activity in brain dopamine systems contribute to the expression of dopamine mediated behaviors. Our analysis also indicates the possibility that the maternal effects on TH activity in CS and SN are the consequences of X-chromosome linked gene effects. We suggest that the influence of the X-chromosome linked gene(s) is dependent upon the action of gonadal steroids during the critical period of ontogenesis, and X-chromosome linked gene(s) play a major role in the genotype dependent expression of sexual dimorphism in TH activity.

Animals↗
PubMed1985

Sympathetic nervous system and control of blood pressure during natural behaviour.

The role of the sympathetic nervous system in generating behaviourally linked blood pressure (BP) responses was investigated in awake rats instrumented for chronic intra-arterial BP recording. All data from the recording sessions were digitalized and processed by a computer. Frequency interval histograms of behaviourally associated changes of BP and heart rate (HR) were generated. 6-Hydroxydopamine (100 and 200 mg/kg intravenously) was used for chemosympathectomy. In the intact rats (n = 8) three different frequency histograms of mean BP values for three behavioural groupings were generated (from lowest to highest average values): (1) resting, (2) exploring-grooming and (3) eating-drinking. Chemosympathectomy (n = 5) abolished this order of BP changes; mean BP did not rise from rest to other behaviours, nor did it vary during different behaviours. It is concluded that the sympathetic nervous system is responsible for producing the changes in BP that are appropriate and characteristic of each behaviour in awake, unrestrained rats.

Animals↗
PubMed1985

Cholinergic neurons of the chick ciliary ganglia express adrenergic traits in vivo and in vitro.

In this study, we sought to determine whether neurons of the chick embryo ciliary ganglia (CG), a parasympathetic cholinergic ganglia, can express catecholaminergic (CA) traits. To accomplish this, we used immunocytochemical techniques to examine the presence of the CA enzymes tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) in CGs removed from chick embryo at day 8 of development (E8). Few neurons containing TH but not PNMT were found in the E8 CG. To examine whether CG neurons express CA enzymes in vitro, CGs removed from E8 chick embryo were dissociated and kept in culture for 3 to 12 days. In 50% of the culture dishes, some neurons contain TH or PNMT after 5 days in vitro. In an equal proportion of culture plates, CG neurons did not express the enzymes. To determine whether the proportion of CG neurons expressing TH or PNMT is increased by tissue influences, ganglion cells were co-cultured with notochord. In 90% of the co-culture experiments, most neurons present in the culture dishes stained with TH or PNMT after 5 days in vitro. To test for the presence of aromatic L-amino acid decarboxylase (AADC), another CA enzyme, cultures of CGs and CGs plus notochord were incubated with levodopa and processed for the detection of CA histofluorescence. Dopamine histofluorescence was present in all neurons after 3 days in vitro irrespective of the presence of notochord, suggesting that the expressions of TH and PNMT and that of AADC are differentially regulated. This study, therefore, demonstrates that cholinergic neurons of the CG contain CA enzymes in vivo and in vitro and that the proportion of neurons expressing CA traits during development in vitro can be increased by environmental cues such as those released by the notochord.

Acetylcholine↗
PubMed1985

Genes for neurotransmitter synthesis, storage, and uptake.

We found that the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH) (EC 1.14.16.2), dopamine beta-hydroxylase (EC 1.14.17.1), and phenylethanolamine N-methyltransferase (EC 2.1.1.28) share similar protein domains in their primary structures and that they share common gene coding sequences. In a recent report we also demonstrated that antiserums directed against choline acetyltransferase (EC 2.3.1.6), glutamic acid decarboxylase (EC 4.1.1.15), and TH cause specific complement-mediated lysis of cholinergic, gamma-aminobutyric acid-ergic, and dopaminergic subpopulations of synaptosomes, respectively. This interaction of specific antibodies to the specific subpopulation of synaptosomal membrane, e.g., recognition of antibody to TH to only the dopaminergic subpopulation of synaptosomal membrane protein, indicates that the neurotransmitter enzyme and membrane protein of its own synaptosomes may also share common protein domains. Therefore, we postulate that the specific neurotransmitter biosynthetic enzyme and a certain membrane protein of the nerve endings may share similar gene coding sequences, and that expression of these proteins may determine the phenotype of the neuron.

Amino Acids↗
PubMed1985

Contributions of arginine vasopressin and the sympathetic nervous system to fulminating hypertension after destruction of neurons of caudal ventrolateral medulla in the rat.

We sought to determine the role in control of arterial pressure (AP) of the caudal ventrolateral medulla (CVL), a region containing noradrenergic neurons of the A1 group. Electrical stimulation of the A1 area in anaesthetized rats elicits a fall of AP and heart rate at low, but not high, stimulus frequencies. Electrolytic lesions of the A1 area produce fulminating hypertension and a 13-fold increase in plasma arginine vasopressin (AVP). A1-hypertension is attenuated by treatment with an AVP antagonist and is also diminished in rats of the Brattleboro strain. After AVP blockade, the residual hypertension is abolished by treatment with ganglionic or alpha adrenergic blockers, but not by adrenalectomy. We conclude that the region of the CVL containing the A1 noradrenergic cells tonically inhibits the discharge of sympathetic nerve activity as well as the release of AVP from the pituitary.

Adrenal Glands↗