bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiovascular effects and modulation of noradrenergic neurotransmission following central and peripheral administration of neuropeptide Y
Authors: Westfall Thomas C. , Martin John , Chen Xiaoli , Ciarleglio Anita , Carpentier Suzanne , Henderson Kristina , Knuepfer Mark , Beinfeld Marge , Naes Linda 
Published: January 2005

AbstractExperiments have been conducted to evaluate the effect of neuropeptide Y (NPY) administered at three distinct levels of the nervous system: (1) the posterior hypothalamic nucleus, (2) the spinal cord, and (3) the vascular noradrenergic neuroeffector junction. It was observed that NPY produced varying cardiovascular effects at these three distinct sites of the nervous system. Microinjections into the posterior hypothalamic nucleus resulted in an increase in blood pressure, which was reduced by prior microinjection of a muscarinic or H1‐histamine antagonist but not an H2‐histamine antagonist. In addition to the involvement of histaminergic and cholinergic pathways, the pressor effect of NPY appers to result from an increase in sympathetic outflow. NPY was also seen to decrease the potassium‐induced release of norepinephrine (NE) from slices obtained from the posterior hypothalamic nucleus. In contrast to what was observed in the hypothalamus, the intrathecal injection of NPY at a level of T4 or T10 in anesthetized or T10 in unanesthetized rats resulted in a depressor effect as well as a decrease in heart rate. Both an α2‐ and β‐adrenoceptor antagonist reduced the NPY effect. The depressor effect of intrathecal NPY was attenuated in rats pretreated with reserpine as well as in Spontaneously Hypertensive rats (SHR). These data suggest that the effects of NPY are closely associated with sympathetic preganglionic neurons in the spinal cord. At the vascular noradrenergic neuroeffector junction, NPY decreased the nerve stimulation‐induced release of NE while potentiating the contractile response. Moreover, NPY potentiated the increase in perfusion pressure of the perfused mesenteric arterial bed in response to angiotensin, vasopressin, or phenylephrine. The potentiation of smooth muscle contraction produced by NPY was shared by the homologous peptide, peptide YY (PYY) and to a lesser extent, pancreatic polypeptide (PPY). The prejunctional effect of NPY was less and the postjunctional effect greater in SHR compared with that in normotensive rats. The evidence obtained in these studies supports a cotransmitter role of NPY with NE in central and peripheral noradrenergic neurons. Moreover, NPY may be implicated in the development and maintenance of hypertension in the SHR.
Hormonal regulation of somatostatin messenger RNA
Authors: Baldino Frank , Fitzpatrick‐McElligott Sandra , M. O'kane Teresa , Gozes Illana 
Published: January 2005

AbstractThe ability of gonadal steroids to regulate the expression of the somatostatin gene in several regions of the CNS was investigated with in situ hybridization histochemistry. The amount of somatostatin mRNA was found to be significantly decreased 2–3 weeks after ovariectomy or orchidectomy in the periventricular hypothalamus, the ventromedial nucleus of the hypothalamus, and the medial and central nuclei of the amygdala. Treatment of gonadectomized rats with estradiol benzoate or testosterone enanthate reversed this decrease in somatostatin mRNA. No significant effect was noted in the cerebral cortex or bed nucleus of the stria terminalis. In some regions, there was a high degree of convergence between the distribution of neurons containing estrogen/ androgen receptors and somatostatin neurons that were responsive to gonadectomy. These results suggest that sex steroids regulate the expression of somatostatin through an action at the level of transcription.
Ultrastructural changes in acetylcholinesterase activity in the deafferented spinal trigeminal nucleus
Authors: Wilson Frances R. , Westrum Lesnick E. , Broderson Stevan H. 
Published: January 2005

AbstractAcetylcholinesterase (AChE) activity was investigated in synaptic areas of the cat spinal trigeminal nucleus (pars interpolaris and pars caudalis) ipsilateral and contralateral to complete retrogasserian rhizotomy. Vibratome sections of tissue taken from animals of 1, 3, 6, 14, and 21 days survival were examined by electron microscopy following a histochemical reaction for AChE activity employing a method based on the Karnovsky‐Roots technique for demonstrating reaction product. As degeneration progressed with survival time, enzymatic activity was initially reduced in synaptic clefts of injured afferent terminals and subsequently was enhanced throughout the extracellular space, including within synaptic clefts of possibly reinnervated sites. These changes in enzymatic activity with primary deafferentation are discussed in relation to the process of reinnervation, the development of neuronal hyperactivity, and possible noncholinergic functions of AChE.
Biphasic modulation of evoked [3H]D‐aspartate release by D‐2 dopamine receptors in rat striatal slices
Authors: Peris Joanna , Dwoskin Linda P. , Zahniser Nancy R. 
Published: January 2005

AbstractIt has been hypothesized that dopamine (DA) inhibits glutamate release from corticostriatal fibers via presynaptically located D‐2 DA receptors although the evidence presented in the literature has not been conclusive. In the present experiments, the effect of D‐2 receptor ligands on K+‐stimulated tritium release from rat striatal slices preloaded with the nonmetabolizable glutamate analog [3H]D‐aspartate ([3H]ASP) was measured. The D‐2 receptor antagonist S‐sulpiride increased stimulated [3H]ASP release by 75% (EC50 value = 240 nM) and the biologically less‐active isomer R‐sulpiride, although equally effective, was tenfold less potent. The D‐2 receptor agonists pergolide and (+)‐4‐propyl‐9‐hydroxynapthoxazine (+PHNO) inhibited [3H]ASP release at nM concentrations; however, this effect was small (20%). This low efficacy of the exogenous agonists was apparently due to competition by high concentrations of endogenous DA since the effect of pergolide was increased in rats whose striatal DA levels were decreased by 97%. These data support the hypothesis that D‐2 DA receptors modulate [3H]ASP release in an inhibitory fashion. However, when the agonists were tested at lower concentrations, [3H]ASP release was increased significantly by 20% in control rats and 60% in DA‐depleted rats. Both the facilitory and inhibitory effects of pergolide were blocked by 10 μM S‐sulpiride, suggesting D‐2 receptor mediation. In addition, the facilitory effect of pergolide was blocked by tetrodotoxin (TTX) and by the GABAA antagonist bicuculline, implying mediation of this D‐2 effect by an inhibitory GABAergic interneuron. The inhibitory effect of pergolide was decreased by the muscarinic antagonist atropine. These data are consistent with the hypothesis that receptors mediating both facilitory and inhibitory D‐2 modulation of [3H]ASP release are located on interneurons rather than directly on the corticostriatal afferents.
Selective cortical infarction reduces [3H]sulpiride binding in rat caudate‐putamen: Autoradiographic evidence for presynaptic D2 receptors on corticostriate terminals
Authors: Filloux F. , Liu T. H. , Hsu C. Y. , Hunt M. A. , Wamsley James K. 
Published: January 2005

AbstractAlthough the existence of presynaptic D2 dopamine receptors on corticostriate terminals has been supported by numerous receptor‐bindding studies, recent autoradiographic data has failed to demonstrate loss of striatal D2 receptors following cortical lesions. In the present study, Long‐Evans rats were subjected to unilateral middle cerebral artery (MCA) infarction in order to produce reproducible lesions of the neocortex without damaging subcortical structures. Animals were sacrificed 2 and 4 wk following lesion and brains were prepared for receptor autoradiography. D2 receptors were studied using the selective ligand [3H]sulpiride, while D1 dopamine receptors were examined using [3H]SCH 23390. Sodium‐dependent, high‐affinity choline uptake sites were labeled with [3H]hemicholinium‐3, thereby providing a quantitative measure of cholinergic neuronal integrity. Unilateral cortical infarction resulted in approximately a 20% reduction in [3H]sulpiride binding in several discrete regions of the ipsilateral caudate‐putamen (CPu), but not in the nucleus accumbens. D2 receptor binding was also reduced significantly in some areas of the contralateral CPu when compared with [3H]sulpiride binding in shamoperated, control animals. In contrast, D1 receptors as identified by [3H SCH 23390 and high‐affinity choline uptake sites labeled with [3H]‐HC‐3] were not affected by the cortical lesion. The results provide autordiographic confirmation of the existence of presynaptic D2 receptors on corticostriate terminals.
Modified coeruleo‐cortical noradrenergic neurotransmission after serotonin depletion by PCPA: Electrophysiological studies in the rat
Authors: Ferron André 
Published: January 2005

AbstractTo detect eventual modifications in the efficacy of the noradrenergic (NA) coeruleo‐cortical system after serotonin (5‐HT) depletion by parachlorophenylalanine (PCPA), three electrophysiological parameters were investigated in urethane‐anesthetized rats which were treated for 2 days with daily injections of this inhibitor of 5‐HT synthesis. (1) The spontaneous activity of locus coeruleus (LC) noradrenergic neurons showed a significant increase in PCPA‐treated compared to control rats (4.3 vs. 2.6 Hz). (2) The sensitivity of NA autoreceptors was measued in the LC by the effect of intravenous administrations of clonidine or microiontophoretic applications of NA on spontaneous neuronal firing. In treated rats, clonidine and NA induced a lesser reduction of LC neuron firing than in the controls (27 vs. 75% decreases and 1,367 vs. 280 nC, respectively). (3) The responsiveness of cortical neurons to electrical stimulation of the LC was assessed by peristimulus time histograms in the dorsal fronto‐parietal cortex. Following stimulation at 2 or 4 Hz, a majority of spontaneously firing cortical units was inhibited by electrical stimulation of the LC, but the percentage of such units was reduced and showed a decreased responsiveness after PCPA treatment. These findings suggest that following 5‐HT depletion by PCPA, cortical NA neurotransmission is makedly reduced in its efficacy in spite of some increase in the spontaneous activity of coeruleo‐cortical NA neurons.
Increased neuronal responsiveness to cholecystokinin and dopamine induced by lesioning mesolimbic dopaminergic neurons: An electrophysiological study in the rat
Authors: Debonnel Guy , de Montigny Claude 
Published: January 2005

AbstractIn the rat, cholecystokinin (CCK) and dopamine (DA) coexist in a subpopulation of neurons of the ventral tegmental area (VTA) projecting to the nucleus accumbens. However, in the dorsal hippocampus, dopaminergic projections from the VTA do not contain CCK, the latter neurotransmitter being mainly localized in intrinsic hippocampal neurons. The present experiments were undertaken in order to compare the interactions of CCK and DA and the effects of lesioning VTA dopaminergic neurons in a region where these neurotransmitters coexist and in one where they do not. The effects of microiontophoretic applications of CCK, kainate (KA), glutamate (GLU) and DA were determined in control rats and in rats pretreated with a local injection of 6‐hydroxydopamine (6‐OHDA) in the VTA. In the nucleus accumbens and in the hippocampus of intact rats, DA exerted a similar depressant effect whether applied during CCK‐, KA‐ or GLU‐induced activations. The 6‐OHDA lesion enchanced responsiveness of accumbens neurons to KA, GLU and CCK (the responsiveness to this latter peptide being increased by more than 15‐fold) and the depressant effect of DA when applied during neuronal activation by KA or GLU but not when the same neurons were activated with CCK. In the dorsal hippocampus, the 6‐OHDA lesion enhanced neuronal responsiveness to KA and DA in the CA1, but not in the CA3 region, whereas the responsiveness to KA and DA in the CA1, but not in the CA3 region, whereas the reponsiveness to CCK remained unchanged in both regions. These results suggest a physiological role for the coexistence of CCK and DA in the nucleus accumbens. The induction of a supersensitivity to DA in the CA1, but not in the CA3, region of the dorsal hippocampus following a VTA lesion is consistent with the regional distribution of the dopaminergic innervation in this structure.
Synaptic structural plasticity: Role of synaptic shape
Authors: Markus Etan J. , Petit Ted L. 
Published: January 2005

AbstractRecent research has indicated that synaptic curvature is an important and potentially critical plastic feature of the synapse. Alterations in synaptic shape are related to synaptic function, being found both during maturation and in adulthood following neuronal activation. In this paper we review the evidence supporting synaptic shape as a plastic feature of synaptic structure. We also propose several mechanisms which might underlie these changes in shape. Finally, we suggest the possible functional role of alterations in synaptic curvature, including its potential in altering synaptic transmission efficacy.
Differential sparing of somatostatin‐neuropeptide y and cholinergic neurons following striatal excitotoxin lesions
Authors: Beal M. Flint , Kowall Neil W. , Swartz Kenton J. , Ferrante Robert J. , Martin Joseph B. 
Published: January 2005

AbstractWe previously found that quinolinic acid striatal excitotoxin lesions result in a relative sparing of somatostatin and neuropeptide Y neurons. In the present study we examined dose‐response effects of excitotoxins acting at the three subtypes of glutamate receptors: N‐methyl‐D‐aspartate (AA1), quisqualate (AA2), and kainic acid (AA3). Concentrations of both somatostatin‐like immunoreactivity (SLI) and neuropeptide a Y‐like immunoreactivity (NPYLI) were compared with those of substance P‐like immunoreactivity (SPLI) and GABA. Kainic acid (AA3), quisqualic acid (AA2), and AMPA (AA2) resulted in dose‐dependent reductions in all four neurochemical markers examined, while N‐methyl‐D,L‐aspartate (AA1) and quinolinic acid (AA1) resulted in relative sparing of SLI and NPYLI. At doses of each excitotoxin which resulted in comparable 50% reductions in both GABA and SPLI only N‐methyl‐D,L‐aspartate and quinolinic acid had no significant effect on concentrations of SLI and NPYLI. The relative sparing of somatostatin‐neuropeptide Y neurons was confirmed histologically by using histochemical staining for NADPH‐diaphorase neurons combined with either Nissl stains, or immunohistochemical staining for enkephalin. Lessions with N‐methyl‐D‐aspartate agonists resulted in preferential sparing of NADPH‐diaphorase neurons while these neurons were more vulnerable than other neurons to kainic acid or AMPA. Choline acetyltransferase neurons were relatively spared, as compared with other neurons, by agents acting at all three glutamate receptor subtypes. N‐methyl‐D,L‐aspartate lesions were blocked with MK‐801, while there was no effect on quisqualic acid or kainic acid lesions. The relative sparing of somatostatin‐neuropeptide Y neurons following striatal excitotoxin lesions with N‐methyl‐D‐aspartate (AA1) agonists probably reflects a paucity of AA1 receptors on these neurons. Since these neurons are also spared in Huntington's disease, excitotoxins acting at the N‐methyl‐D‐aspartate (AA1) site provide an improved neurochemical model of this illness.
Synaptogenesis in the stratum griseum superficiale of the rat superior colliculus
Authors: Warton S. S. , McCart R. 
Published: January 2005

AbstractThe time course of synaptogenesis in the visual part of the superior colliculus (SC) of pigmented rats has been studied. The number of synaptic profiles per unit area and volume of neuropil in the stratum griseum superficiale (SGS) was estimated in seven groups of animals at ages 3, 9, 15, 21, 30, 49 and 85 days after birth.At 3 days only 1.5 ± 0.06 synaptic contacts per unit area and 5.5 ± 0.18 per unit volume were found. Most of them were immature contacts between growing processes. The density of synaptic contacts increased slowly during the first week. By day 9, 4.1 ± 0.25 and 13.4 ± 0.66 synaptic contacts were counted per unit of area and volume, respectively. A rapid synaptic proliferation occurred during the next 3 weeks and there were 7.7 ± 0.27 and 25.5 ± 1.04 synaptic contacts per unit area and volume at 15 days, 21.1 ± 1.70 and 86.4 ± 5.11 at 21 days, and 25.9 ± 1.20 and 96.7 ± 3.48 at 30 days. At the same time, the synaptic population gradually acquired more mature morphological characteristics: the pre‐ and postsynaptic structures became more specialized, the number of synaptic vesicles within presynaptic structures increased, and the synaptic junctional apposition became defined. After 30 days, a decrease in the density of synaptic profiles was recorded: 23.9 ± 0.44 and 79.8 ± 1.43 per unit area and volume of neuropil at 49 days and 13.4 ± 0.53 and 49.7 ± 2.40 at 85 days, respectively. Thus, after the phase of synaptic proliferation, a significant reduction of synaptic density occurred in the SGS neuropil until it was stabilized at the adult level by the third month of life.Considering the data available on the development of the retinal and visual cortical projections to the SC, the process of synaptic elimination, which takes place after the first postnatal month, does not appear to be directly connected with segregation of these particular projections.
Direct demonstration of D1 dopamine receptors in the bovine parathyroid gland using the D1 selective antagonist [125I]‐SCH 23982
Authors: Monsma Frederick J. , Sibley David R. 
Published: January 2005

AbstractThe presence of D1 dopamine receptors in the parathyroid gland has been proposed based on the demonstration of dopaminergic regulation of adenylate cyclase activity and parathyroid hormone release in dispersed bovine parathyroid cells. Using a radioiodinated D1 selective antagonist [125I]‐SCH 23982, we have now directly labeled and characterized the D1 dopamine receptors in bovine parathyroid gland membranes.[125I]‐SCH 23982 binds in a saturable manner with high affinity and low nonspecific binding to membranes prepared from bovine parathyroid glands. D1 dopamine receptors are present in this preparation at a concentration of ≈︁130 fMoles/mg protein and [125I]‐SCH 23982 binding increases with increasing protein concentration in a linear fashion. Determination of the Kd using the association (k1) and dissociation (k‐1) rate constants revealed good agreement with the Kd determined by saturation analysis (390 pM vs. 682 pM, respectively). Inhibition of 0.3 nM [125I]‐SCH 23982 binding by a series of dopaminergic antagonists verified the D1 nature of this binding site, exhibiting appropriate affinities and rank order of potency. The competition curves of all antagonists exhibited Hill coefficients that were not significantly different from 1. Inhibition of [125I]‐SCH 23982 binding by dopamine and other dopaminergic agonists revealed the presence of high and low affinity agonist binding sites. Addition of 200 μM GppNHp effected a complete conversion of high affinity dopamine binding sites to a homogeneous population of low affinity dopamine sites. The D1 receptors identified in the parathyroid gland with [125I]‐SCH 23982 appear to be pharmacologically identical with those previously characterized in the central nervous system.These results demonstrate that the bovine parathyroid gland, which possesses well‐characterized functional responses to dopaminergic stimulation, may provide a single cell‐type model system for future investigation of the molecular events involved in D1 dopamine receptor/response coupling and regulation.
Effects of hypothyroidism on high‐affinity vasopressin binding sites in developing hippocampal synaptosomes
Authors: Rami Abdelhaq , Barberis Claude , Clos Jean 
Published: January 2005

AbstractBinding sites of vasopressin (VP) have been characterized in the hippocampal synaptic plasma membranes of developing normal and hypothyroid rats using a highly specific tritiated VP antagonist, d(CH2)5Tyr(Me)VP (V1 type). This antagonist bound to an apparently homogeneous population of specific sites with an affinity ten times higher than that of VP itself. The total amount of synaptosomal protein in 15‐day‐old normal rats represented about 50% of the adult value, but the density of binding sites was already maximal and remained constant thereafter, supporting the concept of an early development of an extrahypophyseal vasopressinergic hippocampal system. Thyroid deficiency specifically reduced the amount of synaptosomal protein. However, the binding site density in the synaptsomal fraction appeared to be relatively well preserved from hypothyroidism, although there was a transient decrease in the apparent affinity of the ligand. These data suggest that thyroid hormones are slightly involved in the early development of high‐affinity VP receptors.
Inhibitory effect of norepinephrine on the single‐unit activity of caudally projecting paraventricular neurons
Authors: Kim Yang I. , Dudley Carol A. , Moss Robert L. 
Published: January 2005

AbstractThe role of norepinephrine (NE) in controlling the single‐unit activity of paraventricular (PVN) neurons projecting to or passing through the caudal ventrolateral medulla (CVLM) was investigated in adult male rats anesthetized with urethane. Of 72 PVN neurons studied, 19 were antidromically activated by CVLM stimulation (Group I) and 48 were antidromically activated by posterior pituitary (PP) stimulation (Group II). The remaining 5 neurons were antidromically driven by both CVLM and PP stimulation (Group III). In 14 of the 19 Group I neurons and in all the 5 Group III neurons, iontophoretically applied NE was demonstrated to inhibitory to the single‐unit activity. No excitatory effect of NE was observed. In contrast, both excitatory and inhibitory actions of NE were observed in the Group II neurons. Of 37 Group II neurons tested, 28 were excited and 7 were inhibited by NE. The inhibitory effect of NE in Group I and Group III neurons was selectively blocked by the alpha antagonist, phentolamine, that was coiontophoresed with NE, but not by the beta antagonist, timolol (n = 9). The unit activity of Group I neurons that were inhibited by NE was not altered by an increase in arterial blood pressure (n = 3), whereas the unit activity of one NE‐insensitive Group I neuron was decreased by an increase in blood pressure.Taken together, the results suggest that NE plays an alpha‐adrenoreceptor‐mediated inhibitory role in controlling the single‐unit activity of caudally projecting PVN neurons. These neurons include a subpopulation of PVN neurons that project caudally as well as to the PP. The possible function associated with the NE‐sensitive, caudally projecting PVN neurons may be other than the regulation of blood pressure.