bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of luteinizing hormone secretion by neuropeptide Y in rats: Hypothalamic and pituitary actions
Authors: Crowley William R. , Kalra Satya P. 
Published: January 2005

AbstractPrevious studies have suggested that the stimulatory effect of neuropeptide Y (NPY) on the release of luteinizing hormone (LH) in rats may be due to a central action of the peptide that promotes the release of LH‐releasing hormone (LHRH) from the hypothalamus, and to an action in the pituitary gland, to potentiate the release of LH induced by LHRH. The objectives of the present experiments were to test (1) whether NPY stimulation of LHRH release requires extracellular Ca++, and (2) whether NPY can exert direct stimulatory effects on the release of LH from anterior pituitary cells. The in vitro release of LHRH from medial basal hypothalamic fragments induced by KCl depolarization (56 mM), but not the basal release, was blocked by omission of Ca++ and addition of 0.1 mM EGTA to the incubation medium and also by cobalt (1 mM). Depolarizationinduced release of the peptide was unaffected by nifedipine, diltiazem, or lanthanum. However, the stimulation of LHRH release by NPY (1 μM) still occurred in Ca++ free/EGTA medium. In a second set of experiments, 10 min pulses of NPY (1–100 nM) alone were ineffective in stimulating the release of LH from dispersed, perifused anterior pituitary cells obtained from ovariectomized, untreated or ovariectomized, estrogen‐treated rats, under conditions where pulses of LHRH (0.1–10 nM) were consistently effective. A brief increase in LH release was observed during a 30 min exposure to 100 nM NPY in estrogen‐pretreated cells, but not from untreated cells, and the effect was not as marked as that produced by LHRH. The present results confirm previous observations that NPY stimulates the release of LHRH from medial basal hypothalamus in vitro and suggests that NPY does not activate the influx of extracellular Ca++ in order to produce this effect. NPY may also directly stimulate the release of LH from anterior pituitary cells, but is weaker than the physiological releasing hormone, LHRH. The dual actions of NPY may have physiological significance in mediating ovarian hormone positive feedback on LH secretion during the estrous cycle.
Distribution of dopamine D1 receptors in rat cortical areas, neostriatum, olfactory bulb and hippocampus in relation to endogenous dopamine contents
Authors: Diop Laurent , Gottberg Estela , Brière Richard , Grondin Louise , Reader Tomas A. 
Published: January 2005

AbstractThe tritiated dopamine D1 antagonist SCH23390 was employed to determine the densities of D1 receptors in seven discrete and functionally identified cortical areas (cingulate, frontal, parietal, primary somatosensory, primary visual, retrosplenial and entorhinal‐piriform) as well as in the neostriatum, hippocampus and olfactory bulbs. In addition, the tissue levels of the catecholamines NA, AD, DA, the indoleamine 5‐HT and their main metabolites (MHPG, DOPAC, HVA, 3‐MT, 5‐HTP and 5‐HIAA) were measured in the different regions by HPLC with electrochemical detection. The Scatchard analysis of saturation curves revealed the highest density of [3H]SCH23390 binding sites for the neostriatum, while the densities were 10×20 times lower for total cerebral cortex and hippocampus respectively. For the olfactory bulb and other cortical areas, D1 receptor densities were determined by equilibrium binding at a fixed radioligand concentration approaching saturation. The distribution of D1 receptors was heterogeneous with the greatest densities in entorhinal‐piriform and cingulate cortices. The endogenous DA levels measured for all regions correlated with their metabolite (DOPAC, HVA and 3‐MT) contents (r = 0.999; P < 0.001). There was also a very good correlation (r = 0.981; P < 0.001) between tissue DA and D1 receptor densities. This quantitative information reflects particular features of the organization of the DA systems and is discussed in relation to turnover and recently established aspects of the DA innervation.
Acute effects of lithium on dopaminergic responses: Iontophoretic studies in the rat visual cortex
Authors: Gottberg Estela , Montreuil Bernard , Reader Tomas A. 
Published: January 2005

AbstractThe interactions between lithium and cortical dopaminergic receptors were investigated using the iontophoretic technique to record and apply dopaminergic compounds, GABA, acetylcholine and LiCL on neurons in the primary visual cortex of the rat. The main responses to dopamine (DA) or to the D1 agonist (±)SKF38393 on spontaneously‐active (SA) or visually‐driven (VD) units was a prolonged decrease in firing and a reduction in the responsiveness to pulses of acetylcholine. The D1 antagonist SCH23390, applied iontophoretically or intravenously, blocked or attenuated the inhibitory responses to both DA and (±)SKF38393. The D2 agonist quinpirole (LY171555) either produced only slight excitations or had no effects on both VD and SA units. The concomitant application of lithium blocked the inhibitory responses to DA and to (±)SKF38393 but did not modify the responsiveness to LY171555. In addition, the DA‐ and (±)SKF38393‐induced decreases in responsiveness to acetylchline were also suppressed by lithium. These effects were on dopaminergic mechanisms, since the excitatory responses to acetylcholine alone as well as the inhibitions causes by GABA were unchanged by the application of lithium. These results imply that the modifications in sensitivity to dopaminergic agents induced by lithium are mediated by dopamine D1 receptors and are discussed in relation to adenylatecyclase.
Quantitation of nerve terminal populations: Synaptic vesicle‐associated proteins as markers for synaptic density in the rat neostriatum
Authors: Walaas S. Ivar , Jahn Reinhard , Greengard Paul 
Published: January 2005

AbstractThis study has assessed the contributions of the corticostriatal fibers, the ascending striatopetal fibers, and the intrinsic neostriatal neurons to the nerve terminal population found in the rat neostriatum (caudatoputamen). For this purpose, we have analysed the levels of two different synaptic vesicle‐associated proteins, synapsin I and protein p38 (also called synaptophysin), in the neostriatum after specific lesions. Our results indicate that 45–50% of the synaptic vesicle proteins in the rat neostriatum derive from the corticostriatal fibers, that approximately 25–30% of the synaptic vesicle proteins are present in kainic acid‐sensitive structures, presumably intrinsic terminals and local collaterals, and that ascending fibers contain 20–25% of the vesicle‐associated proteins in the neostriatum. These three neuronal populations therefore comprise 95–100% of the synaptic vesicle‐associated proteins in the rat neostriatum, and thus make up most of the nerve terminals in this brain region. The results, which are in general agreement with previous morphometric studies on the rat basal ganglia, therefore indicate that nerve terminals in the central nervous system can be quantitated by use of these biochemical nerve terminal markers. The results also indicate that a somewhat higher percentage of neostriatal nerve terminals belongs to the corticostriatal fibers than previously believed.
Serotoninergic neurites in senile plaques in cingulate cortex of aged nonhuman primate
Authors: Kitt Cheryl A. , Walker Lary C. , Molliver Mark E. , Price Donald L. 
Published: January 2005

AbstractIn immunocytochemical studies, a polyclonal antiserotonin antibody was used to visualize fibers within the cingulate cortex of young and aged rhesus monkeys. Intricate and distinct patterns of serotoninergic processes were seen in anterior and posterior segments of cingulate cortex (Brodmann areas 24 and 23). In these regions of cortex, many multivaricose serotonin‐immunoreactive axonal swellings were identified, and some of these immunostained neurites were associated with deposits of amyloid. These observations suggest that serotoninergic processes are involved in the formation of senile plaques in neocortex of aged macaques.
Localization and regulation of vasopressin mRNA in human neurons
Authors: Rivkees Scott A. , Chaar Maamoun R. , Hanley Daniel F. , Maxwell Marius , Reppert Steven M. , Uhl George R. 
Published: January 2005

AbstractVasopressin (prepropressophysin) mRNA is detected in neurons of the supraoptic, suprachiasmatic, and paraventricular nuclei of human postmortem hypothalamic specimens by quantitated in situ hybridization using 35S‐labeled single‐stranded cDNA probes directed against exon C of the human vasopressin gene. This hybridization displays the anticipated anatomic distribution, as well as several biochemical features supporting its specificity. Hybridization densities in supraoptic neurons, a measure of vasopressin gene expression, display substantial variability from‐brain‐to‐brain. We can attribute much of this brain‐to‐brain variability to differences in antemortem extracellular volume status. This conclusion is based on (a) animal models of the human postmortem process, (b) animal models of common agonal events, (c) good correlations between antemortem volume status and neuronal vasopressin mRNA hybridization densities in human postmortem specimens matched for age and postmortem interval, and (d) our inability to correlate human neuronal vasopressin mRNA hybridization densities with other clinical and postmortem features. These results provide an example of antemortem regulation of a human neuroendocrine gene using postmortem tissue.
Dye‐Coupling in the neostriatum of the rat: II. Decreased coupling between neurons during development
Authors: Walsh John P. , Cepeda Carlos , Hull Chester D. , Fisher Robin S. , Levine Michael S. , Buchwald Nathaniel A. 
Published: January 2005

AbstractPhysiological and morphological evidence for coupling between neostriatal neurons was obtained from the developing rat. Intracellular injections of Lucifer Yellow‐CH (LY) were made in rat neostriatal slices to study dye transfer (coupling) between neurons. The incidence of interneuronal coupling was 70% in early postnatal (P) periods and declined gradually to 10% in the adult. The number of neurons filled by a single intracellular injection also declined with age. LY injection into single neurons commonly marked aggregates of 4 to 6 cells in neonates. Single injections never produced more than one coupled pair in P20 or older rats. Neurons in which fast prepotentials (FPPs) could be evoked were consistently found to be dye‐coupled. FPPs were resistant to collision with action potentials generated by intracellular current injection. When chemical synaptic transmission was blocked by Mn2+, short‐latency depolarization (SLDs) could be evoked by extracellular stimulation. The SLDs were distinguished from chemical synaptic potentials by their “all or none” nature and by their insensitivity to changes in membrane potential. No SLDs were observed in adult neurons. FPPs and SLDs may be indicators of electrotonic transmission between coupled cells. The high incidence of coupling early in development might reflect intercellular communication that contributes to the differentiation and growth of neostriatal neurons.
Distribution of dopamine D1 and D2 receptors in rabbit cortical areas, hippocampus, and neostriatum in relation to dopamine contents
Authors: Dewar Karen M. , Reader Tomás A. 
Published: January 2005

AbstractThe densities of dopamine D1 and D2 receptors were measured by using [3H]SCH23390 and [3H]reclopride, respectively, in the rabbit cingulate, visual, sensorimotor, and entorhinal‐piriform cortical areas; the dorsal and ventral hippocampus; and the putamen as well as the medial and lateral caudate. Endogenous dopamine (DA) and its metabolites 3,4‐dihydroxyphenylacetic acid (DOPAC), 4‐hydroxy‐3‐methoxyphenylacetic acid (HVA), and 3‐methoxytyramine (3‐MT) were assayed by HPLC with electrochemical detection. The distributions of [3H]SCH23390 and [3H]raclopride binding were heterogenous with the greatest densities in the neostriatum. The concentrations of DA and its metabolities were also highest in this structure. Regions with low DA content, i.e., cortex and hippocampus, had lower densities of [3H]SCH23390 and [3H]raclopride binding. Furthermore, these sites were differentially localized within the various regions and there were substantially more D1 and D2 receptors. The functional significance and heterogeneities in the distribution of D1 and D2 receptors are discussed in relation to the dopaminergic innervation and the turnover estimated by the ratios between endogenous DA and its metabolites.
Effect of acute and daily cocaine treatment on extracellular dopamine in the nucleus accumbens
Authors: Kalivas Peter W. , Duffy Patricia 
Published: January 2005

AbstractThe behavioral stimulant effect of peripheral cocaine injection into rats is augmented following daily adminstration. In vivo dialysis in the nucleus accumbens of conscious rats was used to determine if the increased behavioral response following daily cocaine administration is associated with in increase in extracellular dopamine concentration. Acute injection of cocaine (15 mg/kg, ip) produced and elevation in extracellular dopamine concentration in the nucleus accumbens. Following daily pretreatment with cocaine (15 mg/kg, ip × 4 days), a subsequent acute injection of cocaine (15 mg/kg, ip) significantly elevated the extracellular dopamine levels compared to that produced by a single acute injection. Although the levels extracellular dopamine metabolites was significantly lowered by both acute cocaine and daily cocaine, no difference between these two groups of animals was measured. The increase in extrecellular dopamine following a single acute injection of cocaine was not correlated to the motor stimulant response. However, after daily pretreatment with cocaine the motor stimulant response to acute cacaine was positively correlated with the increased extracellular concentration of dopamine in the nucleus accumbens. These data demonstrate that enhanced dopamine release into the nucleus accumbens may mediate the behavioral sensitization produced by daily injections of cocaine, but that other neural systems are influential in mediating the acute motor stimulant effect of cocaine.
Electrophysiological actions of luteinizing hormone‐realeasing hormone: Intracellular studies in the rat hippocampal slice preparation
Authors: Wong Michael , Eaton Misty J. , Moss Robert L. 
Published: January 2005

AbstractThe electrophysilogical effects of luteinizing hormone‐releasing hormone (LHRH) on CA1 pyramidal cells were investigated utilizing intracellular recodings from the in vitro rat hippocampal slce preparation. Bath application of LHRH (10‐7‐10‐12M) resulted in several changes in the electrophysiological properties of CA1 neurons. LHRH induced a long‐lasting depolarization associated with increased input resitance, and decrease in the afterhyperpolarization associated with increased input resistance, ad decrease in the afterhyperpolarization (AHP) following a train of action potentials, and a reduction in accommodation of repetitive cell discharge. These effects were blocked by the synthetic LHRH antagonist [Ac‐δ‐Pro1, pCl‐D‐Phe2, D‐Trp3,6]‐LHRH. These findings provide electrophysiological evidence for the role of LHRH as a neurotransmitter/neuromodulator in the hippocampus.
Glycine site associated with the NMDA receptor modulates long‐term potentiation
Authors: Oliver M. W. , Kessler M. , Larson J. , Schottler F. , Lynch G. 
Published: January 2005

AbstractRecent work has shown that kynurenic acid and several quinoxaline derivatives act as non‐competitive NMDA receptor antagonists by binding to the glycine site associated with this receptor. In this study, we have tested the effect of the most potent and selective of these compounds, 7‐chlorokynurenic acid (C1‐Kyn), on the induction of long‐term potentiation, an event know to involve activation of NMDA receptors. It was found that 30 m̈M C1‐Kyn reversibly abolished the development of both short‐term and long‐term potentiation in the CA1 region of hippocampal slices. The effectiveness of C1‐Kyn matched its ability to inhibit 3H‐glycine binding and the association of 3H‐TCP with the NDMA receptor in binding experiments (Ki 0.7–1 μM). Weak interactions of C1‐Kyn with AMPA receptor sites were observed and may account for a partial, reversible reduction in the epsp. However, blockade of long‐term potentiation by C1‐Kyn was completely reversed by simultaneous application of the glycine site agonist D‐serine and thus must be attributed to its interaction with the glycine site. These results indicate that the glycine site coupled to the NMDA receptor potently modulates channel function during physiological events related to synaptic activation.
Serotonin excitation of facial motoneurons: Receptor subtype characterization
Authors: Rasmussen Kurt , Aghajanian George K. 
Published: January 2005

AbstractThe receptor subtype (s) mediating the enhancement of facial motoneuron exctitability by serotonin (5‐HT) was evaluated by means of single‐cell recording in vivo (in the anesthetized rat) and in vitro in brain slices. In vivo, microiontophoretic application of the broad‐spectrum 5‐HT1 agonist 5‐carboxamidotryptamine (5‐CT), the 5‐HT2/5‐HT1c agonist 1‐[2,5‐demethoxy‐4‐methylphenyl]‐2‐aminopropane (DOM), but not the selective 5‐HT1A agonist 8‐OH‐2[di‐n‐propylamino]tetralin (8‐OH‐DPAT), produced a 5‐HT‐like enhancement of facial motoneuron excitability. Intravenous administration of the 5‐HT2/ 5‐HT1c antagonists ritanserin and LY 53857 in vivo blocked the facilitatory effects of 5‐HT and DOM, but not norepinephrine (NE). Similarly, in brain slices, bath application of ritanserin blocked the effects of 5‐HT, DOM, and 5‐CT, but not NE on facial motoneurons. Intracellular recordings showed that DOM induced a slow depolarization and an increase in evoked spikes, but these effects were of lesser magnitude and longer duration than those produced by 5‐HT. Taken together these result indicate a a role for 5‐HT2 and/or 5‐HT1c but not 5‐HT1A receptors in serotonergic enhancement of facial motoneuron excitability since 5‐HTs effect was (1) at least partially mimicked by the selective 5‐HT2/5‐HTlc agonist DOM, (2) mimicked by the broad‐spectrum 5‐HT1 agonist 5‐CT but not the selective 5‐HTlA agonist 8‐OH‐DPAT, and (3) blocked by the 5‐HT2/5‐HT1c antagonists ritanserin and LY 53857.
Modulation of gonadotropin‐releasing hormone neuronal activity as evidenced by uptake of fluorogold from the vasculature
Authors: Silverman Ann‐Judith , Witkin Joan W. , Silverman Rachel C. , Gibson Marie J. 
Published: January 2005

AbstractPeripheral injections of the tracer fluorogold (EG) and immunocytochemistry were used to study the modulation gonadotropin‐releasing hormone (GnRH) cell secretory activity in adult mice. Intraperitoneal adminstration of FG would make it available to all GnRH terminals outside the blood‐brain barrier. The degree of capture of the dye would be linked to exocytotic (e.g., secretory) events at the nerve terminal. Single injections of tracer were made into intact mice of both sexes, and this resulted in the retrograde labeling of two‐thirds of the GnRH cell bodies. Administration of identical doses to 3 week castrate mice revealed a reduction in the percentage of GnRH cells, with detectable FG, to 40% of the total. Castration did not diminish the number of GnRH cells visualized. When castrate animals received two doses of FG, the number of GnRH cells with tracer was increased to slightly greater than intact levels. This suggests that the secretory rate of individual GnRH cells might be reduced under coditions of castration. In addition, when ovariectomized females treated with estrogen and progeserone to induce luteinizing hormone (LH) surge were injected with FG just prior to that surge, over 80% of the GnRH neurons were robustly labeled with FG. These latter data are interpreted as representing GnRH neurons at maximally synchronized activity. This study suggests that peripheral administration of FG can be used in this species to follow alterations in neurosecretory rates.
Synaptic interactions between GABAergic neurons and trigeminothalamic cells in the rat trigeminal Nucleus Caudalis
Authors: DiFiglia Marian , Aronin Neil 
Published: January 2005

AbstractSynaptic interactions between GABAergic neurons and thalamic projecting cells within the trigeminal nucleus caudalis were examined using a combined method of GABA immunohistochemistry and retrograde WGA‐HRP labeling of the trigeminothalamic pathway. Results showed that GABA‐positive neurons and projecting cells were separate but closely intermingled within the spinal trigeminal nucleus. GABAergic axon terminals formed symmetric synaptic connections with the cell bodies and dendrites of trigeminothalamic neurons. In turn, some WGA‐HRP filled axon terminals, presumed to originate from axon collaterals of the projecting neurons, formed synaptic connections with GABA containing neurons. The results suggest that in the spinal trigeminal nucleus there is a reciprocal modulation between GABA neurons and trigeminothalamic cells.
Immunoreactive calcium‐binding protein (calbindin‐D28k) in interneurons and trigeminothalamic neurons of the rat nucleus caudalis localized with peroxidase and immunogold methods
Authors: Aronin Neil , Chase Kathryn , Folsom Robin , Christakos Sylvia , Difiglia Marian 
Published: January 2005

AbstractCalbindin‐D28k is a highly abundant protein found in neurons in selected brain regions, including cells in sensory system of the brainstem. Because of its capacity to bind cytosolic ca++, calbindin‐D28k is thought to contribute to the regulation of compartmental Ca++ concentration in neurons. In this study of the rat spinal trigeminal nucleus, calbindin‐D28k was localized with immunoperoxidase and immunogold methods. Results showed that immunoreactive calbindin‐D28k neurons were widely distributed to all region of the nucleus, but were particularly numerous in the substantia gelatinosa. Some trigeminothalamic neurons that were identified by retrograde labeling of conjugated wheat‐ germ agglutinin with horseadish perosidase also contained calbindin‐D28k immunoreactivity. Most of the calbindin‐D28k labeling was found in cell bodies and dendrites. Axon terminal were rarely stainded. More discreate labeling with a gold conjugated second antibody showed that the predominant site of calbindin‐D28k was the matrix of the cytoplasm. Gold label was also heavily associated with euchromatin within nuclei.These finding show that immunoreactive calbindin‐D28k is localized to both interneurons and projecting neurons of the spinal trigeminal nucleus. Many of these cells are likely to receive glutamatergic afferent inputs, which may act in part by increasing Ca++ and under some condition may protect neurons against glutamate‐induced excitotoxicity. We speculate that calbindin‐D28k may function to regulate calcium concentration in spinal trigeminal neurons.