bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oscillation of interspike interval length in substantia nigra dopamine neurons: Effects of nicotine and the dopaminergic D2 agonist LY 163502 on electrophysiological activity
Authors: Carlson Joanne H. , Foote Stephen L. 
Published: December 2004

AbstractThe rates and patterns of discharge activity exhibited by 16 spontaneously active substantia nigra pars compacta dopamine neurons were studied in halothane‐anesthetized rats using three types of quantitative measures: (1) mean discharge rates, (2) population characteristics of interspike interval samples, and (3) interspike interval time‐series measures which were used to examine patterns in the ordering of interspike intervals. The mean discharge rate of these 16 cells was 2.9 ± 0.3 spikes/sec, and each cell was classified as bursting (25% of the cells) or non‐bursting (75%). The distribution of interspike intervals of bursting cells was typically positively skewed and sometimes bimodal, while the interspike intervals of non‐bursting neurons were more normally distributed. Time‐series analyses (raw time‐series plots, return maps, and phase portraits) revealed a substantial oscillatory tendency in the magnitudes of consecutive interspike intervals in these neurons under baseline conditions: Successive interspike intervals tended to alternate between short and long durations, although short bursts often occurred. Under baseline conditions, these cells exhibited both multispike bursts and consecutive long intervals less frequently than would have been predicted by chance ordering of the interspike intervals. These results imply that there are mechanisms acting to reduce the probability of these types of events.Locally infused nicotine enhanced discharge rates in these neurons. Burst firing increased in four neurons, while five neurons did not show any change in burst firing. LY 163502 induced significant decreases in both discharge rate and bursting activity in all cells tested. The variation coefficient, skew, and kurtosis of the interspike interval distributions were not consistently altered by either drug. The local infusion of either nicotine or LY 163502 decreased the oscillatory phenomenon seen in the baseline condition. Neither the nicotine or LY 163502 time‐series data exhibited a larger proportion of long‐short and short‐long pairs (relative to the median interval) than would be expected by chance.It is hypothesized that these neurons have intrinsic mechanisms, made manifest under anesthesia, which induce oscillations in interspike interval length. The oscillatory effect of these mechanisms can be overridden by tonic increases in either excitatory or inhibitory tone. © Wiley‐Liss, Inc.
Microiontophoretic studies of the effects of D‐1 and D‐2 receptor agonists on type I caudate nucleus neurons: Lack of synergistic interaction
Authors: Shen Roh‐yu , Asdourian David , Chiodo Louis A. 
Published: December 2004

AbstractSeveral lines of evidence have suggested there may be a physiologically relevant form of synergistic interaction between D‐1 and D‐2 dopamine (DA) receptors located on postsynaptic neurons in the forebrain that receive a dopaminergic innervation. Because of the theoretical importance of such an interaction with respect to understanding the normal physiology of dopaminergic systems, we evaluated effects of D‐1 and D‐2 selective, agonists, applied microiontophoretically, on the spontaneous electrical activity of a single, identifiable subpopulation of neurons within the caudate nucleus, the type I striatal neuron, in locally anesthetized, gallamine‐paralyzed rats. It was observed that the D‐2 receptor agonist quinpirole (QUIN) produced biphasic effects on cell firing rate. Low ejection currents significantly increased firing rate, while higher currents produced an inhibition. Similar effects were observed for the D‐1 agonists SKF 38393; however, the overall excitations observed at low ejection currents were far less than those observed for QUIN. When these two agonists were applied concurrently, a simple additive effect (but not synergism) was always observed. The acute reduction of striatal levels of DA, by as much as 84% (with pretreatment with α‐methyl‐p‐tyrosine, AMPT), did not alter the responsiveness of type I striatal neurons to the DA receptor agonists applied alone or in combination. These observed effects were not altered either by chloral hydrate anesthesia (in which glutamate‐driven activity was studied) or by a more severe depletion of striatal DA levels (98% depletion produced by combined pretreatment with AMPT and reserpine). © Wiley‐Liss, Inc.
Dopamine supersensitivity and D1/D2 synergism are unrelated to changes in striatal receptor density
Authors: Lahoste Gerald J. , Marshall John F. 
Published: December 2004

AbstractExperiments were conducted to elucidate the relationships among striatal dopamine receptor density, behavioral manifestations of D1/D2 synergism (i. e., the requirement of concomitant stimulation of D1 and D2 receptors for the expression of stereotyped sniffing, licking and gnawing), and behavioral supersensitivity to dopamine agonists. The state of D1/D2 synergism was found to be independent of striatal D1 or D2 receptor density in rats as: (1) increasing striatal D1 and/or D2 receptor density (as confirmed by quantitative receptor autoradiography) by chronic treatment with SCH 23390 (0.5 mg/kg/day for 21 days) and/or haloperidol (0.5 mg/kg/day for 21 days) did not alter the normal pattern of D1/D2 synergism as determined by behavioral responsiveness to agonist stimulation of D1 or D2 receptors, and (2) 5 days of reserpine treatment (1 mg/kg/day), although not significantly changing striatal D1 or D2 receptor density, induced a breakdown in D1/D2 synergism (i. e., behavior was elicited by independent stimulation of D1 or D2 receptors).In addition, the density of striatal D2 binding sites was not indicative of behavioral sensitivity to D2 agonists. Chronic haloperidol treatment increased behavioral sensitivity to the D2 agonist quinpirole by a factor of 2. When tested 96 h after bilateral 6‐hydroxydopamine injections or after 5 daily reserpine injections, supersensitivity to quinpirole was at least double that following chronic haloperidol, without accompanying increases in striatal D2 density. This enhanced sensitivity to quinpirole was no greater than that observed in neurologically intact rats treated concomitantly with a maximally stimulating dose of SKF 38393. Furthermore, rats with unilateral 6‐hydroxydopamine lesions that were treated chronically with eticlopride continued to rotate contralateral to the lesion in response to quinpirole despite having hemispheric symmetry of striatal D2 receptor binding. By contrast, when rats with unilateral 6‐hydroxydopamine lesions were given 5 daily reserpine injections, rotation was abolished, having been replaced by intense stereotyped sniffing, indicative of bilateral supersensitivity.The results support the hypothesis that two distinct types of dopamine supersensitivity exist: A modest one associated with increased D2 density, and a more profound one associated with a breakdown in D1/D2 synergism and independent of D2 density.
Somatostatin binding reduced by ammonium acetate in the rat hippocampus can be reversed by treatment with N‐carbamyl‐L‐glutamate plus L‐arginine
Authors: Del Carmen Boyano Maria , Bodega Guillermo , Alvaro Itziar , Arilla Eduardo 
Published: December 2004

AbstractThe effects of short‐term (90 min), mid‐term (5 days), and long‐term (15 days) administration of ammonium acetate (5 mmol/Kg day i. p.) on the somatostatinergic neurotransmitter system of the rat hippocampus have been studied. Scatchard analysis of the binding of 125I‐Tyr11‐somatostatin to hippocampal dissociated cells indicated that administration of ammonium acetate at the times studied were associated with a decrease in the number of somatostatin receptors in this brain area, whereas the affinity of the same receptors remained unchanged. Administration of ammonium acetate did not affect the levels of somatostatin‐like immunoreactivity in the hippocampus. Treatment with N‐carbamyl‐L‐glutamate (1 mmol/Kg, i. p.) plus L‐arginine (1 mmol/Kg), which lead to the conversion of ammonia into urea, prevented the ammonium acetate‐induced changes in somatostatin binding in this brain area. N‐carbamyl‐L‐glutamate plus L‐arginine alone had no observable effect on the somatostatinergic system. The decrease in the number of somatostatin receptors induced by ammonium acetate might reflect a decreased sensitivity of the target cells to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat hippocampus. © 1992 Wiley‐Liss, Inc.
Alteration of 5‐HT1A receptor binding sites following chronic treatment with ipsapirone measured by quantitative autoradiography
Authors: Fanelli Richard J. , McMonagle‐Strucko Katheen 
Published: December 2004

AbstractIpsapirone, a high‐affinity ligand for the 5‐hydroxytryptamine1A (5‐HT1A) receptor subtype, has been shown to be a full agonist at presynaptic serotonergic sites and a partial agonist at postsynaptic sites. Several recent studies have examined the effects of chronic treatment with ipsapirone or other structurally related pyrimidinylpiperazine compounds, including buspirone and gepirone, on 5‐HT1A binding sites with mixed results. Since the neural mechanism responsible for the anxiolytic and antidepressant properties of these compounds is currently uncertain, further investigation of this issue appeared warranted. [3H] 8‐hydroxy‐2‐(di‐n‐propylamino)‐tetralin ([3H] 8‐OHDPAT), a ligand specific for the 5‐HT1A site, has been used successfully to label these sites using both membrane binding assays and autoradiography. Experiments were performed to determine whether chronic treatment with ipsapirone would differentially affect binding to 5‐HT1A receptors at different brain sites. Rats were treated twice daily with ipsapirone (10 mg/kg i. p.) for 1 day or for 1, 2, or 3 weeks. Quantitative analyses were done of autoradiograms of in vitro [3H] 8‐OH‐DPAT binding to selected brain regions. Binding in vehicle‐treated rats was highest in the hippocampus, septal nucleus, interpeduncular nucleus, entorhinal cortex, and dorsal raphe nucleus. Following 3 weeks of treatment with ipsapirone, a large decline in binding was measured in the dorsal raphe nucleus. This decline was not seen with ipsapirone treatments for shorter periods. With the 3‐week treatment, there were less robust declines in [3H] 8‐OH‐DPAT binding in the entorhinal cortex and interpeduncular nucleus. Binding in the other brain regions analyzed was unaltered. These results, together with those in the literature, indicate the importance of dose and length of treatment in producing these alterations. The large decline in binding sites in the dorsal raphe is consistent with the view that the anxiolytic and antidepressant properties of ipsapirone are mediated by a downregulation of the somatodendritic 5‐HT1A autoreceptors. © 1992 Wiley‐Liss, Inc.
Distribution of cocaine recognition sites in monkey brain: II. Ex vivo autoradiography with [3H]CFT and [125I]RTI‐55
Authors: Kaufman Marc J. , Madras Bertha K. 
Published: December 2004

AbstractCFT [WIN 35, 428, 2β‐carbomethoxy‐3β‐(4‐fluorophenyl)tropane] and its 4‐iodinated analog RTI‐55 have been proposed as imaging probes for cocaine recognition sites and for dopamine transporters. The central and peripheral distribution of radiolabeled forms of these compounds was studied 30 minutes after intravenous administration in squirrel monkey (Saimiri sciureus). Quantitative ex vivo autoradiography of brain tissue sections from animals receiving [3H]CFT (2.5 nmol/kg) revealed radioligand distribution primarily in dopamine‐rich brain regions, and treatment with cocaine or mazindol substantially reduced [3H]CFT accumulation. The caudate nucleus, putamen, and nucleus accumbens/olfactory tubercle accumulated the highest levels of [3H]CFT, and within the caudate nucleus, medial‐to‐lateral and anterior‐to‐posterior gradients were observed. Low levels of [3H]CFT were found in the cortex, thalamus, hypothalamus, and background levels in white matter and in the cerebellum (striatal: cerebellar ratio > 3). The in vivo distribution of [3H]CFT closely paralleled its in vitro distribution (Synapse, 9:177–187). Although [125I]RTI‐55 (0.2 nmol/kg) also distributed to dopamine‐rich brain regions (striatal: cerebellar ratio of 3.6), high levels also were detected in cortex, thalamus, and in midbrain/brainstem structures. In the periphery, [125I]RTI‐55 accumulation, measured as percent of administered dose, was higher than [3H]CFT in liver and lung, greater than 90% comigrated with [3H]CFT or [125I]RTI‐55 standards. The results support the hypothesis that dopamine‐rich brain regions may be relevant to the effects of cocaine, and that both CFT and RTI‐55 may be suitable imaging probes for these sites.
Both phasic sensory stimulation and tonic pharmacological activation increase Fos‐like immunoreactivity in the rat locus coeruleus
Authors: Grant S. J. , Bittman K. , Benno R. H. 
Published: December 2004

AbstractNeuronal activation increases levels of Fos protein, the product of the early immediate gene c‐fos. Since most studies used stimuli that evoke sustained elevations in activity; the present study examined Fos‐like immunoreactivity (Fos‐LI) in the nucleus locus coeruleus (LC). Halothane‐anesthetized rats were given either footshock to elicit phasic activation of LC neurons or yohimbine (10 mg/kg, i. p.) to induce a tonic increase in firing. Both treatments markedly increased Fos‐LI in a subpopulation of LC neurons. These results demonstrate that c‐fos induction does not require high tonic levels of neuronal activity and that Fos‐LI may underestimate the proportion of LC neurons neurophysiologically activated by a given stimulus and suggest that factors beyond neuronal activity per se contributes to c‐fos expression. © 1992 Wiley‐Liss, Inc.
LHRH neurons in the medial septal‐diagonal band‐preoptic area do not project directly to the hippocampus: A double‐labeling immunohistochemical study
Authors: Dudley Carol A. , Sudderth Skylar B. , Moss Robert L. 
Published: December 2004

AbstractWhile neurons containing immunoreactive luteinizing hormone‐releasing hormone (LHRH) are scattered primarily in the medial septal‐diagonal band of Broca‐medial preoptic area (mS‐dbB‐PO) complex, autoradiographic studies have demonstrated dense concentrations of LHRH receptors in the hippocampus. The route by which LHRH is transported to its hippocampal receptors is unknown. The present study was designed to test the hypothesis that LHRH‐containing neurons in the mS‐dbB‐PO complex project to hippocampal sites containing LHRH receptors, thereby serving as a source of innervation to these receptors.Large (0.10 m̈l) or small (0.02 m̈l) volumes of the retrograde tracer wheat germ agglutinin (WGA) were injected unilaterally into four separate hippocampal locations in six ovariectomized female rats. In an additional five females, a 0.15 m̈l volume of the retrograde tracer fluorogold (FG) was similarly injected. After a five day survival period, the animals were sacrificed. Vibratome sections of the brain were stained for both WGA and LHRH with a dual immunohistochemical technique. Since FG is a fluorescent chromagen, brains of animals injected with FG only required processing for LHRH immunofluorescence. As a positive control, some sections containing retrogradely labeled cells filled with either WGA or FG were processed for choline acetyltransferase (CHAT) immunoreactivity.The WGA and FG injections covered targeted hippocampal sites and neurons containing retrogradely transported WGA or FG were found in abundance in the mS‐dbB‐PO complex. In accord with previous reports, many CHAT‐positive and fewer LHRH‐positive neurons were found in this complex. Approximately 5–10% of the CHAT‐positive neurons also contained WGA or FG; however, no neurons were found to co‐localize LHRH and either of the retrograde tracers. The results indicate that LHRH neurons in the mS‐dbB‐PO complex do not project directly to hippocampal sites containing LHRH receptors. © 1992 Wiley‐Liss, Inc.
Comparison of chronic intermittent haloperidol and raclopride effects on striatal dopamine release and synaptic ultrastructure in rats
Authors: See Ronald E. , Chapman Mary Ann , Meshul Charles K. 
Published: December 2004

AbstractThe effects of chronic intermittent administration (7 months) of two neuroleptics, haloperidol (HAL) and raclopride (RAC), were compared using several different measures. Both drugs were administered weekly by subcutaneous injection at 7.0 mg/kg. Both neuroleptics consistently produced catalepsy throughout the treatment period, although HAL was generally more cataleptogenic than RAC. Assessment of dopamine (DA) release in the caudate putamen (CPu), through the use of in vivo microdialysis, showed that chronic HAL or RAC administration caused a prolonged decrease of DA release in response to a low dose of the DA D2 agonist quinpirole (0.03 mg/kg, sc). Injection of the muscarinic agonist pilocarpine (1.0 mg/kg, IP) did not have any significant within‐group effects, although both neuroleptic treatment groups showed decreased DA release when compared to controls. Ultrastructural analysis of the dorsolateral CPu showed that both HAL and RAC treatment resulted in a significant increase in the number of perforated synapses, which contain a discontinuous density along the postsynaptic membrane. These results demonstrate that two different DA D2 receptor antagonists produce a similar effect on DA function and ultrastructural changes within the CPu following chronic, intermittent treatment. © 1992 Wiley‐Liss, Inc.
Sigma receptors are associated with cortical limbic areas in the primate brain
Authors: Mash Deborah C. , Zabetian Cyrus P. 
Published: December 2004

AbstractPutative sigma receptors are a current target for antipsychotic drug development. Novel antipsychotic agents which possess selective and high affinity for sigma binding sites may serve as an alternative to the principal neuroleptic drugs currently in clinical use which mediate extrapyramidal side effects and dyskinesias through their blockade of dopamine receptors. We have used in vitro autoradiography to localize putative sigma receptors labelled with (+)‐[3H]‐3‐(3‐hydroxyphenyl)‐N‐(1‐propyl) piperidine [(+)‐[3H]‐3‐PPP] in the brain of the rhesus macaque. The binding characteristics of (+)‐[3H]‐3‐PPP in the primate brain were comparable to those previously described in the rodent. Saturation analysis demonstrated a single class of sites in cerebellar and hippocampal membranes with a Kd value of 28 nM. Sigma receptors labeled with (+)‐[3H]‐3‐PPP in the primate brain displayed the appropriate rank order of potency and stereoselectivity in competition binding assays. Haloperidol displaced (+)‐[3H]‐3‐PPP binding in the low nanomolar range, and the (+) isomer of pentazocine was 50‐fold more potent than (‐) pentazocine. Computerized densitometric analysis of the autoradiograms demonstrated a striking enrichment of sigma binding sites over the paralimbic belt cortices, including the orbitofrontal, cingulate, insular, parahippocampal, and temporopolar gyri. Peak densities of sigma receptors were seen over the medial and central nuclei of the amygdala and were widely distributed within the hippocampal formation. Sigma binding sites densities were elevated over the suprachiasmatic and supraoptic nuclei of the hypothalamus. Moderate sigma receptor densities were observed over the ventromedial sectors of the caudate and the putamen. Sigma receptors were also elevated over autonomic relay nuclei of the brainstem, including the nucleus of the solitary tract and the dorsal motor nucleus of the vagus. The distribution of sigma receptors in the primate brain suggests that the paralimbic belt cortices, amygdala, hippocampus, hypothalamus, and autonomic relay nuclei of the brainstem may be interrelated by a topographic chemical linkage. The autoradiographic visualization of sigma receptor distributions in the primate brain provides further support for a role of sigma receptor mechanisms in the functions of the limbic system. © 1992 Wiley‐Liss, Inc.
Multiple metabotropic glutamate receptors regulate hippocampal function
Authors: Desai Manisha A. , Smith Timothy S. , Conn P. Jeffrey 
Published: December 2004

AbstractSelective activation of metabotropic glutamate receptors withtrans‐1‐amino‐1, 3‐cyclopentanedicarboxylic acid (trans‐ACPD) stimulates phosphoinositide hydrolysis and elicits three major physiological responses in area CA1 of the hippocampus. These include direct excitation of pyramidal cells, blockade of synaptic inhibition, and decreased transmission at the Schaffer collateral‐CA1 pyramidal cell synapse. Physiological effects oftrans‐ACPD are thought to be mediated by activation of phosphoinositide hydrolysis. However, it is now clear that multiple metabotropic glutamate receptor subtypes exist, some of which are not coupled to phosphoinositide hydrolysis. Thus, we performed a series of studies aimed at determining whether the physiological effects oftrans‐ACPD in the hippocampus are mediated by activation of the predominant phosphoinositide hydrolysis‐linked glutamate receptor. We report thatL‐2‐amino‐3‐phosphonopropionic acid (L‐AP3), an antagonist oftrans‐ACPD‐stimulated phosphoinositide hydrolysis, does not inhibit the physiological effects oftrans‐ACPD in area CA1 at concentrations that maximally inhibittrans‐ACPD‐stimulated phosphoinositide hydrolysis in this region. Furthermore, 1S, 3S‐ACPD activates the phosphoinositide hydrolysis‐linked glutamate receptor but does not reduce evoked field excitatory postsynaptic potentials (EPSPs) in area CA1. However, we report that the physiological effects of 1R, 3S‐ and 1S, 3R‐ACPD are consistent with the hypothesis that these effects are mediated by activation of a metabotropic glutamate receptor. Thus, our data are consistent with the hypothesis that the physiological effects oftrans‐ACPD in area CA1 of the hippocampus are mediated by metabotropic glutamate receptors that are distinct from the AP3‐sensitive phosphoinositide hydrolysis‐linked glutamate receptor. © 1992 Wiley‐Liss, Inc.
Systemic and microiontophoretic administration of morphine differentially effect ventral pallidum/substantia innominata neuronal activity
Authors: Napier T. Celeste , Chrobak James J. , Yew Jay 
Published: December 2004

AbstractIn vivo electrophysiological recording techniques were employed to examine responses of ventral pallidum/substantia innominata (VP/SI) neurons to systemic and local administration of morphine. Using a cumulative dosing protocol, intravenous administration (0.1–30 mg/kg i. v.) produced a suppression of firing in 82% of neurons tested. The suppression was dose‐related and blocked by the opioid antagonist, naloxone. In contrast, microiontophoretic applications of morphine resulted in current‐related suppression (32% of neurons tested) or excitation (26%). Concurrent application of naloxone attenuated or blocked both effects of local morphine applicatio. It was demonstrated that acute tolerance did not develop with repeated morphine exposures following either systemic or local administration. The present findings establish the sensitivity of VP/SI neurons to morphine and provide functional relevance at the level of a single neuron for opioid peptides and their receptors in this region. As reported for most other opioid receptive brain areas, neuronal rate suppression was the predominate response observed, and it is proposed that excitations to iontophoresed morphine reflect a disinhibitory phenomenon. The differntial morphine‐induced rate changes, and number of responding neurons, observed with systemic vs. iontophoretic morphine administration suggest that extra‐VP/SI regions that also are opioid sensitive can subsequently direct neuronal responsivensess to opioids within the VP/SI. © 1992 Wiley‐Liss, Inc.