bluuebunny/crossref_metadata_2025_split huggingface dataset:
Different mechanisms may be required for maintenance, of NMDA receptor‐dependent and independent forms of long‐term potentiation
Authors: Grover Lawrence M. , Teyler Timothy J. 
Published: December 2004

AbstractIn hippocampal area CA1, long‐term potentiation (LTP) is induced by tetanic stimulation protocols that activate N‐methyl‐D‐aspartate (NMDA) receptors. In addition, some stimulation protocols can induce LTP during NMDA receptor blockade. An initial signal in both NMDA receptor‐dependent and independent LTPs is increased intracellular Ca2+ concentration in postsynaptic neurons. It therefore seems possible that subsequent steps leading to expression and maintenance of potentiation are shared whether or not LTP is induced through NMDA receptor activation. We tested this hypothesis by applying a broad spectrum protein kinase, inhibitor, previously shown to inhibit NMDA receptor‐dependent LTP. In agreement with earlier reports, we found that H‐7 inhibited NMDA receptor‐dependent LTP when applied either during tetanic stimulation, or beginning 30 min following tetanic stimulation. In contrast, NMDA receptorindependent LTP was not inhibited by H‐7 applied during or following tetanic stimulation. We also tested for mutual occlusion between NMDA receptor‐dependent and independent LTPs. Although induction of NMDA receptor‐independent LTP did not occlude later induction of NMDA receptor‐dependent LTP, induction of NMDA receptordependent LTP did occlude NMDA receptor‐independent LTP. While the kinase inhibitor experiment showed a clear difference between NMDA receptor‐dependent and independent LTPs, the occlusion experiments suggest an interaction between the signalling pathways for the two LTPs. © 1995 Wiley‐Liss, Inc.
How can exocytosis account for the actual properties of miniature synaptic signals?
Authors: Vautrin Jean , Barker Jeffery L. 
Published: December 2004

AbstractIt is broadly accepted that a postsynaptic “miniature” is the most elementary chemically transmitted signal and results from the all‐or‐none release of transmitter packaged in a single presynaptic vesicle. Hitherto, it has not been possible to directly verify this renowned representation, although it is consistent with evidence of vesicle traffic and, following an intense period of release, vesicle depletion. However, vesicle traffic involving molecular components similar to those implicated in transmitter release has been attributed to other functions including membrane repair. Furthermore, as a number of investigators have recently proposed, miniature signals recorded at peripheral and central synapses may actually reflect several rather than a single discharge of transmitter. It is not clear whether such putative multiple‐discharge miniatures represent near‐synchronous exocytoses of several vesicles or a burst of openings in a pore that couples a vesicle with the outer membrane. In any case, despite the popularity of the vesicular hypothesis, the molecular mechanism involved in synchronizing fast elementary secretion has not yet been elucidated. Interdependencies among subminiature discharges composing a miniature have suggested that the underlying process is a regenerative signal restricted to a presynaptic terminal unit, confirming Fatt and Katz's first speculation on miniatures, which was not vesicular exocytosis [Fatt and Katz (1952), J. Physiol., 117:109–128]. Here we discuss the possibility that this regenerative signal might be a localized cytosolic Ca2+ transient and attempt to reconcile this hypothesis with the exocytotic models proposed to explain fast transmitter release. © 1995 Wiley‐Liss, Inc.
Neuropeptide Y and dynorphin‐immunoreactive large dense‐core vesicles are strategically localized for presynaptic modulation in the hippocampal formation and substantia nigra
Authors: Pickel Virginia M. , Chan June , Veznedaroglu Erol , Milner Teresa A. 
Published: December 2004

AbstractNeuropeptide Y (NPY) and dynorphin elicit regionally selective presynaptic modulation in the hippocampal formation and the pars reticulata of the substantia nigra, respectively. We examined potential anatomical substrates for their presynaptic modulation by determining the distribution and size of large (80–120 nm) dense‐core vesicles (DCVs), organelles previously shown to be immunoreactive for each peptide. Throughout the hippocampal formation, NPY‐immunoreactive DCVs were located primarily in axon terminals and were more sparingly distributed in dendrites. In comparison with other portions of the hippocampal formation, NPY‐labeled DCVs were most abundant in axons and terminals of the CA1 region. The DCVs in the CA1 region of the hippocampus also more frequently had larger mean cross‐sectional diameters when located along portions of the terminal in contact with unlabeled axons. In both the CA1 region of the hippocampus and the dentate gyrus, NPY‐labeled DCVs in contact with portions of the axonal membrane apposed to astrocytes also were larger than those located more centrally in the axon terminal. Dynorphin‐immunoreactive DCVs in axon terminals 'of the substantia nigra were significantly larger when found near portions of the axonal membrane in contact not only with other axons and astrocytic processes, but also occasionally with postsynaptic dendrites. The parallels between diameters of DCVs and known selectivity of NPY for presynaptic modulation in the CA1 region of the hippocampus suggest a direct correlation between the size and distribution of immunoreactive DCVs and their sites of exocytotic release. By analogy, we can conclude that dynorphin in the pars reticulata of the substantia nigra is also principally a presynaptic modulator, but may additionally elicit functional changes through interactions with receptive sites on astrocytes or postsynaptic neurons. © 1995 Wiley‐Liss, Inc.
Pet imaging studies of dopamine D2 receptors: Comparison of [18F]N‐Methylspiperone; and the benzamide analogues [18F]MABN and [18F]MBP in baboon brain
Authors: Mach Robert H. , Ehrenkaufer Richard L. E. , Greenberg Joel H. , Shao Lingxiong , Morton Thomas E. , Evora Paul H. , Nowak Peggy A. , Luedtke Robert R. , Cohen David , Reivich Martin 
Published: December 2004

AbstractA series of positron emission tomography (PET) imaging studies was conducted in a baboon with the benzamide derivatives [18F]2,3‐dimethoxy N‐9‐(4‐fluorobenzyl)‐9‐azabicyclo[3.3.1]nonan‐3β‐yl]benzamide ([18F]MABN) and [18F]2,3‐dimethoxy‐N‐[1‐(4‐fluorobenzyl)piperidin‐4‐yl]benzamide ([18F]MBP). Studies were also conducted with the butyrophenone [18F]N‐methylspiperone (NMSP) for comparison. Tissue‐time activity curves of [18F]MABN are similar to those of [18F]NMSP since both compounds displayed approximately the same uptake in the basal ganglia and displayed irreversible binding kinetics in vivo. However, the rapid rate of clearance from the cerebellum and high basal ganglia: cerebellum ratio of [18F]MABN indicate that this compound has a much lower amount of nonspecific binding than [18F]NMSP. [18F]MBP displayed a higher uptake in the basal ganglia relative to [18F]NMSP and [18F]MABN and exhibited reversible binding kinetics in vivo. This property of [18F]MBP is desirable since the uptake of radioactivity in D2‐rich ligands is less likely to be influenced by changes in cerebral blood flow. The current data suggest that both [18F]MABN and [18F]MBP are promising ligands for studying dopamine D2 receptors with PET. © 1995 Wiley‐Liss, Inc.
Long‐lasting inhibition of in vivo cocaine binding to dopamine transporters by 3β‐(4‐Iodophenyl)Tropane‐2‐Carboxylic acid Methyl Ester: RTI‐55 or βCIT
Authors: Volkow N. D. , Gatley S. J. , Fowler J. S. , Chen R. , Logan J. , Dewey S. L. , Ding Y.‐S. , Pappas N. , King P. , Gregor R. R. Mac , Kuhar M. J. , Carroll F. I. , Wolf A. P. 
Published: December 2004

AbstractCocaine analogs such as 3β‐(4‐iodophenyl)tropane‐2β‐carboxylic acid methyl ester (RTI‐55 or βCIT) with a higher affinity for the dopamine transporter (DAT) may be potentially useful in interfering with cocaine's actions in brain. This study evaluates the time course of the effects of RTI‐55 on cocaine binding in baboon brain using PET and [11C]cocaine. [11C]Cocaine binding was measured prior to, and 90 minutes, 24 hours, 4–5 days and 11–13 days after RTI‐55 (0.3 mg/kg i.v.). Parallel studies with [3H]cocaine and RTI‐55 (0.5 mg/kg i.v. or 2 mg/kg i.p.) were performed in the mouse. RTI‐55 significalitly inhibited [11C]cocaine binding at 90 minutes and 24 hours after administration.The half‐life for the clearance of RTI‐55 from the DAT was estimated to be 2 to 3 days in the baboon brain. In the mouse brain, RTI‐55 significantly inhibited [3H]cocaine binding at 60 and 180 minutes after administration and recovery was observed at 12 hours. These results document long‐lasting inhibition of cocaine binding by RTI‐55 and corroborate that binding kinetics of RTI‐55 in striatum observed in imaging studies with [123I]RTI‐55 represents binding to DATs. © 1995 Wiley‐Liss, Inc.
Brain transcription factor gene expression, neurotransmitter levels, and novelty response behaviors: Alterations during rat amphetamine withdrawal and following chronic injection stress
Authors: Persico Antonio M. , Schindler Charles W. , Zaczek Robert , Brannock Michael T. , Uhl George R. 
Published: December 2004

AbstractTranscription factors are known to act as gene expression regulators, possibly linking extracellular stimuli to long‐term modifications at the neuronal level. Such modifications may potentially ‐underlie chronic psychostimulant‐ and stress‐induced behavioral alterations. This study illustrates how a 2 week, twice daily 7.5 mg/kg d‐amphetamine or saline regimen alters rat brain regional expression of transcription factor genes, including c fos, fos‐B, jun‐B, c jun, and zif268, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.Amphetamine withdrawal‐induced decreases in transcription factor mRNA levels, assessed using Northern blot analysis, appear most prominent in prefrontal cortex, begin approximately 12 h after the last injection, and largely recover to control levels by 54 h. Prefrontal cortical and striatal dopamine content, assessed using HPLC, decrease and recover over a similar time course. Behavioral “stereotypy time” manifest by animals exposed to a novel environment, a measure sensitive to psychostimulant withdrawal, also decreases beginning 12 h after the last injection, is still significantly reduced at 54 h, and recovers at 72 h.Chronic saline injections are followed by a consistent decrease in transcription factor gene expression, observed 6 h after the last injection, followed by a “rebound” increase at 12 h. These changes are accompanied by dramatic, mostly biphasic alterations in prefrontal cortical biogenic amines and by a short‐lived increase in striatal dopamine turnover. At the same time, rats display much longer‐lasting decreases in locomotor responses when exposed to a novel environment, with recovery occurring only 54 h after the last injection.The delayed recovery of behavioral responses to novelty is consistent with potential involvement of changes in transcription factor‐mediated gene expression in neurochem‐ ical mechanisms underlying psychostimulant withdrawal and chronic injection stress‐ induced behavioral alterations. © 1995 Wiley‐Liss, Inc.
Biological mechanisms and perinatal exposure to abused drugs
Authors: Thadani Pushpa V. 
Published: December 2004

AbstractUse of illicit and licit drugs during pregnancy is a major public health concern, as it can have adverse effects on the developing fetus. Infants born of women addicted to narcotics, cocaine, alcohol, or polydrugs often undergo a characteristic withdrawal syndrome and may have physical, behavioral, and/or neurological abnormalities. As it is not feasible to ascertain whether these functional changes in human infants are produced by abused substance(s) per se or by a combination of complex socioeconomic factors and polydrug use, researchers in recent years have developed and utilized various innovative animal models to assess drug‐induced alterations and their biological mechanisms during the developmental period under a controlled environment. To promote interdisciplinary communications as well as to assess the progress and the future needs in this area, the National Institute on Drug Abuse (NIDA) held a technical review at which biomedical researchers discussed their current findings in various physiological systems. This report summarizes the major findings and the methodological and experimental issues discussed at the conference. The meeting was held in Washington, DC, on May 25 and 26, 1994. © 1995 Wiley‐Liss, Inc.
Modulation of dopamine D1‐mediated turning behavior and striatal c‐fos expression by the substantia nigra
Authors: Fenu S. , Carta A. , Morelli M. 
Published: December 2004

AbstractIn order to study the possible contribution of the substantia nigra (SN) in the positive interaction between dopamine D1 receptor agonists and glutamate antagonists in unilaterally 6‐hydroxydopamine (6‐OHDA) lesioned rats, the effect of the D1 agonist, SKF 38393, was studied in combination with intranigral infusions of glutamate antagonists of the NMDA (MK 801, CPP) or AMPA (NBQX) type of receptor. Local infusion into the SN of the 6‐OHDA lesioned side of MK 801, CPP or NBQX at doses inducing no or minimal behavioral effects significantly increased the turning behavior and the expression of c‐fos induced, in the lesioned caudate‐putamen (CPu), by a parenteral administration of SKF 38393. The same result was obtained after intra‐SN infusion of the GABA agonist, muscimol. High doses of MK 801, CPP or muscimol infused into the SN produced intense contralateral turning per se and induced a sparse c‐fos expression in the lesioned CPu which was antagonized by parenteral administration of MK 801. The results indicate that a depression of SN pars reticulata efferent neurons potentiates D1‐mediated responses and suggest that this area may play a role in the positive interaction between glutamate antagonists and D1 receptor agonists. © 1995 Wiley‐Liss, Inc.
Effects of the σ receptor ligand SR 31742A on neurotensin biosynthesis in rat basal ganglia
Authors: Labie Christophe , Saubusse Patricia , Keane Peter E. , Fur Gérard Le , Soubrié Philippe 
Published: December 2004

AbstractThe effects of SR 31742A, a specific σ ligand, were investigated on neurotensin (NT) biosynthesis in the basal ganglia of the rat. Both single and repeated treatments with either SR 31742A (20 mg/kg i.p.) or haloperidol (1 mg/kg i.p.) increased the concentration of NT‐like immunoreactivity (NT‐1i) in the nucleus accumbens. In contrast to haloperidol, the administration of SR 31742A failed to increase the concentration of NT‐li in the caudate‐putamen. We have further investigated drug‐induced variations in NT biosynthesis by studying NT/neuromedin N (NT/NN) mRNA levels in the nucleus accumbens and the ventral tegmental area of the rat following SR 31742A administration. The NT/NN mRNA levels in the ventral tegmental area were increased by a maximum of fifteen fold (7 h at 20 mg/kg i.p.). A lower increase in NTINN mRNA levels was elicited in the nucleus accumbens. These results suggest that the increase in NT‐li observed after SR 31742A treatment, like that produced by haloperidol, may result from an increase of NT biosynthesis. Furthermore, the effects of SR 31742A on NT metabolism are similar to those of atypical antipsychotics, since they appear to be selective for the limbic system. © 1995 Wiley‐Lies, Inc.
Synaptic reorganisation in the rat striatum after dopaminergic deafferentation: An ultrastructural study using glutamate decarboxylase immunocytochemistry
Authors: Nitsch Cordula , Riesenberg Rainer 
Published: December 2004

AbstractThe ultrastructure of GABAergic and non‐GABAergic synapses in the adult rat neostriatum was examined 6‐8 months after unilateral removal of the nigrostriatal dopaminergic pathway by 6‐hydroxydopamine injection into the medial forebrain bundle. GABAergic profiles were identified by preembedding glutamate decarboxylase (GAD) immunocytochemistry performed on parasagittal vibratome sections. In three representative fields of the striatum, the nature and number of boutons and their postsynaptic partners were determined and the differences between the striata ipsi‐ and contralateral to the lesion analyzed. The percentage of GAD‐immunoreactive boutons was increased from 23% on the intact side to 28% on the lesioned side. In addition, the GABAergic boutons underwent significantly more multiple contacts with several independent postsynaptic profiles, preferentially with dendritic spines. This could reflect a lesion‐induced sprouting of local GABAergic axon terminals. On the other hand, although the vast majority of GABAergic boutons underwent synaptic contacts with dendrites (77% vs. 80%), the number of boutons per dendrite or per dendritic circumference remained unchanged. Thus, the higher frequency of GABAergic boutons may simply reflect the loss of the dopaminergic nerve endings, without a heterosynaptic replacement by GABAergic boutons. The deafferentation also induced structural changes of the postsynaptic profiles. Some dendritic spines had a shortened neck; others were completely integrated in the dendrite which now contained a spine apparatus and was contacted by boutons with the features of axospinous synapses. The spine retraction resulted in a quantitative decrease in the number of spines. Analysis of the synaptic curvature revealed that only spines with a flat contact zone were lost. Concurrently, the number of dendrites was increased, of the GAD‐containing in particular, suggesting that the denrites of GABAergic interzeurons tend to elongate and/or arborize. Taken together, the results of the present study show that the dopaminergic denervation caused a remodeling of the postsynaptic neurons. The relative increase of the number of GABAergic boutons and their synaptic contacts suggests that an altered wiring of the intrinsic GABAergic system contributes to the changes in the striatal output activity. © 1995 Wiley‐Liss, Inc.
Chronic corticosterone treatment maintains synaptic activity of CA1 hippocampal pyramidal cells: Acute high corticosterone administration increases action potential number
Authors: Birnstiel Susanne , List Troy J. , Beck Sheryl G. 
Published: December 2004

AbstractThe hypothalamic‐pituitary‐adrenocortical (HPA) axis controls the levels of plasma corticosterone (CT) in the rat and the levels of cortisol in man. CT is important in maintaining homeostasis and regulating energy production. Homeostasis is maintained by basal activation of the hippocampal‐HPA axis. In response to stress CT secretion is increased. CT activation of receptors in the hippocampus provides feedback inhibition of the HPA axis to return the system to basal activity. There are two types of CT receptors: the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). CT has a 10‐fold higher affinity for MR than GR. Normal basal levels of CT occupy the majority of the MR. During the diurnal surge of CT and following the presentation of a stressful stimulus, the MR and GR are both maximally occupied. To begin to understand how CT influences the hippocampal‐HPA axis, intracellular recording techniques in the hippocampal brain slice preparation were used to determine how high concentrations of CT may alter cell characteristics and/or evoked synaptic activity. Two treatment groups were used, i.e., adrenalectomized (ADX) and ADX with CT pellet replacement (ADX + CT) that produced plasma blood levels equal to that seen in a normal rat in the morning. Acute administration of 100 nM CT decreased action potential threshold and the number of action potentials elicited by a depolarizing current pulse in cells from both the ADX and ADX + CT treated rats. The amplitude of the evoked excitatory postsynaptic potentials (EPSP) or inhibitory postsynaptic potentials (IPSP) declined in cells recorded from ADX animals and ADX rats acutely treated with high concentrations of CT (ADWCT). The EPSPs and IPSPs were stable in cells from ADX + CT rats exposed to high CT concentrations. We conclude from these data that chronic CT treatment is necessary to maintain EPSP and IPSP amplitude. Also, acute administration of a high concentration of CT alters the output of the CA1 hippocampal pyramidal cells by increasing the number of action potentials elicited by a depolarizing current pulse but does not alter the amplitude of subthreshold EPSPs and IPSPs. © 1995 Wiley‐Liss, Inc.
Neonatal excitotoxic ventral hippocampal damage alters dopamine response to mild repeated stress and to chronic haloperidol
Authors: Lipska Barbara K. , Chrapusta Stanislaw J. , Egan Michael F. , Weinberger Daniel R. 
Published: December 2004

AbstractThe effects of neonatal excitotoxic ventral hippocampus (VH)lesions on dopamine release in response to repeated stress (saline injections) and to chronic haloperidol treatment were investigated in Sprague‐Dawley rats infused with ibotenic acid or vehicle into the VH on day 7 of postnatal life (PD7). Beginning on PD35, lesioned and sham‐operated rats were injected i.p. with saline (INJ) once daily for 3 weeks or were not treated (NO INJ). Another cohort of rats was given haloperidol (HAL, 0.4 mg/kg, i.p.) or vehicle beginning on PD35 and thereafter once daily for 3 weeks. 3‐Methoxytyramine (3‐MT) was measured by combined gas chromatography/mass spectrometry in the frontal cortex (FC), nucleus accumbens (NAcc), and striatum (STR) at PD56 following MA0 inhibition with pargyline. At baseline (NO INJ), 3‐MT was reduced in STR of lesioned rats. Repeated saline injections resulted in a further 3‐MT reduction in STR, FC, and NAcc of lesioned animals, but had no effect in sham rats. Chronic HAL, compared with vehicle, suppressed locomotor activity, and increased 3‐MT accumulation in the FC, NAcc, and STR in sham and lesioned rats. This increase was enhanced in the FC of lesioned rats. These data show that mild repeated stress attenuates dopamine release in FC, NAcc, and STR of lesioned rats, while chronic HAL augments it in FC of lesioned animals versus controls. We conclude that the neonatal excitotoxic lesion of VH alters the functioning of midbrain dopamine systems during environmental and pharmacological challenge. © 1995 Wiley‐Liss, Inc.