bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of the effects of the cholecystokinin‐B receptor antagonist, PD 134308, and the cholecystokinin‐A receptor antagonist, L‐364,718, on dopamine neuronal activity in the substantia nigra and ventral tegmental area
Authors: Meltzer Leonard T. , Christoffersen Curt L. , Serpa Kevin A. , Razmpour Ahmad 
Published: December 2004

AbstractExtracellular single‐unit recording techniques were used to study the effects of the cholecystokinin‐A (CCK‐A) antagonist, L‐364, 718, and the CCK‐B antagonist, PD 134308, on DA neuronal activity in chloral hydrate anesthetized rats. Neither L‐364, 718 (0.1‐1.6 mg/kg i.v.) nor PD 134308 (0.1‐6.4 mg/kg) altered the basal firing rate of substantia nigra or ventral tegmental area DA neurons. The ability of PD 134308 and L‐364, 718 to alter the apomorphine‐induced inhibition of substantia nigra DA neurons was assessed. Pretreatment with L‐364, 718 (0.6 or 4.16 mg/kg i.v.) did not shift the apomorphine dose‐response curve (0.5‐32 μg/kg i.v.). In contrast, PD 134308 (0.6 or 6.4 mg/kg i.v.) produced dose‐related, significant shifts to the right of the apomorphine dose‐response curve. However, these effects were small in comparison to the haloperidol (0.1 mg/kg i.p.)‐induced shift of the apomorphine curve. These data suggest that in the substantia nigra there may be a tonic level of CCK release that, through actions on CCK‐B receptors, may modulate DA agonist‐induced inhibition of DA neuronal activity. © 1993 Wiley‐Liss, Inc.
Cytoplasmic structure in organotypic cultures of rat hippocampus prepared by rapid freezing and freeze‐substitution fixation
Authors: Miller Lucas D. Pozzo , Landis Dennis M. D. 
Published: December 2004

AbstractWe have compared rapid freezing followed by freeze‐substitution fixation with conventional aldehyde fixation as preparative methods for the electron microscopic study of organotypic cultures of neonatal rat hippocampus. Rapid freezing by contact with a copper block chilled by liquid helium was accomplished without mechanical distortion of superficial structures, and preserved structure to a depth of at least 20 μM without visible ice crystals. Freeze‐substitution fixation in acetone/osmium tetroxide, followed by en bloc staining with tannic acid and uranyl acetate, provided satisfactory staining of cytoplasm and organelles. While both preparative techniques yielded generally satisfactory results, rapid freezing provided much better preservation of astrocytic lysosomal inclusions, and afforded new views of intermediate filament substructure. Rapid freezing and freeze‐substitution fixation seemed especially well suited to the preservation of short filamentous proteins, such as those forming the membrane cytoskeleton of dendritic spines or those associated with synaptic vesicles. The combination of rapid freezing methods and organotypic culture provides an opportunity to examine cytoplasmic structure in tissue from deep regions of the brain which had previously been inaccessible to rapid freezing techniques. © 1993 Wiley‐Liss, Inc.
Quantitative autoradiographic mapping of delta‐opioid receptors in the rat central nervous system using [125I][D.Ala2]deltorphin‐I
Authors: Gouarderes Christine , Tellez Stephane , Tafani Jean André M. , Zajac Jean‐Marie 
Published: December 2004

AbstractThe distribution of β‐opioid binding sites was studied by quantitative autoradiography in rat brain and spinal cord using the highly selective ligand [125I][D. Ala2]deltorphin‐I. The binding properties of [125I][D. Ala2]deltorphin‐I were investigated by microdensitometry of autoradiographic films with the aid of a computerassisted image‐analysis system. [125I][D. Ala2]deltorphin‐I appeared to interact with a single class of sites in all brain areas (KD = 0.9 nM). In 23 regions tested, whatever the δ site concentration, DTLET, a δ agonist, appears to be 2 orders of magnitude more effective than DAGO, a μ agonist, in inhibiting specific [125I][D. Ala2]deltorphin‐I binding. The distribution of [125I][D. Ala2]deltorphin‐I sites is globally consistent with that of other δ ligands and does not support the existence of a δ‐receptor subtype recognized by [D. Ala2]deltorphin‐I. [125I][D. Ala2]deltorphin‐I binding sites were highly confined, exhibiting selective localization in the neocortex and a diffuse pattern in the striatum, accumbens nucleus, claustrum, layer of bulb, amygdaloid nucleus, pontine nuclei, and inferior colliculus. In several areas a rostro‐caudal gradient of site concentration was indicated. [D. Ala2]deltorphin‐I binding sites were also present in the substantia gelatinosa at all levels of the spinal cord and, unexpectedly, in deeper laminae and the ventral horn. These results demonstrate the ability of [125I][D. Ala2]deltorphin‐I to characterize low concentrations of binding sites and to reveal new localizations of δ receptors. © 1993 Wiley‐Liss, Inc.
Local cerebral glucose utilization after D1 receptor stimulation in 6‐OHDA lesioned rats: Effect of sensitization (priming) with a dopaminergic agonist
Authors: Morelli Micaela , Pontieri Francesco E. , Linfante Italo , Orzi Francesco , Di Chiara Gaetano 
Published: December 2004

AbstractIn rats bearing unilateral 6‐hydroxydopamine (6‐OHDA) lesions of the dopaminergic nigro‐striatal neurons, a single administration of a D‐2 agonist (LY 17155) potentiates the contralateral turning induced by a D‐1 agonist (SKF 38393). To identify the neural substrate of this form of sensitization (priming), we studied the local cerebral glucose utilization (lCMRglc) in 6‐OHDA lesioned animals treated, 3 days apart, as follows: (1) saline‐saline, (2) LY 171555‐saline, (3) saline‐SKF 38393 and (4) LY 171555‐SKF 38393. The unilateral 6‐OHDA lesion per se (Sal‐Sal) produced increases in lCMRglc in the globus pallidus (GP) and in the lateral habenula (LH) of the lesioned hemisphere. lCMRglc in LY‐Sal group were similar to those measured in the Sal‐Sal group. Administration of SKF 38393 to drug‐naïve rats (Sal‐SKF) abolished the lesion‐induced metabolic asymmetry in the LH but did not have any effect on the GP; furthermore, it increased lCMRglc in the substantia nigra pars reticulata (SNr) of the lesioned side. After priming with LY 171555, administration of SKF 38393 (LY‐SKF) produced marked metabolic asymmetries by increasing lCMRglc in the SNr and entopeduncular nucleus (EP), and decreasing it in the LH of the lesioned side. These changes were also significant when compared to the corresponding values of the other experimental groups. Again, in LY‐SKF group no modification of the lesion‐induced metabolic asymmetry in the GP was found. These results indicate that priming exerts a facilitatory influence on the ability of D‐1 receptors to stimulate the striato‐nigral and striato‐entopeduncular pathway, suggesting that changes in the effectiveness of dopamine in activating its postsynaptic target elements might contribute to the mechanism of sensitization to drugs stimulating dopaminergic transmission. © 1993 Wiley‐Liss, Inc.
Electrophysiological characterization of rat striatal neurons in vitro following a unilateral lesion of dopamine cells
Authors: Twery M. J. , Thompson L. A. , Walters J. R. 
Published: December 2004

AbstractThe effects of a unilateral 6 to 19‐week lesion of dopamine cells on the excitability of rat striatal neurons were investigated in vitro using the intracellularly recorded membrane properties of neurons obtained ipsilateral and contralateral to 6‐hydroxydopamine (6‐OHDA) injection sites. Neurons ipsilateral to the lesion site and in striatal tissue depleted of dopamine exhibited resting membrane potentials and membrane resistances similar to those recorded in contralateral striatal neurons. Denervation appeared to have no appreciable effect on the proportion of neurons exhibiting various patterns of neuronal spiking (repetitive, bursting, or single spike) evoked by depolarizing current pulses. Current‐voltage determinations revealed nominal rectification in the majority of neurons and marked nonlinearty consistent with inward rectification at potentials hyperpolarized and depolarized to rest in a large proportion of the remaining neurons. Neurons ipsilateral to 6‐OHDA lesion sites exhibited these relationships in the same proportion as contralateral control cells. However, ipsilateral neurons with nominal rectification exhibited an average rate constant for the early onset of small hyperpolarizing membrane transients which was significantly smaller than that of controls. This finding suggests that intrinsic membrane parameters regulating the excitability of certain striatal neurons may be under the influence of dopamine or other factors closely associated with nigrostriatal nerve terminals. Published 1993 Wiley‐Liss, Inc.
Expression of c‐fos protein in the experimental epilepsy induced by pilocarpine
Authors: Barone Paolo , Morelli Micaela , Cicarelli Giulio , Cozzolino Alberto , DeJoanna Gabriella , Campanella Giuseppe , DiChiara Gaetano 
Published: December 2004

AbstractThe expression of the c‐fos proto‐oncogene, as estimated by immunohistochemistry of the FOS nuclear protein, was studied in both focal and generalized seizures induced in rats by systemic administration of pilocarpine. Focal seizures, as indicated by the occurrence of stereotyped oral movements, chewing and sniffing, were evoked by either a subconvulsant dose of pilocarpine (200 mg/kg) or the association of a convulsant dose of pilocarpine (400 mg/kg) with SCH 23390, a selective D‐1 dopamine receptor antagonist. This seizure pattern resulted in FOS accumulation in certain limbic areas, namely, the piriform cortex, amygdala, and olfactory tubercle. On the other hand, in rats developing generalized seizures, accumulation of FOS was also found in hippocampus, cingulate cortex, frontal cortex, striatum, accumbens, as well as in certain thalamic nuclei. Generalized seizures, including motor limbic seizures and status epilepticus, were induced by either a convulsant dose of pilocarpine (400 mg/kg) or a low dose of pilocarpine (15–200 mg/kg) combined with either lithium or the D‐1 selective agonist SKF 38393. These findings indicate a close correlation between the sequence of behavioural alterations induced by pilocarpine and the proto‐oncogene activation. The results provide the basis for mapping the areas of origin and the pathways of generalization of seizure activity. As shown by the effects of dopamine receptor agonists and antagonists, the process of generalization appears to be controlled by the dopamine system. © Wiley‐Liss, Inc.
Robustness of G protein changes in cocaine sensitization shown with immunoblotting
Authors: Striplin Caryn D. , Kalivas Peter W. 
Published: December 2004

AbstractDaily cocaine administration has been shown to alter G proteins in mesolimbic nuclei, and these changes have been implicated in the initiation and expression of behavioral sensitization. To evaluate the robustness of changes in G proteins induced by daily cocaine treatments capable of producing behavioral sensitization, the levels of Gi1α, Gi2α, Goα, Gsα, and Gβ protein were measured by immunoblotting at 1 hr after an acute injection of cocaine or saline given 1 or 14 days following the last injection of daily cocaine or saline. A significant decline in Gi1α was seen in the nucleus accumbens at 14 days following daily cocaine administration regardless of whether they received an acute challenge with cocaine or saline 1 hr prior to decapitation. No alterations were observed in the ventral tegmental area, substantia nigra, dorsolateral striatum, or prefrontal cortex in the levels of Gi1α, Gi2α, or Goα. No change in G protein immunoreactivity was measured in the nucleus accumbens or ventral tegmental area of rats decapitated 1 hr after discontinuing daily cocaine. The possibility that a long‐term change in Gi1α in the nucleus accumbens may be related to cocaine‐induced behavioral sensitization is discussed. © Wiley‐Liss, Inc.
Endogenous GABA release from rat striatal slices: Effects of the GABAB receptor antagonist 2‐hydroxy‐saclofen
Authors: Mayfield R. Dayne , Zahniser Nancy R. 
Published: December 2004

AbstractThe reproducibility of endogenous GABA release evoked by multiple periods of electrical field stimulation was examined in rat striatal slices. In these experiments, NO‐328 was used to block GABA uptake, and evoked GABA release (overflow) was completely Ca2+ dependent. A seemingly invariant observation in these experiments was that spontaneous GABA release (outflow) progressively decreased as a function of superfusion time and that GABA overflow decreased 25–30% in response to the second of two periods of stimulation (S2/S1 ratios = 0.70 to 0.75). The attenuation of GABA release was not explained by the amount of GABA lost to the superfusion buffer (fractional release), direct depletion of releasable pools of GABA, or slice viability. Furthermore, the decreases in GABA release were not dependent on stimulation frequency (5–15 Hz) or the absolute amount of GABA evoked by electrical stimulation. However, the GABAB receptor antagonist 2‐hydroxy‐saclofen (2‐OH‐saclofen; 316 μM) not only enhanced GABA overflow, when superfused throughout both periods of stimulation, but also resulted in S2/S1 ratios of unity. When 2‐OH‐saclofen was superfused throughout the second stimulation period only, GABA overflow was almost two‐fold greater than that evoked by the initial period of stimulation (2‐OH‐saclofen‐free). In addition, these S2 responses were ∼30% greater than S1 responses that were observed when 2‐OH‐saclofen was present throughout the entire superfusion period. These results indicate that activation of GABAB receptors was involved in the progressive attenuation of GABA release and further emphasize that GABAB receptors play an important role in modulating endogenous GABA release from striatal slices. © Wiley‐Liss, Inc.
Autoradiographic distribution of [3H]neurotensin receptors in the brains of superoxide dismutase transgenic mice
Authors: Cadet Jean Lud , Kujirai Kayoko , Carlson Elaine , Epstein Charles J. 
Published: December 2004

AbstractSuperoxide dismutase (SOD) plays an important role in the protection of cells against the deleterious effects of free radicals by dismutating the toxic superoxide anion radical. Although oxygen‐based radicals have been implicated in the process of aging and in neurodegenerative disorders such as Parkinson's disease, the contribution of these free radicals to the pathology of these entities has yet to be clarified. It is also not certain that increased levels of free radical scavenging enzymes would attenuate the molecular and cellular processes that lead to these pathological states. In order to asses the contribution of increased SOD gene dosage to the pathogenesis of Down's syndrome, transgenic mice have been constructed that overexpress the human CuZnSOD. We are also using this model to evaluate the role of free radicals in age‐associated changes in brain neurotransmitters and their receptors. In the present study, transgenic mice and their nontransgenic littermates, aged 6 weeks and 21 months, were used in an autoradiographic receptor study of the distribution of brain neurotensin receptors. At 6 weeks of age, there were no significant differences between the two groups of mice in most brain regions. In addition, [3H]NT binding sites showed parallel age‐related decreases in the majority of the areas examined in both groups. However, significant age‐related decreases in the septum, the diagonal band of Broca, and in some subdivisions of the caudate‐putamen were observed only in SOD‐Tg mice. In contrast, significant age‐related decreases in the core area of the nucleus accumbens and the dorsal aspect of the dentate gyrus of the hippocampus were seen only in non‐Tg mice. Interestingly, there were increases in NT binding sites in the CA2 area of the hippocampus in both groups of mice. These results suggest that oxygen‐based radicals might play a role in the biochemical changes that occur in NT receptors during the process of aging since these receptors were differentially affected in some regions of the brains of SOD‐Tg mice and of their littermates, which contrast in their ability to scavenge the superoxide radical. Published 1993 Wiley‐Liss, Inc.
Discrete expression of Ca2+/calmodulin‐sensitive and Ca2+ ‐insensitive adenylyl cyclases in the rat brain
Authors: Mons Nicole , Yoshimura Masami , Cooper Dermot M. F. 
Published: December 2004

AbstractPhysiological studies and inferences from invertebrate models implicate Ca2+/calmodulin‐sensitive adenylyl cyclase with memory processes. However, Ca2+/calmodulin‐insensitive adenylyl cyclase also occurs in brain, and its neuronal functions are less clear. Two oligonucleotide probes, based on rat cDNAs for Types I and II adenylyl cyclase, which appear to correspond to these functional forms, were used to conduct in situ hybridization analysis of the relative abundance and localization of these two species in the rat brain as a first step in evaluating their neuronal role. Quite discrete patterns of expression were encountered; in some areas, both species were co‐expressed, but in others, little overlap was observed. The differential expression of the two mRNAs suggests that discrete roles may be fulfilled by the two adenylyl cyclases in neural tissues. © Wiley‐Liss, Inc.
Drug‐ and behavior‐associated changes in dopamine‐related electrochemical signals during intravenous heroin self‐administration in rats
Authors: Kiyatkin Eugene A. , Wise Roy A. , Gratton Alain 
Published: December 2004

AbstractHigh‐speed chronoamperometry was used to monitor dopamine‐related electrochemical signals in the nucleus accumbens of rats allowed to self‐administer heroin intravenously and rats that received similar injections passively. Rats self‐administered 100 μg/kg of heroin at ∼20‐min intervals. Dopamine‐related electrochemical signals increased monotonically after the first injection of each day; the effect was weaker on the first than on the second and subsequent days. The second and subsequent injections in each session caused biphasic effects: the initial effect was a decrease in signal‐a minor one when compared to the increase caused by the first injection‐and this was followed by an increase that brought the signal back to or somewhat higher than the level at the time of the injection. Over the course of each 4‐h session, the electrochemical signal reached and fluctuated around an elevated plateau; doubling the injection dose did not elevate this plateau but did cause larger phasic decreases and subsequent increases. Qualitatively similar electrochemical changes were seen in the animals passively receiving the drug, but there were two notable quantitative differences. First, in the passive animals the initial depressions in signal were of shorter duration. Second, in the passive animals (which were injected at intervals determined by the self‐administering animals) the electrochemical signal reached a maximum and began to fall prior to the time of the next injection; in the animals that self‐administered the drug, the signal was still rising at the time of the next injection. The changes in electrochemical signal are unlikely to represent fluctuations of ascorbate or dopamine metabolites; thus it appears that whereas self‐administered heroin injections cause a slow and long‐lasting elevation of extracellular dopamine concentration, short‐term increases in dopamine concentration are associated with the behavioral activation that precedes the injections and it is short‐term decreases that appear to be associated with the period usually thought to be most significant for positive reinforcement. © 1993 Wiley‐Liss, Inc.
Kinetic and pharmacological examination of stimulation‐induced increases in synaptic efficacy in the chick ciliary ganglion
Authors: Poage Robert E. , Zengel Janet E. 
Published: December 2004

AbstractWe have characterized the kinetic and pharmacological properties of stimulation‐induced increases of synaptic efficacy in the embryonic chick ciliary ganglion. We found what appear to be four components of increased ganglionic efficacy with average time constants of decay of about 60 msec, 400 msec, 30 sec, and 200 sec. These time constants are similar to the those describing the decay of the four components of stimulation‐induced increases in neurotransmitter release characterized at other synapses. These components have been termed first and second components of facilitation, augmentation, and potentiation. We found that the addition of small amounts of Ba2+ to the low Ca2+ bathing solution led to an increase in the magnitude of the augmentation‐like component, whereas Sr2+ enhanced the magnitude and time course of the component resembling the second component of facilitation. These effects of Ba2+ and Sr2+ are similar to the effects of these same divalent cations on augmentation and the second component of facilitation, respectively, at the frog neuromuscular junction and rabbit superior cervical ganglion. Based on these similar kinetic and pharmacological properties, we conclude that the four components of stimulation‐induced increases in release that have been described in other synaptic preparations also appear to be present in the chick ciliary ganglion. Published 1993 Wiley‐Liss, Inc.
Septal efferent axon terminals identified by anterograde degeneration show multiple sites for modulation of neuropeptide Y‐containing neurons in the rat dentate gyrus
Authors: Milner Teresa A. , Veznedaroglu Erol 
Published: December 2004

AbstractThe ultrastructure and cellular associations of septal efferent terminals identified by anterograde degeneration with neurons containing neuropeptide Y (NPY) in the rat dentate gyrus were examined quantitatively. For this, the septal complex (i. e., medial septal and diagonal band nuclei) of adult male rats was injected with the neurotoxin ibotenic acid (1%; 150 nl) and following a 2–4‐day survival period, the hippocampal formation was processed for the electron microscopic immunocytochemical demonstration of NPY using the avidin‐biotin complex method.Terminals with the morphological characteristics of anterograde degeneration, in particular an increase in osmiophilia, and neurons containing NPY‐like immunoreactivity (NPY‐LI) were most abundant in the hilus of the dentate gyrus. In this region, degenerating terminals (n = 109) were usually small (0.2–0.4 μm in diameter) and formed both asymmetric and symmetric synapses with small (distal) dendrites. The degenerating terminals contacted either single NPY‐containing (19%) perikarya or dendrites or unlabeled (48%) perikarya or dendrites. Some degenerating terminals contacted the same perikarya or dendrites as an NPY‐containing terminal (11%); these neurons were either immunoreactive for NPY or unlabeled. The remaining degenerating terminals were either directly apposed without glial intervention to unlabeled and NPY‐labeled terminals (11%) or lacked associations with any neuronal processes in the plane of section analyzed (11%). The findings demonstrate that ibotenic acid injections in the septal complex can identify septal efferent terminals by degeneration and provide cellular substrates for the direct synaptic regulation as well as presynaptic modulation of hippocampal NPY‐containing neurons by septal efferent terminals. © 1993 Wiley‐Liss, Inc.