bluuebunny/crossref_metadata_2025_split huggingface dataset:
Calcium‐, calcium/calmodulin‐, and calcium/phospholipid‐stimulated protein phosphorylation in the rat anterior pituitary
Authors: Pryor James C. , Cain Scott T. , Nemeroff Charles B. 
Published: December 2004

AbstractCalcium‐dependent protein phosphorylation may be a critical step in the stimulated secretion of anterior pituitary hormones. We have noted the existence of a number of calcium‐calcium/calmodulin‐, and calcium/phospholipid‐dependent phosphoproteins in the normal rat anterior pituitary. Cell extracts were prepared from anterior pituitary glands of male rats and phosphorylated with [γ32P]ATP in the presence or absence of calcium, calmodulin, and phosphatidylserine. The samples were electrophoresed on SDS‐PAGE gels, autoradiographs prepared, and phosphate incorporation into specific proteins quantitated with microdensitometry. Calcium alone significantly stimulated the phosphorylation of proteins with molecular weights of 80.0‐, 62.0‐, 51.0,‐ 30.5‐, and 25.0‐kDa. The phosphorylation of 21.5‐, 51.0‐, and 80.0‐kDa MW phosphoproteins was found to be phospholipid dependent. The phosphorylation of 62.0‐, 51.0‐, 33.0‐, 30.5‐, and 25.0‐kDa MW phosphoproteins was found to be calcium/calmodulin kinase dependent. Calcium/calmodulin also inhibited phosphorylation of the 80.0‐kDa phosphoprotein. © Wiley‐Liss, Inc.
Long‐Term frontal brain metabolic changes in cocaine abusers
Authors: Volkow Nora D. , Hitzemann Robert , Wang Gene‐Jack , Fowler Joanna S. , Wolf Alfred P. , Dewey Stephen L. , Handlesman Leonard 
Published: December 2004

AbstractNeurological complications from cocaine use are well recognized. We propose that chronic cocaine use can also cause clinically silent brain dysfunction.We investigated brain glucose metabolism with positron emission tomography (PET) and 2‐deoxy‐2[18F] fluoro‐D‐glucose (FDG) in 21 neurologically intact chronic cocaine abusers (C) and 18 normal controls (N). The cocaine abusers were tested 1–6 weeks after the last use of cocaine and seven were retested after a 3 month drug‐free period.Global cerebral glucose metabolism was not significantly different between controls and cocaine abusers (N = 38.4±3, C = 36.5±5 μmol/100 g of tissue, min). However, cocaine abusers had significantly (P< 0.05) lower metabolic activity in 16 of the 21 left frontal regions and 8 of the 21 right frontal regions. These decreases persisted after 3–4 months of detoxification and were correlated with the dose (P ≤ 0.01) and the years of cocaine use (P ≤ 0.05).This study shows reduced rates of frontal metabolism in neurologically intact cocaine abusers that persist even after 3–4 months of detoxification. © Wiley‐Liss, Inc.
Effects of the novel NMDA receptor antagonist, CGP 39551, on field potentials and the induction and expression of LTP in the dentate gyrus in vivo
Authors: Maren Stephen , Baudry Michel , Thompson Richard F. 
Published: December 2004

AbstractThe effects of the novel competitive N‐methyl‐D‐aspartate (NMDA) receptor antagonist, CGP 39551 [the carboxyethylester of CGP 37849; DL‐(E)‐2‐amino‐4‐methy‐5‐phosphono‐3‐pentenoic acid], on extracellular field potentials and long‐term potentiation (LTP) induced in the dentate gyrus by stimulation of the perforant path were studied in anesthetized rats. CGP 39551 attenuated the population spike (PS) and excitatory postsynaptic potential (EPSP) amplitude of dentate field potentials, reduced the NMDA receptor‐mediated component of train‐evoked burst potentials, and prevented the induction of LTP. The decrease in PS and EPSP amplitude produced by CGP 39551 was observed mainly in non‐potentiated synaptic populations; potentiated field potentials were only minimally affected by drug treatment. These results are consistent with the in vivo blockade of NMDA receptors by CGP 39551. They also indicate that NMDA receptors may contribute in a tonic manner to the state of dentate granule cell excitability. Finally, the differential modulation of potentiated and non‐potentiated synapses by CGP 39551 suggests that a change in some properties of postsynaptic AMPA receptors is involved in the expression of LTP. © Wiley‐Liss, Inc.
GABAB receptor‐mediated inhibitory postsynaptic potentials evoked by electrical stimulation and by glutamate stimulation of interneurons in Stratum lacunosum‐moleculare in hippocampal CA1 pyramidal cells in vitro
Authors: Williams Sylvain , Lacaille Jean‐Claude 
Published: December 2004

AbstractFollowing micropressure application of glutamate (500 μM) in stratum lacunosum‐moleculare (L‐M), inhibitory postsynaptic potentials (glut‐IPSPs) were recorded in CA1 pyramidal cells. These glut‐IPSPs were blocked by tetrodotoxin (1 μM) and, thus, were probably generated by the activation of local interneurons. The effects of pharmacological antagonists on glut‐IPSPs and on electrically‐evoked early and late IPSPs were assessed in the same cells during the same application of the antagonist. Local application of the GABAB antagonist 2‐OH saclofen (1–4 mM) reduced both glut‐IPSPs and late IPSPs but not early IPSPs. In contrast, the GABAB antagonist phaclofen (20 mM) reduced late IPSPs but not early IPSPs or glut‐IPSPs. Early IPSPs were blocked by the GABAA antagonists bicuculline and picrotoxin but late IPSPs and glut‐IPSPs were not. Repetitive electrical stimulation depressed early and late IPSPs as well as glut‐IPSPs, suggesting that interneurons activated with glutamate were also stimulated electrically. Thus, interneurons in str. lacunosum‐moleculare appear to inhibit pyramidal cells via a GABAB receptor‐mediated IPSP. The discrepancy in the pharmacological profile of the GABAB glut‐IPSPs and of the GABAB late IPSPs may suggest the presence of two GABAB mechanisms in CA1 pyramidal cells. © 1992 Wiley‐Liss, Inc.
Induction of long‐term potentiation in the basolateral amygdala does not depend on NMDA receptor activation
Authors: Chapman Paul F. , Bellavance Lisa L. 
Published: December 2004

AbstractLong‐term potentiation (LTP) can be induced in the lateral and basolateral amygdala by stimulating synaptic afferents in the external capsule (EC). We examined the sensitivity of amygdaloid LTP to the NMDA receptor antagonist 2‐amino‐5‐phosphonopentanoate (AP5), which is known to block LTP induction in the Schaffer collateral/CA1 synapses in the hippocampus. While relatively high concentrations (100 μM) of DL‐AP5 were effective in preventing LTP induction in the lateral and basolateral amygdala in vitro, the same concentrations also significantly depressed synaptic responses to low‐frequency stimulation. Furthermore, at 50 μM, a concentration sufficient to block both synaptic responses mediated by NMDA receptors and LTP induction in the hippocampus and neocortex, AP5 did not affect the probability of inducing LTP in the amygdala. Application of 10 μM 6‐cyano‐7‐nitroquinoxaline‐2, 3‐dione (CNQX), which blocks non‐NMDA excitatory amino acid receptors, reduced the monosynaptic response to EC stimulation by 85%. The remaining CNQX‐insensitive response did not appear to be mediated by NMDA‐type receptors, since it was not reduced by 50 or 100 μM AP5, and showed none of the voltage sensitivity characteristic of NMDA responses. These data suggest that while the induction of LTP in the amygdala produced by EC stimulation is blocked by high doses of AP5, plasticity at these synapses probably does not require activation of NMDA receptors. © Wiley‐Liss, Inc.
Differential modulation by dopamine of responses evoked by excitatory amino acids in human cortex
Authors: Cepeda Carlos , Radisavljevic Zivotije , Peacock Warwick , Levine Michael S. , Buchwald Nathaniel A. 
Published: December 2004

AbstractThe responses of human neocortical neurons to iontophoretic application of excitatory amino acids and their modulation by dopamine (DA) were studied in vitro. Brain slices were obtained from children undergoing surgery for intractable epilepsy. Application of N‐methyl‐D‐aspartate (NMDA) to the slices induced slow depolarizations accompanied by decreased input conductances and sustained action potentials in cortical neurons. Glutamate produced rapid depolarizations and firing with few changes in input conductances. Quisqualate also induced depolarization and firing, but input conductances increased during the rising phase of the membrane depolarization. Iontophoretic application of DA alone produced no change in membrane potential or input conductance. However, when DA was applied in conjunction with the excitatory amino acids, it produced contrasting effects. With either bath application of DA or when iontophoresis of DA preceded application of NMDA, the amplitude of the membrane depolarizations and the number of action potentials were increased, whereas the latency of these responses decreased. In contrast, DA decreased the amplitude of the depolarizations and the number of action potentials evoked by glutamate or quisqualate. The fact that DA affects responses to NMDA and glutamate or quisqualate in opposite directions is of considerable importance to the understanding of cellular mechanisms of neuromodulation and the role of DA in cognitive processing and in epilepsy. © Wiley‐Liss, Inc.
Fine structure of presynaptic axonal terminals in sympathetic autonomic ganglia of aging and diabetic human subjects
Authors: Schroer Jo Anna , Plurad Santiago B. , Schmidt Robert E. 
Published: December 2004

AbstractThe neuropathologic changes that may underlie autonomic nervous system dysfunction in nondiabetic elderly human subjects or as a complication of diabetes have been systematically examined in sympathetic ganglia of a series of autopsied human subjects. As in animal models of aging and diabetes, enormously swollen terminal axons were found closely apposed to the perikarya of principal sympathetic neurons in prevertebral superior mesenteric sympathetic ganglia of aged and diabetic human subjects. Dystrophic axons consisted of two stereotyped forms: the first was composed of large numbers of misalligned aggregates of neurofilaments surrounded by variable numbers of small dense core vesicles; the second was characterized by large numbers of mitochondria, vacuoles, and dense and multivesicular bodies. The fine structural characteristics of neuroaxonal dystrophy, its predilection for prevertebral rather than paravertebral sympathetic ganglia, and the tendency for multiple dystrophic axons to cluster preferentially around selected neurons were identical in aged and diabetic human ganglia and were similar to changes seen in animal models of aging and diabetes. Neither diabetic nor aging ganglia demonstrated evidence of neuronal degeneration. Such structural changes may represent a degenerative influence of diabetes and aging on the normal remodeling of nerve terminals in autonomic ganglia, i. e., the continually ongoing process of turnover and replacement of axonal terminals. Similarity of lesions in human diabetes and aging suggests the possibility of pathogenetic mechanisms that are common to diabetes and the aging process. The substantial parallels between humans and animal models provide support for the validity of testing some proposed pathogenetic mechanisms directly in animal models. © 1992 Wiley‐Liss, Inc.
High‐affinity binding of [125I]RTI‐55 to dopamine and serotonin transporters in rat brain
Authors: Boja J. W. , Mitchell W. M. , Patel A. , Kopajtic T. A. , Carroll F. I. , Lewin A. H. , Abraham P. , Kuhar M. J. 
Published: December 2004

AbstractRTI‐55 (3β‐(4‐iodophenyl)tropan‐2β‐carboxylic acid methyl ester), one of the most potent inhibitors of dopamine uptake reported to date, was radioiodinated and tested as a probe for the cocaine receptor in Sprague‐Dawley rat brain. Saturation and kinetic studies in the striatum revealed that [125I]RTI‐55 bound to both a high‐ and low‐affinity site. The Kd for the high‐affinity site was 0.2 nM, while the Kd for the low‐affinity site was 5.8 nM. The corresponding number of binding sites in the striatum was 37 and 415 pmol/g protein. The pharmacological profile of specific [125I]RTI‐55 binding in the striatum was consistent with that of the dopamine transporter. Additionally, [125I]RTI‐55 was found to bind with high affinity to the cerebral cortex. Scatchard analysis revealed a single high‐affinity component of 0.2 nM with a density of 2.5 pmol/g protein. The pharmacological profile demonstrated by [125I]RTI‐55 in the cerebral cortex matched that of the serotonin transporter. Autoradiographic analysis of sagittal brain sections with [125I]RTI‐55 binding was consistent with these findings. Specific binding of [125I]RTI‐55 was blocked by dopamine uptake inhibitors in areas rich in dopaminergic nerve terminals. Conversely, serotonin uptake inhibitors blocked the binding of [125I]RTI‐55 in brain areas rich in serotonergic neurons. These results demonstrate that [125I]RTI‐55 may be a very useful ligand for the dopamine and serotonin transporters. Published 1992 Wiley‐Liss, Inc.
Regional distribution of neuropeptide somatostatin gene expression in the human brain
Authors: Mengod G. , Rigo M. , Savasta M. , Probst A. , Palacios J. M. 
Published: December 2004

AbstractThe regional distribution of mRNA coding for the neuropeptide somatostatin has been studied in the human brain by in situ hybridization histochemistry using 32P‐labeled oligonucleotides. We show that somatostatin mRNA‐containing neurons are widely distributed in a number of nuclei and grey areas of the human brain, including neocortex, putamen, nucleus caudatus, nucleus accumbens, amygdala, midbrain, medulla oblongata, hippocampal formation, reticular nucleus of the thalamus, and posterior nucleus of the hypothalamus. No significant hybridization signal was observed in the substantia nigra, claustrum, globus pallidus, thalamus, and cerebellum. The topographic localization of neurons containing SOM mRNA in the human brain is in agreement with previous studies using immunocytochemical or radioimmunoassay techniques. These results show that in situ hybridization histochemistry with oligonucleotide probes can be used to map the distribution of neurons expressing SOM mRNA in human postmortem materials. © 1992 Wiley‐Liss, Inc.
SPECT Imaging of the benzodiazepine receptor: Autoradiographic comparison of receptor density and radioligand distribution
Authors: Sybirska Elzbieta , Al‐Tikriti Mohammed , Zoghbi Sami S. , Baldwin Ronald M. , Johnson Eric W. , Innis Robert B. 
Published: December 2004

AbstractSPECT imaging of benzodiazepine (BZ) receptor using the antagonist [123I]iomazenil in nonhuman primates was correlated with ex vivo autoradiography and in vitro receptor autoradiography of postmortem tissue sections taken at the time of maximal brain uptake of the radiotracer. Cryostat sections prepred from brain tissue blocks at the orientation of the SPECT imaging plane showed high activity in gray matter regions, with gray to white matter ratios of greater than 30:1. After at least one week decay of 123I, these same tissue sections were used to localize and quantify the distribution of BZ receptors with the standard technique of in vitro receptor autoradiography using [125I]iomazenil. The ex vivo autoradiographic distribution of activity was highly correlated (r = 0.89) with the distribution of BZ receptors, although a few brain regions showed reproducible discrepancies between ex vivo and in vitro results. The ex vivo autoradiograms provided quantitative data from a realistic “biological phantom,” which may be used to assess the accuracy of image reconstruction and to investigate differences between the distribution of an intravenously (i. v.) administered tracer and that of its target in brain tissue. © 1992 Wiley‐Liss, Inc.
Reduction of GABAB inhibitory postsynaptic potentials by serotonin via pre‐ and postsynaptic mechanisms in CA3 pyramidal cells of rat hippocampus in vitro
Authors: Oleskevich Sharon , Lacaille Jean‐Claude 
Published: December 2004

AbstractThe action of serotonin (5‐HT) on GABAergic synaptic transmission was investigated with intracellular recordings in CA3 pyramidal cells of rat hippocampal slices. Local application of 5‐HT (500 m̈M) hyperpolarized CA3 pyramidal cells, decreased cellular input resistance, and reduced slow afterhyperpolarizations. Serotonin attenuated the late (GABAB) component of polysynaptic inhibitory postsynaptic potentials (IPSPs; 47% of control) without affecting the early (GABAA) component. During bath application of the excitatory amino acid antagonists 6‐cyano‐7‐nitroquinoxaline‐2, 3‐di‐one (CNQX) (20 m̈M) and 2‐amino‐5‐phosphonovalerate (AP‐5) (40 m̈M), 5‐HT similarly decreased the amplitude of the late (GABAB) component (17% of control) of monosynaptic IPSPs but did not affect the early (GABAA) component. The mean reversal potentials of poly‐ and monosynaptic IPSPs were unaffected by 5‐HT. The conductance increases associated with the late component of poly‐ and monosynaptic IPSPs were reduced by 5‐HT.Hyperpolarizing responses evoked in CA3 pyramidal cells by somatic applications of gamma‐aminobutyric acid (GABA) were unaffected by 5‐HT. During bath application of bicuculline (20–50 m̈M), hyperpolarizing responses elicited by dendritic GABA application were reduced by 5‐HT (71% of control). The effect of 5‐HT on these direct GABAB hyperpolarizations (29% decrease in response) does not appear sufficient to fully account for the effect of 5‐HT on late GABAB IPSPs (53–83% decrease in response). Therefore, 5‐HT may reduce GABAB IPSPs in CA3 pyramidal cells 1) by a postsynaptic action on pyramidal cells and 2) by a selective presynaptic action on GABAergic interneurons mediating the GABAB IPSP. This presynaptic action of 5‐HT does not appear to involve excitatory afferents onto inhibitory interneurons. © 1992 Wiley‐Liss, Inc.
Involvement of the nigrotectal and nigrothalamic pathways in kappa opioid‐induced circling
Authors: Thompson Lisa A. , Walker J. Michael 
Published: December 2004

AbstractThe relationship between kappa opioid‐induced movement and output stations of the substantia nigra pars reticulata (SNpr) was examined using the rodent circling model. Contralateral rotation produced by intranigral microinjection of the kappa opiate U50,488 was lower in animals with ibotenic acid lesions of either the ipsilateral ventromedial thalamus or superior colliculas than in control animals without lesions. These results suggest that endogenous kappa opioids in the SNpr may influence movement through action on the nigrothalamic and nigrotectal pathways. In contrast, animals with ipsilateral lesions of the striatum showed an increase in circling relative to controls, possibly due to kappa receptor supersensitivity in the SNpr. © 1992 Wiley‐Liss, Inc.
Comparative PET studies of the kinetics and distribution of cocaine and cocaethylene in baboon brain
Authors: Fowler J. S. , Volkow N. D. , MacGregor R. R. , Logan J. , Dewey S. L. , Gatley S. J. , Wolf A. P. 
Published: December 2004

AbstractRecent studies have suggested that cocaethylene, an active metabolite of cocaine found in blood and postmortem brain of individuals self‐administering 2 drugs. We have used positron emission tomography (PET) and carbon‐11 (t1/2: 20.4 min) labeled cocaine and cocaethylene to compare the short‐term kinetics of cocaine and cocaethylene in baboon brain. The regional uptake of [11C]cocaine ([11C]COC) and [11C]cocaethylene ([11C]CE), 5–8 mCi and 4–6 m̈g, in baboon brain (n = 7) were similar but clearance from whole brain (global, GL) and from striatum (SR), thalamus (TH), and cerebellum (CB) was slower for cocaethylene. Steady‐state distribution volumes (DV) were not significantly different in the striatum but were greater for cocaethylene in the thalamus, cerebellum, and whole brain. Debenzoylation of cocaethylene proceeded at about one‐third the rate of cocaine, as determined by in vitro incubation of labeled cocaethylene and labeled cocaine with baboon plasma and with purified horse butyryl‐cholinesterase (EC 3. 1. 1. 8). Even though the slower clearance of cocaethylene could lead to longer tissue exposures and potentially accentuated or different physiological effects relative to cocaine, the difference between the 2 drugs is not large. Thus it is more likely that the direct actions of cocaine and alcohol on some organs, rather than cocaethylene, account for this enhanced toxicity. © 1992 Wiley‐Liss, Inc.
Chronic treatment with sabeluzole protects cultured rat brain neurons from the neurotoxic effects of excitatory amino acids
Authors: Pauwels Petrus J. , Van Assouw Harrie P. , Peeters Luc , Moeremans Marc , Leysen Josée E. 
Published: December 2004

AbstractThe neuroprotective properties of the cognitive enhancer sabeluzole were investigated in rat brain neuronal cultures derived from the hippocampal formation of 17‐day‐old rat embryos. Measurement of the neuronal cytoskeletal microtubule‐associated protein, MAP2, was used to assess survival of neurons after exposure of neuronal cultures to glutamate. MAP2 was quantified in neuronal cell homogenates by means of an enzyme‐linked immunosorbent assay (ELISA) using a mouse monoclonal MAP2 antibody, peroxidase‐labeled goat anti‐mouse Jg antiserum, and 2,2′‐azido‐di‐[3‐ethylbenzthiazoline] sulphonate (ABTS) as substrate. Exposure of 7‐day‐old neuronal cultures to 1mM glutamate for 16 hours led to a three‐fold increase in released lactate dehydrogenase (LDH) and a 40% decrease in cellular MAP2 content. Acute treatment of neuronal cultures with 10m̈M sabeluzole yielded a 40% drop in released LDH induced by glutamate. Cultures treated chronically with 0.1 m̈M sabeluzole on days 1 and 4 in culture showed, after 1 week in culture, a MAP2 content and total LDH activity that was not different from control cultures. A 16‐hour exposure to 1mM glutamate did not induce LDH release or changes in MAP2 levels in sabeluzole‐treated cultures. A single treatment with 0.1 m̈M sabeluzole between day 1 to 5 induced a 70–80% drop in glutamate‐induced released LDH in 7‐day‐old neuronal cultures. Full and partial neuronal protection after chronic sabeluzole treatment at 0.1m̈M was also observed for neurotoxicity induced by 5mM N‐methyl‐D‐aspartate (NMDA) and 1mM kainic acid or 30 m̈M veratridine, respectively. Within a series of compounds such as Ca++and Na+ channel antagonists, glutamate receptor antagonists and various neurotransmitter receptor antagonists, sabeluzole, chronically given, were the most potent for inhibition of released LDH induced by 1mM glutamate (IC50‐ value: 34 ± 13nM). In conclusion, chronic sabeluzole treatment protects cultured rat brain neurons from excitotoxic aggression. © 1992 Wiley‐Liss, Inc.
Effect of differential rearing on synapses and soma size in rat medial amygdaloid nucleus
Authors: Ichikawa Masumi , Matsuoka Masato , Mori Yuji 
Published: December 2004

AbstractThe effects of differential rearing on synaptic morphology and neuronal size were examined in the medial amygdaloid nucleus (MAN) of adult rats. Forty‐day‐old male rats were housed in one of three ways: individually (isolated condition, IC); with four males per cage (unisexual condition, UC); or with two males and two females per cage (social condition, SC). After 2 months, the animals were prepared for electron and light microscopy Although there was no statistically significant difference in number of synapses per unit volume in MAN, the number of perforated (P) synapses, which are characterized by discontinuities in the postsynaptic density, were significantly greater in the UC and the SC than in the IC. The length of synaptic contact zone of P synapses was also longer in both the UC and the SC compared with the IC, whereas the length of nonperforated synapses was longer only in the SC. Some area was also larger in the SC compared with the IC. These results demonstrate that exposure to different rearing conditions, in which the pheromonal environment can be substantially different, can induce striking morphological changes in both synapses and neurons in the MAN of adult rats. © 1993 Wiley‐Liss, Inc.