bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term blockade of the dopamine uptake complex by metaphit, an isothiocyanate derivative of phencyclidine
Authors: Zimänyi Ildikó , Jacobson Arthur E. , Rice Kenner C. , Lajtha Abel , Reith Maarten E. A. 
Published: January 2005

Abstract[3H]Mazindol was used to label the dopamine uptake complex in mouse striatum in vitro in the presence and absence of metaphit, an isothiocyanate derivative of phencyclidine. In some experiments, metaphit was present in the incubation fluid throughout the procedure in other experiments it was eliminated by several washings and centrifugations. It was found that after removal of the metaphit by washing and centrifugation, the mazindol binding was not restored. Membranes that were pretreated with metaphit and washed had a lower density of mazindol binding sites than control membranes; the remaining mazindol sites had the same afinity for [3H]mazindol. These findings are in agreement with the previous studies on [3H]cocaine and [3H]methylphenidate binding. The following observations support that metaphit is irreversibly acting and not slowly dissociating from the mazindol recognition sites of the dopamine uptake carrier complex: (1) Metaphit did not change the off‐rate of [3H]mazindol binding, arguing against an allosteric action at a distinct site. (2) The presence of cocaine protected the mazindol binding sites from the action of metaphit, supporting binding of metaphit and mazindol to the same site. (3) Nine hours after metaphit pretreatment and removal, the degree of inhibition of mazindol binding was the same as immediately after pretreatment, consonant with an irreversible effect of metaphit. (4) The potency of metaphit in inhibiting mazindol binding was greater under slightly alkaline conditions, consistent with acylation of the mazindol sites. Furthermore, it was found that intracerebroventricular application of metaphit did not result in a decrease in the binding of [3H]mazindol 5 hr after the administration.
Review: Fine structure of synaptogenesis in the vertebrate central nervous system
Authors: Vaughn James E. 
Published: January 2005

AbstractThis article reviews studies of the formation of synaptic junctions in the vertebrate central nervous system. It is focused on electron microscopic investigations of synaptogenesis, although insights from other disciplines are interwoven where appropriate, as part of the review is concerned with the morphological maturation of synapses as described from both qualitative and quantitative perspectives. Next, epigenetic influences on synaptogenesis are examined, and later in the article the concept of epigenesis is integrated with that of hierarchy. It is suggested that the formation of synaptic junctions may take place as an ordered progression of epigenetically modulated events wherein each level of cellular affinity becomes subordinate to the one that follows. The ultimate determination of whether a synapse is maintained, modified or dissolved would be made by the changing molecular fabric of its junctional membranes. In closing, a hypothetical model of synaptogenesis is proposed, and an hierarchial order of events is associated with a speculative synaptogenic sequence. Key elements of this hypothesis are (1) epigenetic factors that facilitate generally appropriate interactions between neurites; (2) independent expression of surface specializations that contain sufficient information for establishing threshold recognition between interacting neurites; (3) exchange of molecular information that biases the course of subsequent junctional differentiation and ultimately results in (4) the stabilization of synaptic junctions into functional connectivity patterns.
Immunochemical identification of desmin in Torpedo postsynaptic membranes and at the rat neuromuscular junction
Authors: Sealock Robert , Murnane Amy A. , Paulin Denise , Froehner Stanley C. 
Published: January 2005

AbstractPreparations of acetylcholine receptor‐rich (AChR‐rich) postsynaptic membranes from electric tissue of electric rays often contain an Mr 55,000 protein (55kD protein) that has not been previously characterized. Using a monoclonal antibody (MAb 1403) against the 55kD protein from Torpedo californica and a pan‐specific, anti‐intermediate filament antibody (Pruss et al., 1981; Cell 27:419–428), we show that the 55kD protein has the properties expected of Torpedo desmin. By the electron microscope immunogold method applied to perfusion‐fixed electric tissue, MAb 1403 labeled only cytoplasmic filaments in the electroplax. These filaments were neither more concentrated nor arranged detectably differently in postsynaptic regions relative to nonpostsynaptic regions. The 55kD protein could also be fractionated away from isolated postsynaptic membranes by gradient centrifugation. The protein is thus a minor component of the postsynaptic membrane in situ and after isolation. On semithin cryosections of rat skeletal muscle, on the other hand, MAb 1403, which recognizes rat desmin but not rat vimentin, gave strong fluorescent labeling of the postsynaptic region, weaker labeling of the Z‐line, and still weaker labeling of the cell surface immediately surrounding extrajunctional nuclei. The pattern of postsynaptic labeling suggests that desmin, presumably in the form of intermediate filaments, occurs near the AChR‐rich crests of the junctional folds, but is particularly concentrated among and around the ends of the folds. Similar results were obtained with a second monoclonal antibody raised against authentic desmin. These results suggest that desmin intermediate filaments may have an important role in organization of the postsynaptic cytoplasm in rat muscle.
Presence of calcium/calmodulin‐dependent protein Kinase II in Nerve terminals of rat brain
Authors: Walaas S. Ivar , Gorelick Fred S. , Greengard Paul 
Published: January 2005

AbstractCalcium/calmodulin‐dependent protein kinase type II, a multimeric 550‐650 kilodalton enzyme composed of major alpha (50 kilodalton) and beta/beta' (60/58 kilodalton) subunits, is present in high concentrations in mammalian brain. Previous immunocytochemical studies indicated that the enzyme is enriched in cell bodies and dendrites, but did not show a clear‐cut localization in nerve terminals. The present study present evidence, using lesion‐induced degenerations of pre‐ and postsynaptic neuronal populations in the neostriatum and substantia nigra, that calcium/calmodulin‐dependent protein kinase II, as measured both by autophosphorylation of enzyme subunits and by synapsin I kinase activity, is present in high concentrations in several populations of presynaptic terminals. Lesions of the corticostriatal tract decreased the amount of enzyme by 30‐40% in the neostriatum, a decrease similar to that seen in the same region of synapsin I, a general nerve terminal market. Lesions of the striatonigral tract induced an even more pronounced decrease of the enzyme in the substantia nigra; this decrease was larger than the lesion‐induced change of synapsin I seen in the same region. Our data therefore indicate that certain nerve terminal population in the rat brain contain high levels of calcium/calmodulin‐dependent protein kinase II.
Phencyclidine and sigma receptors in rat spinal cord: Binding characterization and quantitative autoradiography
Authors: Aanonsen Linda M. , Seybold Virginia S. 
Published: January 2005

AbstractThese experiments were designed to compare phencyclidine (PCP) and s̀ (sigma) receptor binding sites in the rat spinal cord by using receptor binding and autoradiographic techniques. Binding sites for 3H‐TCP (3H‐1‐[1‐(2‐thienyl)cyclohexy]piperidine), a PCP receptor agonist, and (+)3H‐3‐PPP (3H‐(+)‐3‐(3‐hydroxyphenyl)‐N‐(1‐propyl)piperidine), a s̀ receptor agonist, in the rat spinal cord were shown to represent two populations of recognition sites. Inhibition studies revealed that ligands with high affinity for the PCP receptor (MK‐801 and PCP) were potent competitors at 3H‐TCP binding sites whereas the putative s̀ receptor ligands (±)pentazocine and haloperidol were potent competitors at (+)3H‐3‐PPP binding sites. The autoradiographic distribution of 3H‐TCP and (+)3H‐3‐PPP binding sites in adjacent sections of rat spinal cord demonstrated the occurrence of two distinct populations of binding sites. 3H‐TCP binding sites were localized primarily in laminae I and II in cervical and thoracic spinal segments. Binding sites in lamina I decreased in density along a rostral to caudal gradient in the spinal cord. The highest density of (+)3H‐3‐PPP binding sites was found in the ventral horn (lamina VIII and IX) and over perikarya in dorsal root ganglia. Significantly elevated densities of (+)3H‐3‐PPP binding sites were also found in lamina X within thoracic and lumbar segments and in the intermediolateral cell column. The results of the present study show that PCP and s̀ receptor binding sites are differentially localized in the rat spinal cord and suggest that separate binding sites exist for PCP and s̀ agonists.
Long‐term potentiation in hippocampal CA3 neurons: Tetanized input regulates heterosynaptic efficacy
Authors: Bradler James E. , Barrionuevo German 
Published: January 2005

AbstractThree excitatory synaptic inputs to hippocampal CA3 neurons—the mossy fibers, Schaffer collateral/commissural fibers, and fimbrial fibers—were determined to be separate and independent in the pharmacologically disinhibited in vitro slice. Long‐term synaptic potentiation (LTP) was induced in one of these three synaptic inputs, and subsequent synaptic efficacy changes in the other two nontetanized inputs were characterized using current and voltage clamp techniques. LTP in the mossy fiber input was accompanied by potentiation of Schaffer and fimbrial responses, whereas the induction of LTP in the Schaffer pathway was associated with the potentiation of fimbria responses and a depression of mossy fiber responses. LTP induced in the fimbrial response was confined to that input alone.
Structural alterations of dendritic spines induced by neural degeneration of their presynaptic afferents
Authors: Benshalom Gadi 
Published: January 2005

AbstractMorphological parameters were compared for dendritic spines of spiny stellate neurons in layer IV of the barrel region of mouse somatosensory cortex, which synapse with degenerated thalamocortical afferents (TC spines) and with intact, unidentified axon terminals (UI spines). Spiny stellate neurons were labeled for light and electron microscopic identification by Golgi impregnation and gold toning. Dendritic spines were examined in series of thin sections, and TC spines were ultrastructurally detectable because of the degeneration‐induced characteristic appearance of the TC axon terminals. Results show that the means of the width of the spine head and of the length of the spine stalk were significantly higher in TC spines than in UI spines by about 11 and 25%, respectively. The variability of these two morphological parameters was significantly lower for TC spines. The mean of the spine stalk width at the narrowest cross section of the stalk was about 0.12 μm, with no significant difference observed between the two spine groups. No specific relationship was found in either the TC or the UI groups of spines between the length of the spine stalk and the width of the spine stalk at its narrowest profile.As structural features typifying transneuronal degeneration were not observed along the dendritic spines examined, it is speculated that the morphological differences encountered between the TC and UI spines may result, at least in part, from the degeneration‐induced synaptic inactivity of the TC axospinous synapses, rather than exclusively from any direct effects of the degeneration process.
Concentrations of mRNAs encoding for preprosomatostatin and preprocholecystokinin are increased after kainic acid‐induced seizures
Authors: Olenik C. , Meyer D. K. , Marksteiner J. , Sperk G. 
Published: January 2005

AbstractConcentrations of preprosomatostatin‐mRNA and preprocholecystokinin‐mRNA were determined by Northern blot analysis in rats 2, 10, and 30 days after strong seizures induced by a single intraperitoneal injection of kainic acid. At all time intervals examined, levels of preprosomatostatin‐mRNA were increased in the frontal cortex; so were levels of preprosomatostatin‐mRNA in the striatum. Transient increases, i.e., 2 days after kainic acid, of preprocholecystokinin‐mRNA were observed in the frontal cortex and the substantia nigra. Preprocholecystokinin‐mRNA was reduced in the hippocampus 2 and 10 days after kainic acid. Both preprosomatostatin‐ and preprocholecystokinin‐mRNA levels showed a tendency to be reduced in the amygdala/pyriform cortex at all three time intervals.The increases in mRNA levels suggest enhanced rates of synthesis of the respective neuropeptides subsequent to kainic acid‐induced seizures. They may also reflect a prolonged increase in the activity of the respective peptide‐containing neurons. This is of special interest in the frontal cortex, since in this area both neuropeptides are found in interneurons and are widely colocalized with γ‐aminobutyric acid.
Peripheral induction of burst firing in locus coeruleus neurons by nicotine mediated via excitatory amino acids
Authors: Tung C.‐S. , Ugedo L. , Grenhoff J. , Engberg G. , Svensson T. H. 
Published: January 2005

AbstractThe effect of systemic nicotine administration (50 μg kg−1 i.v.) on the activity of brain noradrenaline neurons in the locus coeruleus (LC) of chloral hydrateanesthetized rats was analyzed with single cell recording techniques and quantitative computer assessment of firing rate, degree of bursting, and regularity of firing. Nicotine caused an increased firing rate of the cells, with an average time of onset of 1.7 s. An increase in burst activity was observed, as well as deregularization of the firing pattern. Intraventricularly administered kynurenic acid (1 μmol), an antagonist of excitatory amino acids (EAA), did not change the firing rate of the LC cells, but did induce a marked regularization of their firing pattern into a pacemaker‐like activity and completely abolish burst firing. The EAA antagonist also blocked all of the above effects of nicotine on the LC neurons as well as their typical burst‐activation response to a peripheral, noxious stimulus such as paw‐pinch. Since the circulation time in the rat is about 20 s, these results provide unequivocal evidence for a peripheral site of origin for the rapid LC activation induced by systemic nicotine administration. The data also allow the conclusion that the nicotine‐induced LC activation is indirect and dependent on EAA in brain. Our results provide evidence for a tonically active EAA input to the LC, being of importance for induction of changes in the spontaneous, pacemaker activity of LC neurons into burst firing or more irregular firing patterns. It is suggested that the LC activation by nicotine may be significant in relation to tobacco dependence.
Dopamine control of seizure propagation: Intranigral dopamine D1 agonist SKF‐38393 enhances susceptibility of seizures
Authors: Turski Waldemar A. , Cavalheiro Esper A. , Ikonomidou Chrysanthy , Bortolotto Zuner A. , Klockgether Thomas , Turski Lechoslaw 
Published: January 2005

AbstractThe involvement of dopamine (DA) in human and experimental epilepsy has been discounted as DAergic drugs have little effect on convulsions. This work presents evidence that bilateral microinjection of the DA D1 agonist SKF‐38393 into the substantia nigra enhances the susceptibility of rats to seizures, with and ED50 fo 20 pmol (range 13‐31 pmol), converting subconvulsant doses of the cholinergic agonist pilocarpine (200 mg/kg; i.p.) into convulsant ones. The proconvulsant action of SKF‐38393 was reversed by blocking D1‐mediated transmission in the substantia nigra with the D1 antagonist SCH‐23390. The D2 agonist LY‐171555 did not modulate the threshold for limbic seizures when injected into the substantia nigra. In the striatum, the D2 agonist LY‐171555 protected rats against limbic seizures induced by systemic administration of pilocarpine (380 mg/kg; i.p.), with an ED50 of 2 pmol (range 1.4–2.8 pmol). The anticonvulsant action of LY‐171555 in the striatum was reversed by haloperidol. The D1 agonist SKF‐38393 did not affect pilocarpine seizures following administration into the striatum. Systemic administration of DAergic drugs showed that the D1 agonist SKF‐38393 decreased the threshold for pilocarpine seizures, with an ED50 of 0.81 mg/kg (range 0.45–1.47 mg/kg), whereas the D2 agonist LY‐171555 had no effect on susceptibility of rats to pilocarpine. Thr proconvulsant action of SKF‐38393 was blocked by the D1 antagonist SCH‐23390. These results suggest that DA differentially modulates seizure threshold in the forbrain acting via D1 mechanisms in the substantia nigra and D2 mechanisms in the striatum.
Direct effect of 17β‐estradiol on striatum: Sex differences in dopamine release
Authors: Becker Jill B. 
Published: January 2005

AbstractThe nigrostriatal dopamine (DA) system is sexually dimorphic. In female but not male rats, striatal DA activity is modulated by gonadal steroid hormones. Ovariectomy (OVX) decreases striatal DA release and turnover. Estrogen replacement restores the response to that of the intact female in estrus. In contrast, castration (CAST) of male rats has no effect on the stimulated release of DA from striatal tissue. This report addresses the question: Dose estrogen act directly on the striatum to induce changes in DA release? Physiological concentrations of 17b̃‐estradiol and other steroids or a nonsteroidal estrogen analog were applied directly to striatal tissue maintained in an in vitro superfusion system. The effect of hormonal treatments on the responsiveness of striatal DA terminals to stimulation was examined in tissue from OVX females and intact and CAST male rats. The results are summarized as follows: (1) Infusion of 17b̃‐estradiol (p < 0.01) and diethylstilbesterol (p < 0.05) increased amphetamine (AMPH)‐stimulated striatal DA release from striatal tissue of OVX female rats compared with the effect of cholesterol. 17alpha‐Estradiol also tended to potentiate the striatal DA response to AMPH, but this result was not statistically significant (p < 0.062). 17b̃‐Estradiol had no effect on AMPH‐stimulated DA release from striatal tissue of intact male rats. (2) The KCl‐stimulated release of DA from striatal tissue of OVX rats exposed in vitro to 100 pg/ml 17b̃‐estradiol (a physiological dose) was significantly greater (p < 0.05) than the response after exposure to vehicle. In contrast, 1,000 pg/ml 17b̃‐estradiol produced a decrease in KCl‐induced striatal DA release (p < 0.05), whereas 17alpha‐estradiol (100 pg/ml or 1,000 pg/ml) did not significantly influences the response to KCl. (3) The pulsatile administration of 17b̃‐estradiol stimulated DA release from strital tissue of OVX females (p < 0.05; compared with tissue from an OVX group that received vehicle or CAST male rats exposed to either 17b̃‐estradiol or vehicle). It is concluded that with tissue from OVX rats, physiological concentrations of estrogen can act directly on striatal tissue in vitro to stimulate DA release and to increase striatal DA responsiveness to stimulation, whereas prolonged exposure or high concentrations of 17b̃‐estradiol decreases striatal DA responsiveness. The striatum and/or the striatal DA system are sexually dimorphic in this regard.
Postsynaptic structure may account for variations in miniature endplate current shapes along frog neuromuscular junctions
Authors: Fortier L. P. , Tremblay J. P. 
Published: January 2005

AbstractIntracellular recordings were made in the presence of 6–9 m̈M neostigmine with an electrode placed halfway between the distal end and the proximal region of a long simple branch of a frog neuromuscular junction. During the intracellular recording period, an extracellular electrode was placed alternatively at a distal and at a proximal site. The temporal correspondence between the extracellular miniature endplate current and intracellular miniature endplate potential permitted us to identify two miniature endplate potential (MEPP) populations originating, respectively, from the distal and proximal regions. The frequency and intracellular amplitude of MEPPs were higher in the proximal than in the distal region. The rise time and the decay time of the extracellularly recorded MEPC were longer in the proximal region. A significant correlation was observed between the amplitude (in mV) and surface (in mV · ms) of MEPCs. The slope of this regression line was steeper for the proximal region. Furthermore, the correlation coefficient was lower for that region owing to variations of MEPC shape. Our observations suggest that in the presence of anticholinesterase, ACh rebinds more often to acetylcholine receptors in the proximal region because of the presence of longer postjunctional folds.
Effects of haloperidol and clozapine on preprotachykinin‐A messenger RNA, tachykinin tissue levels, release and neurokinin‐1 receptors in the striato‐nigral system
Authors: Christian Humpel , Andrea Knaus Gabriele , Bernhard Auer , Hans‐Gunther Knaus , Christian Haring , Elvar Theodorsson , Alois Saria 
Published: January 2005

AbstractThe effects of haloperidol and clozapine on tachykinin tissue lelvels, preprotachykinin‐A messenger RNA, spontaneous and potassium‐evoked tachykinin release, dopamine D2 receptors, and [125]Bolton‐Hunter‐substance P binding sites in the striato‐nigral system were examined. Chronic administration (10 days) of the dopamine receptor antagonist haloperidol (2 mg/kg, i.p.) significantly decreased tissue levels of substance P like‐immunoreactivity and neurokinin A like‐immunoreactivity in the striatum and the substantia nigra. The corresponding preprotachykinin‐A mRNA was decreased ub tge struatyun, Haloperidol did not affect the potassium‐evoked tachyikinin release in the substantia nigra but significantly increased the spontaneous release. Haloperidol increased the number of D2‐receptors but left [125]Bolton‐Hunter‐substance P binding sites, representing neurokinin 1 (NK‐1) receptors, as determined by competition experiments with selective ligands, unchanged. Clozapine (30 mg/kg, i.m.) did not influence nigral and striatal tachykinin tissue levels, preprotachykinin‐A mRNA and potassium‐evoked release or spontaneous efflux in the substantia nigra, or D2‐receptors and [125I]Bolton‐Hunter‐substance P bindin sites. The present data indicate that neuroleptics influence the striato‐nigral tachykinin system in different ways. Tachykinins may therefore, contribute to the therapeutic and/or untoward effects of certain neuroleptic drugs.