bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrosensory systems in fish
Authors: Heiligenberg Walter 
Published: January 2005

AbstractA close integration of behavioral, neurophysiological, and neuroanatomical approaches has guided research on the neural basis of electrosensation and the generation of behaviors associated with this modality. By postulating neuronal implementaions of specific computations in sensory information processing, behavioral studies have been curcial in focusing studies at the neuronal level onto behaviorally relevant structural and functional aspects. Physiological and anatomical studies have analyzed (a) neural networks underlying the distributed processing of sensory information, (b) the role of descending recurrent pathways and eference copy mechanisms for the filtering of incoming information, c) the significance of multiple topographic representations for sensory information processing, and d) the modulation of sensory and motor structures through various transmitters and receptor subtypes. Developmental studies have explored the significance of steroid hormones for the tuning of electroreceptors to the frequency of an endogenous neuronal oscillator which drives the electric current pulses necessary for their stimulation. Embryological studies have revealed that the development of mechanoreceptors and electroreceptors in the fish's skin is induced by the innervation of primary afferent nerve fibers which are specific with regard to their central connections as well as with regard to the type of receptor induced in the periphery.
Synaptic remodelling of perforated synapses during development and maturation in a visual projection area in birds
Authors: Nixdorf Barbara E. 
Published: January 2005

AbstractPerforated synapses are characterized by the appearance of one or more discontinuities in the postsynaptic density (PSD). These synapses are thought to represent intermediate stages in synaptic remodelling and turnover. To determine the dynamic level of these processes, the development of perforated synapses at different ages was examined in the neuropil of the ectostriatum, a visual projection area in birds. The overall number of perforated synapses per unit volume increases during development. Single and multeple perforated synapses, however, show a differnt developmental trend. Between 20 and 100 days, when the number of multiple perforated synapses decreases by 46%, single perforated synapses increase by 83% in number per unit volume. No significant changes in single or multiple perforated synapses can be observed at younger ages (i.e., 5 or 10 days). Various parameters increase between 10 and 20 days, followed by a reduction at 100 days: The relative frequency of perforations per synaptic contact, the length of the postsynaptic density including the size of the perforation, the length of the synaptic contact zone in perforated synapses excluding the size of the perforation, and the size of the perforation follow the same trend.
Paradoxical anticonvulsant acitivity of the γhyphen;Aminobutyrate antagonist bicuculline methiodide in the rat striatum
Authors: Turski Lechoslaw , Diedrichs Stefan , Klockgether Thomas , Schwarz Michael , Turski Waldemar A. , Sontag Karl‐Heinz , Brotolotto Zuner A. , Chlderazzo‐Filho Lineu S. , Cavalheiro Esper A. 
Published: January 2005

AbstractBicuculline methiodide (BMI), a γ‐aminobutyrate (GABA) antagonist, is a powerful convulsant agent when injected into the cerebral ventricles amygdala, hippocampus thalamus, neocortex and deep prepiriform cortex in rats. In contrast, bilateral microinjection of BMI into the rat striatum confers protection against seizures induced by the cholinergic agonist pilocarpine (380 mg/kg, i.p.), with an ED50 of 94 fmol (range 45–195 fmol). No topogrphical variation in the anticonvulsant action of BMI was detected throughout rostrocaudal and dorsoventral aspects of the striatum. The anticonvulsant action of BMI in the striatum was reversed by coadministration of the GABA agonist muscimol or by blocking GABA‐mediated inhibition in either the substantia nigra pars reticulata or in the entopeduncular nucleus. The results show that blockade of GABA‐mediated inhibition in the striatum has a powerful anticonvulsant effect in the pilocorpine model, suggesting that GABAergic transmission in the striatum modulates the seizure propagation in the forebrain.
Chemically distinct rat olivocochlear neurons
Authors: Vetter Douglas E. , Adams Joe C. , Mugnaini Enrico 
Published: January 2005

AbstractWe have produced a neurochemical map of the cell bodies of origin of the cochlear efferent terminals in rat by combining glutamic acid decarboxylase (GAD), choline acetyltransferase (ChAT) or calcitonin gene‐related peptide (CGRP)immunocytochemistry with retrograde transport of horseradish peroxidase.The location of cochlear efferent cell bodies are in general agreement with the medial and lateral systems described by White and Warr (J. Comp. Neurol. 219:203–214, 1983) with some minor modifications. The lateral system consists of at least two pools of chemically distinct neurons located within the lateral superior olive (LSO) ipsilateral to the injected cochlea. One pool immunostains with an antibody to GAD while the other immunostains with antibodies to ChAT and to CGRP. The medial efferent system consists of periolivary neurons that are almost exclusively large and ChAT‐positive but CGRP‐negative. They are located both ipsilateral and contralateral to the cochlea they project to. There are a few GAD‐positive small neurons in the medioventral and rostral periolivary regions that project ipsilaterally, but these may prove to be ectopic neurons. The ipsilateral lateroventral periolivary region (LVPO) contains some efferent neurons, all of which are ChAT‐positive but CGRP‐negative. Additional cochlear efferent neurons, some of which are ChAT‐positive and others GAD‐positive, are present within and immediately dorsal to the fiber capsule surrounding the medial limb, and to a lesser extent the lateral limb, of the ipsilateral LSO. Not all GAD‐positive or ChAT‐positive olivary cells project to the cochlea.We have complemented the results in the brainstem by demostrating two immunocytochemically distinct populations of efferent terminals in the cochlea simultaneously, one CGRP‐positive and the other GAD‐positive. Approximately, equal numbers of boutons immunoreactive for both markers are present beneath inner hair cells throughout the entire length of the cochlea. Surprisingly high numbers of GAD‐positive and CGRP‐positive boutons are also present on outer hair cells, with each class having its spatially and morphologically ditinct features. The lack of CGRP‐positive periolivary cells that are retrogradely labeled by cochlear injections of HRP suggests that the lateral olivocochlear system sends projections to outer hair cells. Our results raise questions about species differences in the organization of targets of the lateral and medial olivocochlear systems.
Contribution of the amygdala and nucleus accumbens to ventral pallidal responses to dopamine agonists
Authors: Napier T. Celeste 
Published: January 2005

AbstractNeurons recorded from ventral pallidum/substantia innominata (VP) of the basal forebrain respond to dopaminergic agonists that activate either the D1 or D2 the receptor subtype. Major afferent systems to the VP originate within amygdaloid nuclei (AMN) and the nucleus accumbens (NA). Since both the AMN and the NA are dopaminoceptive, the present study sought to analyze the contribution of these afferent systems to VP responses to dopaminergic agonists. Single VP neurons were electrophysiologically recorded in vivo from chloral hydrate‐anesthetized rats, and the following determinations were made. (1) Effects of pharmacologic inactivation of an afferent system were assessed by monitoring VP neurons during intracerebral microinjections of the local anesthetic procaine, administered directly into either the AMN or the NA. (2) With procaine‐induced VP rate changes used to indicate an afferent influence on the recorded neuron, VP responses to apomorphine (an agonist that acts at D1 and D2 receptor subtypes), SKF38393 (a D1 agonist), or quinpirole (a D2 agonist) were determined and compared with responses in rats not receiving the procaine pretreatment. Following pharmacologic inactivation of either the AMN or the NA, approximately 80% of the VP neurons monitored demonstrated rate changes, illustrating that spontaneous neuronal firing in the VP is dependent on tonically active input systems. Following afferent cessation, responses to apomorphine and quinpirole remained intact, suggesting that the AMN or NA is not necessary for VP responding to the systemic administration of dopaminergic agonists that act at D2 receptors. In contrast, the number of neurons that responded to SKF38393 was diminished follow intra‐AMN (but not intra‐NA) procaine. This suggests that D1‐induced VP responses are mediated, at least in part, via the AMN.
Iontophoretically administered drugs acting at the N‐methyl‐D‐aspartate receptor modulate burst firing in A9 dopamine neurons in the rat
Authors: Overton Paul , Clark David 
Published: January 2005

AbstractExtracellular single‐unit recording and iontophoresis were used to examine the effect of N‐methyl‐D‐aspartate (NMDA) and the competitive NMDA antagonist (+/−)‐4‐(3‐phosphonopropyl)‐2‐piperazine carboxylic acid (CPP) on the firing rate and firing pattern of A9 dopamine (DA) neurons in the rat. Administration of NMDA produced a dose‐dependent increase in firing rate (up to nearly 300% of baseline at the highest ejection current), which could be blocked by iontophoretic CPP. Low currents (<10 nA) were sufficient to induce apparent depolarisation inactivation in some neurons. In addition to this effect on firing rate, NMDA also caused a dramatic increase in burst firing, which was also dose dependent; cells made more bursts, and each burst consisted of more spikes. The only measured aspect of burst morphology that was not affected was the mean burst interspike interval. All nonbursting cell (n = 10) were converted to burst firing by the drug. CPP administered alone was found to reduce burst firing, without affecting the firing rate. These data suggest that a tonically active excitatory amino acid input to A9 DA neurons is responsible for inducing burst firing in vivo and that this input seems to operate via the NMDA receptor, possibly by virtue of its link to a Ca2+ ionophore.
Clinical and biochemical aspects of depressive disorders: III. Treatment and controversies
Authors: Caldecott‐Hazard Sally , Schneider Lon S. 
Published: January 2005

AbstractThe present document is the final of three parts of a review that focuses on recent data from clinical and animal research concerning the biochemical bases of depressive disorders, diagnosis, and treatment. Various treatments for depression, including psychotherapy, pharmacological, and somatic treatments, will be described in this third part. Also, some of the controversies in the field, as well as a summary of the most salient points of the review, will be discussed. Previous sections of this review dealt with the classification of depressive disorders and research techniques for studying the biochemical mechanisms of these disorders (Part I) and various transmitter/receptor theories of depressive disorder (Part II).
Direct muscarinic and nicotinic receptor‐mediated excitation of rat medial vestibular nucleus neurons in vitro
Authors: Phelan Kevin D. , Gallagher Joel P. 
Published: January 2005

AbstractWe have utilized intracellular recording techniques to investigate the cholinoceptivity of rat medial vestibular nucleus (MVN) neurons in a submerged brain slice preparation. Exogenous application of the mixed cholinergic agonists, acetylcholine (ACh) or carbachol (CCh), produced predominantly membrane depolarization, induction of action potential firing, and decreased input resistance. Application of the selective muscarinic receptor agonist muscarine (MUSC), or the selective nicotinic receptor agonists nicotine (NIC) or 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP) also produced membrane depolarizations. The MUSC‐induced depolarization was accompanied by decreased conductance, while an increase in conductance appeared to underlie the NIC‐ and DMPP‐induced depolarizations. The muscarinic and nicotinic receptor mediated depolarizations persisted in tetrodotoxin and/or low Ca2+/high Mg2+ containing media, suggesting direct postsynaptic receptor activation. The MUSC‐induced depolarization could be reversibly blocked by the selective muscarinic‐receptor antagonist, atropine, while the DMPP‐induced depolarization could be reversibly suppressed by the selective ganglionic nicotinicreceptor antagonist, mecamylamine. Some neurons exhibited a transient membrane hyperpolarization during the depolarizing response to CCh or MUSC application. This transient inhibition could be reversibly blocked by the γ‐aminobutyric acid (GABA) antagonist, bicuculline, suggesting that the underlying hyperpolarization results indirectly from the endogenous release of GABA acting at GABA receptors. This study confirms the cholinoceptivity of MVN neurons and establishes that individual MVN cells possess muscarinic as well as nicotinic receptors. The data provide support for a prominent role of cholinergic mechanisms in the direct and indirect regulation of the excitability of MVN neurons.
Prenatal cocaine produces deficits in serotonin mediated neuroendocrine responses in adult rat progeny: Evidence for long‐term functional alterations in brain serotonin pathways
Authors: Cabrera Theresa M. , Yracheta Joseph M. , Li Qian , Levy Andrew D. , Van De Kar Louis D. , Battaglia George 
Published: January 2005

AbstractCocaine produces biochemical alterations in brain serotonin (5‐HT) neurons. Since 5‐HT is critical to the development of fetal 5‐HT neurons and target tissues, we hypothesized that in utero exposure to cocaine could result in long‐term alterations in postnatal 5‐HT systems. Pregnant Sprague‐Dawley rats were administered either saline or (−)cocaine (15 mg/kg, s.c., b.i.d.) from gestational day 13 to 20. Prenatal cocaine exposure did not alter litter size, gender number, or progeny birth weights. Functional alterations in serotonergic systems were determined in postnatal day (PD) 70 male progeny by measuring changes in 5‐HT mediated plasma hormones following a single 8 mg/kg injection of the 5‐HT releaser p‐chloroamphetamine (PCA). Cocaine exposed male progeny exhibited significant reductions in adrenocorticotropic hormone (ACTH, −43%) and renin (−62%) responses to PCA. However, no alterations were observed in the corticosterone or prolactin response to PCA. In utero exposure to cocaine did not alter basal levels of ACTH, renin, corticosterone, or prolactin. There were no significant differences in the density of either hypothalamic or cortical 5‐HT uptake sites. Likewise, there were no significant differences in the densities of any of the 5‐HT1 receptor subtypes or in the density of 5‐HT2 receptors in cortex. These data, which provide the first demonstration of deficits in 5‐HT mediated neuroendocrine function in adult progeny following in utero exposure to cocaine, indicate long‐term functional alterations of brain 5‐HT systems. © 1993 Wiley‐Liss, INe.
Further characterization of the effects of BMY 14802 on dopamine neuronal activity
Authors: Zhang Jing , Chiodo Louis A. , Freeman Arthur S. 
Published: January 2005

AbstractFurther evaluation of the effects of BMY 14802 on dopamine (DA) neuronal activity in the rat substantia nigra pars compacta (A9) was conducted with single‐unit recording and microiontophoresis in anesthetized rats. Microiontophoretic administration of BMY 14802 (sigma, serotonin (5‐HT)‐1A and α‐1 adrenoceptor ligand) had no effect on DA neurons. Microiontophoretic administration of (+)‐3‐PPP (weak D2 agonist with high affinity for sigma receptors) and quinpirole (D2/D3 agonist) inhibited A9 DA neuronal activity. Coiontophoresis or i.v. pretreatment with BMY 14802 had no effect on the current‐response curves for the effects of microiontophoretic (+)‐3‐PPP or quinpirole on A9 DA neurons. Coiontophoretic administration of (−)‐sulpiride, a selective D2 antagonist, blocked the inhibitory effects of microiontophoretic (+)‐3‐PPP. The effects of BMY 14802 (0.25‐8 mg/kg, i.v.) on DA neurons (increased firing rate, increased burst‐firing, reduced regularity of firing pattern) were not altered by acute brain hemitransection, but were blocked by pretreatment with NAN‐190, an antagonist of 5‐HT‐1A and α‐1 receptors. The α‐1 receptor antagonist, prazosin, did not block these effects of BMY 14802.In conclusion, the effects of BMY 14802 on DA neuronal firing rate and firing pattern are indirect, perhaps due in part to the occupation of 5‐HT‐1A receptors. © 1993 Wiley‐Liss, Inc.
Development of dopamine‐beta‐hydroxylase—positive fiber innervation in co‐cultured hippocampus‐locus coeruleus organotypic slices
Authors: Moudy Anna M. , Kunkel Dennis D. , Malouf Alfred T. , Schwartzkroin Philip A. 
Published: January 2005

AbstractDevelopment of the noradrenergic innervation of the rat hippocampus by the nucleus locus coeruleus was examined immunohistochemically in the roller tube organotypic cultured slice preparation. Slices of rat hippocampus and locus coeruleus were co‐cultured on glass coverslips for 2–6 weeks and evaluated for the presence of dopamine‐beta‐hydroxylase (DBH) and tyrosine hydroxylase (TH) immunoreactive cells and fibers. Large, multipolar DBH‐ and TH‐positive cells were visible within the locus coeruleus; an occasional cell appeared near or just within co‐cultured hippocampal tissue and in connecting fiber tracts. DBH‐positive cells tended to concentrate near the edges of locus coeruleus tissue. Locus coeruleus slices cultured alone showed little indication of fiber outgrowth in any direction. In co‐cultures, however, beaded DBH‐ and TH‐positive fibers were directed toward the hippocampus. The majority of these fibers entered the hippocampus in the hilar/CA3 region and formed extensive collateral branches. Light microscopy suggests that DBH‐positive fiber growth was densest at or near the pyramidal cell layer in CA3b and CA3c and in the infragranular region of the dentate hilus. This pattern of noradrenergic innervation of hippocampus by co‐cultured locus coeruleus in vitro appears very similar to the pattern established in vivo (see Moudy et al., companion article, this issue). © 1993 Wiley‐Liss, Inc.
GABAergic projection from the ventral pallidum and globus pallidus to the subthalamic nucleus
Authors: Bell Ken , Churchill Lynn , Kalivas Peter W. 
Published: January 2005

AbstractThere exists a topographically organized projection from the globus pallidus and ventral pallidum to the subthalamic nucleus and adjacent lateral hypothalamus. The participation of GABA as a neurotransmitter in this projection was evaluated by retrograde labeling of cells in the pallidal area from an iontophoretic deposit of Fluoro‐Gold in the subthalamus combined with in situ hybridization for mRNA of the GABA synthetic enzyme, glutamate decarboxylase (GAD). A rostrocaudal gradient in the contribution of GABA to the projection was demonstrated with a relatively small percentage of retrogradely labeled cells in the rostra1 ventral pallidum containing GAD mRNA (7%) compared to the caudal globus pallidus which had over 70% of the Fluoro‐Gold containing cells double‐labeled for GAD mRNA. Overall the ventral pallidum contribution to the subthalamic nucleus was less GABAergic than the portion arising from the globus pallidus (35% vs. 61%, respectively). © 1995 Wiley‐Liss, Inc.
Synaptic transmission blockade increases plasminogen activator activity in mouse skeletal muscle poisoned with botulinum toxin type A
Authors: Tian Wen‐Hao , Festoff Barry W. , Blot Stéphane , Diaz Jorge , Hantaï Daniel 
Published: January 2005

AbstractExperimental denervation, either by nerve crush or axotomy, leads to a dramatic increase in muscle plasminogen activator (PA) activity, suggesting a regulation of muscle PA levels by some neural influence (Festoff et al., 1986, J. Cell Biol., 103:1415–1421; Hantaï et al., 1990, Proc. Natl. Acad. Sci. U.S.A., 87:2926–2930). The Botulinum toxin (BoTx) type A is known to selectively interrupt the release of acetylcholine without structurally altering synaptic morphology. In the present study we have used acute BoTx poisoning of hind limb muscles to further explore the neural regulation of muscle PA activities directly after poisoning and during the process of collateral reinnervation. Electromyographic recording and study of ultraterminal sprouting after zinc iodideosmium and silver‐cholinesterase staining were used to monitor “denervation” and reinnervation. Muscle choline acetyltransferase activity did not decrease, as is observed after experimental denervation, but in contrast increased and, therefore, reflected the functional integrity of intramuscular nerve endings. Within 2 days of BoTx poisoning, muscle urokinase‐PA, and to a lesser extent, tissue‐PA activities, rose in muscle extracts as shown by an amidolytic assay and fibrin zymography. When reinnervation occurred, muscle urokinase‐PA activity decreased but did not return to baseline levels within the 80 days of our study. These results suggest that cholinergic transmission‐regulated events determine activity of muscle PAs and that PAs likely have a role in neuromuscular formation and plasticity. © 1995 Wiley‐Liss, Inc.
Increase in synaptic vesicle proteins in synapsin‐transfected NG108‐15 cells: A subcellular fractionation study
Authors: Fried Gabriel , Han Hui‐Quan 
Published: January 2005

AbstractWe have examined the subcellular distribution of synapsins and synaptophysin in density gradients from synapsin‐ and vector‐transfected NGlO8‐15 cells, since we recently found that transfection of synapsin IIb cDNA into neuroblastoma X glioma hybrid cells (NG108‐15) resulted in cell lines that had a more neuronal phenotype than controls. The increase in synapsins and synaptophysin in the transfected cells was maximal in the region of the gradient containing small synaptic vesicles. The transferrin receptor, a marker for early endosomes, did not increase in the synapsin‐containing fractions in the transfected cells. Secretogranin I, a soluble protein stored in and secreted from large dense cored vesicles, showed a very pronounced increase in the dense regions of gradients from transfected cells. These subcellular fractionation data suggest a possible role for the synapsins in the regulation of synaptic vesicle function. © 1995 Wiley‐Liss, Inc.
NMDA antagonists and clonidine block c‐fos expression during morphine withdrawal
Authors: Rasmussen Kurt , Brodsky Marina , Inturrisi Charles E. 
Published: January 2005

AbstractThe c‐fos gene is expressed in the central nervous system (CNS) in response to neuronal stimuli. Induction of c‐fos in certain CNS regions occurs following naltrexone precipitated withdrawal in morphine dependent rats. Non‐competitive (MK801) and competitive (LY274614) NMDA receptor antagonists and clonidine, an alpha2 partial agonist, attenuate the intensity of naltrexone precipitated withdrawal. We determined the levels of c‐fos mRNA by solution hybridization in several brain regions in control and morphine dependent rats following pretreatment with saline, MK801 (1 mg/kg, s.c.), LY274614 (100 mg/kg, i.p.), or clonidine (1.5 mg/kg, i.p.). Morphine treatment increased c‐fos mRNA levels in striatum (STR) and amygdala (AMY). Naltrexone did not alter c‐fos mRNA levels in placebo‐treated rats. However, naltrexone increased c‐fos mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord. Pretreatment with MK801 blocked this effect of naltrexone in AMY but not in NA, FC, or HIP, while pretreatment with LY274614 or clonidine blocked this effect of naltrexone in AMY and NA but not in FC or HIP. These results further delineate both the neuroanatomical pathways involved in morphine withdrawal and the locus of action of compounds that reduce morphine‐withdrawal symptoms. © 1995 Wiley‐Liss, Inc.