bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accurate Synapse Regeneration Despite Ablation of the Distal Axon Segment
Authors: Mason Adrian , Muller Kenneth J. 
Published: April 2006

AbstractIn each body ganglion of the leech Hirudo medicinalis there is a single S‐cell. After an S‐cell axon is severed, it regenerates along its surviving distal segment and reconnects with its synaptic target, the axon of the neighbouring S‐cell. In approximately half the cases the regenerating axon forms a temporary electrical synapse specifically with the distal segment, which remains active and connected to the target, thereby functioning as a splice until regeneration is complete. To determine whether the distal axon segment is required for successful regeneration, distal segments of severed S‐cell axons were ablated by intracellular injection of bacterial protease. Fifty‐seven preparations were examined from 2 to 212 days after injection of the axon segment. The extent of S‐cell axon regeneration was assessed electrophysiologically by intracellular and extracellular recording, and anatomically by intracellular injection of markers followed by light microscopy and electron microscopy. The S‐cell axons regenerated successfully in almost 90% of animals examined after 2 weeks or more. In a further four animals the target S‐cell was ablated in addition to the distal axon segment, permanently disrupting conduction along the S‐cell pathway. Nevertheless, the regenerating axon grew along its usual pathway and there was no evidence that alternative connections were formed. It is concluded that, although the distal axon segment can provide a means for rapid functional repair, the segment is not required for reliable regeneration of the axon along its usual pathway and accurate formation of an electrical synapse.
Ontogenetic Development of 5‐HT1D Receptors in Human Brain: An Autoradiographic Study
Authors: del Olmo Elena , del Arco Carmen , Díaz Alvaro , Pascual Julio , Mengod Guadalupe , Palacios José M. , Pazos Angel 
Published: April 2006

AbstractThe pattern of pre‐ and postnatal appearance of 5‐HT1D receptors throughout the different areas of the human brain was studied by quantitative in vitro autoradiography, using [125I]GTI (serotonin O‐carboxymethyl‐glycyl‐[125I]tyrosinamide) as a ligand. The anatomical distribution of 5‐HT1D receptors in neonatal, infant and children's brain was in good agreement with that observed in the adult, the basal ganglia and substantia nigra being the most intensely labelled areas. The development of these receptors throughout the human brain was mainly postnatal: low densities of [125I]GTI binding sites were observed at the fetal/neonatal stage in most regions analyzed, in contrast with the high levels of labelling found in infant and children's brains. Indeed, in a number of regions, including the globus pallidus, substantia nigra and visual cortex, a peak of overexpression of 5‐HT1D receptors was observed in the first decade of life. Such overexpression could support a regulatory role for 5‐HT1D receptors in advanced periods of the CNS developmental process. Our results also indicate that the administration of drugs acting on 5‐HT1D receptors during the early postnatal period of life could result in modifications of their properties, as these receptors are already functional in this period.
Further Observations on the Role of Nitric Oxide in the Feline Lateral Geniculate Nucleus
Authors: Cudeiro J. , Rivadulla C. , Rodriguez R. , Martinez‐Conde S. , Martinez L. , Grieve K. L. , Acuña C. 
Published: April 2006

AbstractWe have examined the responses of a population of 77 cells in the dorsal lateral geniculate nucleus (dLGN) of the anaesthetized, paralysed cat. Here the synthetic enzyme for the production of nitric oxide, nitric oxide synthase, is found only in the presynaptic terminals of the cholinergic input from the brainstem. In our hands, iontophoretic application of inhibitors of this enzyme resulted both in significant decreases in visual responses and decreased responses to exogenous application of NMDA, effects which were reversed by coapplication of the natural substrate for nitric oxide synthase, L‐arginine, but not the biologically inactive isomer, D‐arginine. Nitroprusside and S‐nitroso‐N‐acetylpenicillamine (SNAP), nitric oxide donors, but not L‐arginine, were able to increase markedly both spontaneous activity and the responsiveness to NMDA application. Furthermore, SNAP application facilitated visual responses. Responses of cells in animals without retinal, cortical and parabrachial input to the LGN suggest a postsynaptic site of action of nitric oxide. This modulation of the gain of visual signals transmitted to the cortex suggests a completely novel pathway for nitric oxide regulation of function, as yet described only in primary sensory thalamus of the mammalian central nervous system.
Neurotensin Excitation of Serotonergic Neurons in the Dorsal Raphe Nucleus of the Rat In Vitro
Authors: Jolas Thierry , Aghajanian George K. 
Published: April 2006

AbstractNeurotensin‐containing terminals and radioligand binding sites are present in the dorsal raphe nucleus. The purpose of this study was to test, in brain slices containing this nucleus, the effect of neurotensin on the electrical activity of serotonergic neurons. In extracellular recordings, the cells were identified by the ability of the α1‐adrenoceptor agonist phenylephrine to induce firing, and serotonin to reduce this effect. After washout of phenylephrine, neurotensin (10 nM to 10 μM) induced a concentration‐dependent increase in the firing rate of serotonergic neurons (EC50= 142 nM; maximum effect ˜1 μM). The neurotensin excitation, which was mimicked by neurotensin fragments 8–13 but not neurotensin peptide fragment 1–8 and selectively blocked by SR 48692 (100 nM), was observed mainly in the ventral part of the nucleus. Most serotonergic neurons showed marked desensitization to neurotensin, even at low concentrations. The neurotensin response was occluded by supramaximal concentrations of phenylephrine. In intracellular recordings using KCl‐containing electrodes, neurotensin induced an inward current associated in some cases with a decrease in apparent input conductance. In conclusion, neurotensin was found to have an excitatory action on serotonergic neurons in the ventral part of the dorsal raphe nucleus, an effect which could be subject to desensitization and was occluded by phenylephrine. This occlusion phenomenon may be important for the physiological role of neurotensin in the dorsal raphe nucleus.
Differential Oscillatory Properties of Cholinergic and Non‐cholinergic Nucleus Basalis Neurons in Guinea Pig Brain Slice
Authors: Alonso Angel , Khateb Asaid , Fort Patrice , Jones Barbara E. , Mühlethaler Michel 
Published: April 2006

AbstractEvidence has suggested that the nucleus basalis magnocellularis has the potential to influence the functional state of the cerebral cortex through topographically organized, widespread projections of the cholinergic cells in that nucleus. It has also been shown that, in addition to the cholinergic neurons, other non‐cholinergic magnocellular basal forebrain neurons, some of which have been identified as gamma‐aminobutyric acid‐ergic, project into the cerebral cortex and thus may also participate in the modulation of its activity. We have performed a comparative study of the intrinsic rhythmic properties of immunohistochemically and morphologically characterized choline acetyltransferase (ChAT)‐positive and ChAT‐negative cells of the nucleus basalis by means of intracellular recordings in guinea pig brain slices. Our results demonstrate that relatively large, multipolar cholinergic and non‐cholinergic neurons each display differential voltage‐dependent properties that allow them to discharge rhythmically in spike bursts and spike clusters, respectively, at low frequencies (<10 Hz). Cholinergic cells display bursts of 2–4 action potentials (at ‐200 Hz) riding on low‐threshold spikes recurring at a low frequency (<5 Hz) when depolarized from a membrane potential more negative than ‐55 mV and display low‐frequency (<10–15 Hz) tonic firing when depolarized from a more positive level. In contrast, non‐cholinergic cells fire in a unique mode, displaying non‐adapting clusters of spikes interspersed with rhythmic subthreshold membrane‐potential oscillations when depolarized from levels less negative than ‐55 mV. The spike clusters repeat rhythmically at relatively low frequencies (2–10 Hz). The intracluster spiking frequency is relatively high and coincides approximately with that of the intervening membrane‐potential oscillations (‐20–70 Hz). The cluster frequency of the non‐cholinergic cells corresponds, in the same manner as the burst frequency of the cholinergic cells, to a delta (1–4 Hz) or theta (4–10 Hz) range of activity, whereas the intra‐cluster and tonic spike frequencies of the non‐cholinergic cells correspond to high beta to gamma ranges of electroencephalographic activity (19–30 Hz and 30–60 Hz, respectively). We propose that the different modes of oscillatory firing by the cholinergic and non‐cholinergic basal forebrain cell populations could collectively contribute to the rhythmic modulation of slow and fast rhythms within the cerebral cortex.
Unique Distribution of Somatostatin‐immunoreactive Cells in the Retina of the Tree Shrew (Tupaia belangeri)
Authors: Engelmann Ralf , Peichl Leo 
Published: April 2006

AbstractSomatostatin‐like immunoreactive cells in the tree shrew retina were studied with the monoclonal antibody S8 against the neuropeptide somatostatin 14. As in some other mammals, immunoreactive somata are exclusively found in the ganglion cell layer. Immunoreactive processes form a sparse main plexus in the inner plexiform layer near the border of the inner nuclear layer; fewer additional processes are found closer to the ganglion cell layer. With retrograde labelling of retinal ganglion cells by injections of the tracer Fast Blue into the superior colliculus and lateral geniculate body and counterstaining of the retinae with S8, ˜5% of the immunoreactive somata were double‐labelled at any retinal location. The vast majority of somatostatin‐like immunoreactive cells are thus displaced amacrine cells. Their somata are distributed over the entire retina. Their population density is highest in the temporal retina, with peak densities of ˜5000 cells/mm2 near the central area and a steep density gradient. In the remaining retina densities are 200–400 cells/mm2, falling to ˜100 cells/mm2 at the retinal margins. This is in stark contrast to the somatostatin‐like immunoreactive cells in other mammalian retinae which have densities of 10–40 cells/mm2 and are confined to restricted retinal regions (inferior retina and/or retinal margin).
Copper Modulation of NMDA Responses in Mouse and Rat Cultured Hippocampal Neurons
Authors: Vlachová Viktorie , Zemková Hana , Vyklický Ladislav 
Published: April 2006

AbstractThe effect of Cu2+ on NMDA receptors was studied in cultured mouse and rat hippocampal neurons using whole‐cell patch‐clamp and a fast perfusion system. Analysis of the Cu2+ concentration‐response curve for inhibition of NMDA‐induced currents suggests that free Cu2+ directly inhibits NMDA receptors with an IC50 of 0.27 μM. Cu2+ was ineffective in blocking NMDA receptor activity when complexed with NMDA or glycine; NMDA‐Cu2+ and glycine‐Cu2+ complexes acted as agonists of similar potency to the free amino acids. The inhibition by Cu2+ (10–100 μM) of responses to 10 μM NMDA was essentially voltage‐independent. The onset of inhibition by 100 μM Cu2+ of responses to 2 FM glutamate acting at NMDA receptors was significantly faster than NMDA receptor deactivation evoked by a sudden decrease in the concentration of glycine or glutamate, or of both agonists. This suggests that CU2+ acts as a non‐competitive antagonist, and does not directly interfere with the binding of glutamate or glycine to their recognition sites on the NMDA receptor complex. In the absence of NMDA the apparent association rate constant for binding of Cu2+ to NMDA receptors, calculated from the rate of onset of block by Cu2+ of test responses to NMDA, was 19 times slower than in the presence of 30 μM NMDA, suggesting that Cuz+ interacts preferentially with agonist‐bound receptors. Our results show that Cu2+ is a potent inhibitor of NMDA receptor‐mediated responses.
Immunohistochemical Localization of Dopamine D Receptors in Rat Retina
Authors: Veruki Margaret L. , Wässle Heinz 
Published: April 2006

AbstractWe have localized the dopamine D1 receptor in rat retina using a subtype‐specific monoclonal antibody. Immunolabelling can be detected in the inner and outer plexiform layers and in a number of cells in the inner nuclear layer. In the inner plexiform layer, labelled processes form four distinct horizontal bands and a series of patches. In order further to characterize the labelling pattern of the D1 receptor antibody, double‐labelling experiments were performed with antibodies against population‐specific neuronal markers in the retina. Antibodies against tyrosine hydroxylase. choline acetyltransferase, calretinin, calbindin, the glutamate transporter GLT‐I, protein kinase C, recoverin and parvalbumin were co‐applied with the D, receptor antibody. With these cell markers we demonstrate that horizontal cells, at least three types of cone bipolar cells and a small number of amacrine cells are immunolabelled for the D1 receptor. In the inner plexiform layer, processes labelled by the D1 receptor antibody are co‐stratified with processes labelled by the GLT‐1 antibody. D1 receptor‐labelled processes are not co‐localized with the processes of amacrine cells and ganglion cells labelled by antibodies against tyrosine hydroxylase, choline acetyltransferase or calretinin. Our results indicate that dopamine Dl receptors are localized predominantly to horizontal cells and cone bipolar cells. Furthermore, the spatial disparity between dopaminergic processes and the site of the majority of D1 receptors supports the idea that in the retina dopamine acts as a neuromodulator that diffuses through extracellular space. The localization of D1 receptors to a number of identified cell types enables future physiological work to be directed towards specific synaptic circuits within the retina.
Cholera and Pertussis Toxins Reveal Multiple Regulation of cAMP Levels in the Rabbit Carotid Body
Authors: Cachero T. G. , Rigual R. , Rocher A. , Gonzalez C. 
Published: April 2006

AbstractIt is known that hypoxia (PO2∼66–18 mm Hg), acting via unknown receptors, increases carotid body cAMP levels in Ca2+‐free solutions, indicating that low PO2 activates adenylate cyclases independently of the action of the released neurotransmitters. The aim of the present work was to investigate the involvement of G proteins in the genesis of the basal level of cAMP and on the increase in cAMP induced by low P02. In carotid body homogenates, cholera toxin‐ and pertussis toxin‐induced [32P] ADP‐ribosylation of two protein bands of =42 and 45 kDa, and =39 and 40 kDa respectively; in both cases, prior incubation of the carotid bodies with the toxins reduced [32P] ADP‐ribosylation by >90%. In intact carotid bodies, cholera toxin treatment increased cAMP levels more in normoxic than in hypoxic organs, indicating that hypoxia releases neurotransmitters acting on receptors negatively coupled to adenylate cyclases. Cholera toxin‐treated carotid bodies incubated in Ca2+‐free solution had identical cAMP levels in normoxia and in hypoxia. In pertussis toxin‐treated normoxic carotid bodies the cAMP level was close to control, but in pertussis toxin‐treated hypoxic carotid bodies cAMP rose to a level similar to those seen in normoxic cholera toxin‐treated organs, indicating that low PO2 releases neurotransmitters acting on receptors positively coupled to adenylate cyclases. Pertussis toxin‐treated carotid bodies incubated in Ca2+‐free solution lost their capacity to increase cAMP in response to hypoxia, indicating that a G protein sensitive to pertussis toxin is needed for this response. This implies that the carotid bodies express a pertussis toxin‐sensitive G protein positively coupled to adenylate cyclases, or that a Gs protein requiring the cooperative action of Go/Gi donated by subunits mediates the increase in cAMP level produced by hypoxia.
Colocalization of Oestrogen Receptor lmmunoreactivity and Preproenkephalin mRNA Expression to Neurons in the Superficial Laminae of the Spinal and Medullary Dorsal Horn of Rats
Authors: Amandusson Åsa , Hermanson Ola , Blomqvist Anders 
Published: April 2006

AbstractA double‐labelling procedure combining immunohistochemical staining with in situ hybridization using a radiolabelled cRNA probe was employed to demonstrate oestrogen receptor‐like immunoreactivity and preproenkephalin‐A mRNA in the medullary and spinal dorsal horn of female rats. Both markers labelled large numbers of neurons in the substantia gelatinosa and its trigeminal homologue. Many of these neurons were double‐labelled, displaying both oestrogen receptor‐like‐ immunoreactivity and preproenkephalin‐A mRNA; cell counts showed that 40–60% of the of the oestrogen receptor‐like‐immunoreactive cells in the superficial laminae also were labelled for preproenkephalin‐A mRNA, and that 60–70% of the preproenkephalin‐A mRNA‐labelled neurons in the same laminae displayed oestrogen receptor‐like immunoreactivity. Previous studies have shown that oestrogen receptors can bind to the promoter region of the preproenkephalin‐A gene, and studies on the hypothalamus have demonstrated that oestrogen regulates enkephalin expression in select neuronal populations. The present results demonstrate that enkephalinergic neurons in the superficial dorsal horn contain oestrogen receptors and suggest that oestrogen may play an important role in the modulation of sensory and nociceptive processing in the lower medulla and spinal cord.
Macrophage Inflammatory Protein‐1β (MIP‐1β) Produced Endogenously in Brain During E. coli Fever in Rats
Authors: Miñano Francisco J. , Fernández‐Alonso Antonio , Benamar Khalid , Myers R. D. , Sancibrián Manuel , Ruiz Rosa M. , Armengol José A. 
Published: April 2006

AbstractMacrophage inflammatory protein‐1 (MIP‐1) evokes an intense fever, independent of a prostaglandin mechanism, and is now thought to play an important role in the defence response to bacterial pyrogens. The purpose of this study was 2‐fold: (i) to determine whether the potent doublet of this cytokine, MIP‐1β, is actually produced in the brain in response to a pyrogenic dose of a lipopolysaccharide of Escherichia coli and (ii) to determine the anatomical site of synthesis of this cytokine in the brain. Following the intense fever produced by intraperitoneal administration of lipopolysaccharide in the unrestrained rat, MIP‐1β immunoreactivity was identified post mortem in two regions of the brain implicated in fever: the organum vasculosum laminae terminalis (OVLT) and the anterior hypothalamic, preoptic area (AH/POA). Microinjection of goat anti‐mouse MIP‐1β antibody (anti‐MIP‐1β) directly into the AH/POA markedly suppressed fever in rats in response to lipopolysaccharide. Further, anti‐MIP‐1β administered 180 min after the injection of lipopolysaccharide acted as an antipyretic and reversed the fever induced by the endotoxin. Anti‐MIP‐1β or control immunoglobulin G antibody microinjected into the hypothalamus immediately before the intraperitoneal injection of the control saline did not alter the temperature of the rats. Taken together, the present results demonstrate that MIP‐1β is produced in the brain in response to a bacterial endotoxin. These observations, in the light of earlier data on fever induced by MIP‐1β, further support the hypothesis that endogenously synthesized MIP‐1β acts as an intermediary factor in the evocation of fever by acting on the thermosensitive cells of the brain.
Differential Effects of an L‐type Ca2+ Channel Antagonist on Activity‐ and Phosphorylation‐enhanced Release of Acetylcholine at the Neuromuscular Junction of the Frog In Vitro
Authors: Arenson M. S. , Gill D. S. 
Published: April 2006

AbstractThe effects of the selective L‐type Ca2+‐channel antagonist nimodipine on changes in the electrophysiological correlates of acetylcholine release induced by activity in the motor nerve or by inhibition of protein dephosphorylation were studied in the isolated sartorius muscle of the frog. Nimodipine (1 μM) had no effect on basal miniature endplate potential (mEPP) frequency or on the quantal content of the endplate potential (EPP) evoked at 0.33 Hz. Stimulation of the motor nerve at frequencies of 20, 40 and 50 Hz progressively increased the quantal content and at 50 Hz caused an increase in mEPP frequency measured at the end of the train. Nimodipine (1 μM) had no effect on the change in either parameter caused by activity in the motor nerve. The L‐channel agonist BAYK 8644 had inconsistent effects, causing at 0.33 Hz an increase in quantal content at 55% of the neuromuscular junctions examined. Application of the phosphatase inhibitor okadaic acid (1 μM) caused an increase in miniature endplate potential and/or current [mEPP(C)] frequency but not in quantal content. The increase in spontaneous frequency was reduced by the Ca2+‐channel blockers nimodipine (1 μM) and cadmium (75 μM). The amplitude of mEPP(C)s was increased by okadaic acid (1 μM), but neither the decay time constant of miniature endplate currents (mEPC) nor the amplitude of endplate currents evoked by iontophoretic application of carbachol was so altered. The activity of electric eel acetylcholinesterase was unchanged by okadaic acid. The present data do not support the concept that the recruitment of normally silent L‐type Ca2+‐channels contributes to activity‐dependent increases in acetylcholine release. The results obtained with okadaic acid suggest that protein phosphorylation and dephosphorylation may regulate the activity of L‐type channels and the packaging of acetylcholine.
Correlations between Water Maze Performance and Cortical Somatostatin mRNA and High‐affinity Binding Sites During Ageing in Rats
Authors: Dournaud Pascal , Jazat‐Poindessous Frédérique , Slama Annie , Lamour Yvon , Epelbaum Jacques 
Published: April 2006

AbstractSomatostatin levels and high‐affinity (somatostatin‐1) binding sites are decreased in post‐mortem cortical samples of Alzheimer's disease patients but the relationships between such modifications and the cognitive deficits remain to be established. We investigated these relationships in the ageing rat. Three age groups (3–4, 14–15 and 26–27 months) were tested in a modified version of the Morris water maze. Somatostatin mRNA levels were quantified by in situ hybridization and somatostatin binding sites by radioautography using the selective agonist octreotide (SMS 201995) as a competing drug to evaluate high‐affinity (somatostatin‐1) and low‐affinity (somatostatin‐2) binding sites. The number of somatostatin mRNA‐containing cells was not modified with age or memory performance in cortical, hippocampal and hypothalamic regions, but somatostatin mRNA densities were significantly decreased with age and with memory performance in the frontal and parietal cortex. In the frontal cortex somatostatin mRNA densities were already decreased in 14‐ to 15‐month‐old rats, whereas the decrease was observed only in 26‐ to 27‐month‐old rats in the parietal cortex. A decrease in somatostatin‐1 binding was observed with memory performance, independently of age, in the basolateral amygdala only, while somatostatin‐2 binding sites were not affected. In the frontal and parietal cortex, a significant correlation occurred between the latency to find the invisible platform in the water maze and somatostatin mRNA (r= ‐0.54 and 0.59 respectively, P > 0.02). These results indicate that ageing rats with memory impairments display some of the features of the somatostatinergic deficits observed in Alzheimer's disease.