bluuebunny/crossref_metadata_2025_split huggingface dataset:
NADPH Diaphorase‐Containing Nonpyramidal Cells in the Rat Hippocampus Exhibit Differential Sensitivity to Kainic Acid
Authors: Miettinen R. , Kotti T. , Halonen T. , Riekkinen P. 
Published: April 2006

AbstractNeurons containing nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase exhibit high resistance to several excitotoxins. In the neocortex and striatum, however, these neurons are sensitive to kainic acid. Here we report that, 2 weeks after i.p. injection of kainic acid, the number of NADPH diaphorase neurons in the hilus and CA1 subfield was decreased, whereas the cell counts in the other hippocampal areas were to a great extent similar to those for the controls. We propose that the loss of NADPH diaphorase neurons in the hippocampus after systemic injection of kainic acid is associated with the pathophysiological processes involved in the spreading of epileptic seizure activity rather than to the direct neurotoxic effect of the kainic acid per se.
Cerebral Energy Metabolism and Immediate Early Gene Induction Following Severe Incomplete Ischaemia in Transgenic Mice Overexpressing the Human Ornithine Decarboxylase Gene: Evidence that Putrescine is not Neurotoxic In Vivo
Authors: Lukkarainen Jouko , Kauppinen Risto A. , Koistinaho Jari , Halmekytö Maria , Alhonen Leena , Jänne Juhani 
Published: April 2006

AbstractCerebral ischaemia causes activation of ornithine decarboxylase followed by accumulation of putrescine, and these biochemical phenomena have been thought to contribute to the development of neuronal damage. We have used a transgenic mouse line overexpressing the human ornithine decarboxylase gene in their neurons with constitutively high putrescine to study the possible role of putrescine in development of neuronal damage in forebrain ischaemia. An incomplete forebrain ischaemia model was developed in which common carotid arteries were bilaterally occluded and reduction of blood pressure caused by orthostatic reaction was used as a way of decreasing cerebral circulation. Cerebral high‐energy metabolites, intracellular pH and lactate were monitored by means of 31P and 1H nuclear magnetic resonance spectroscopy respectively. Incomplete ischaemia for 15 min resulted in severe energy failure, as indicated by an increase in the inorganic phosphate/phosphocreatine ratio, intracellular acidification from a pH of ∼7.1 to ∼6.5 and an increase in lactate concentration from <1 to ∼10 mmol/kg in both syngenic and transgenic mice. Following deocclusion, recovery of energy metabolites, intracellular pH and lactate were identical in both animal groups. Ornithine decarboxylase activity rose 9‐ and 3‐fold in syngenic and transgenic mice respectively 6 h after ischaemia. Activation of ornithine decarboxylase resulted in extensive accumulation of putrescine in the brains of transgenic animals 12–24 h after ischaemia, which was ∼50‐fold greater than the basal level in syngenic mice. In situ hybridization experiments revealed induction of transcription factors c‐Fos and zif‐268 in the hippocampus, throughout the cerebral cortex and striatum 1–3 h after ischaemia. Messenger RNA of heat shock protein 70 was induced in dentate gyrus and CA3 and CA4 subfields of the hippocampus 1 h after ischaemia. The distribution and extent of induced mRNAs were similar in syngenic and transgenic animals. Histological evaluation did not reveal any difference between the two animal groups despite large variation in their cerebral putrescine content. Neuronal necroses were observed in the CA4 layer of hippocampi in both syngenic and transgenic mice. These data suggest that ornithine decarboxylase activation and accumulation of endogenous putrescine are indicative of an ischaemic insult and that these changes reflect an adaptive response rather than acting as causative factors of neuronal damage.
Neonatal Rat Cerebellar Granule and Purkinje Neurons in Culture Express Different GABAA Receptors
Authors: Zempel John Martin , Steinbach Joe Henry 
Published: April 2006

AbstractWe have established a culture system for microexplants of rat cerebellar cortical tissue in which cells develop morphologically, express type‐A receptors for the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) and form GABAergic synaptic connections. Criteria of cell size and shape allow reliable identification of granule and Purkinje neurons, criteria confirmed by studies of the binding of antibodies to calbindin D28K and GABA. Both granule and Purkinje neurons express GABAA receptors, but granule neurons fall into two classes in terms of their sensitivity. Granule neurons which do not show spontaneous synaptic currents are relatively insensitive to GABA, while granule neurons with synaptic currents are much more sensitive. The responses of Purkinje neurons to applications of 1 μM GABA are relatively insensitive to Zn2+ ions (10 μM), and are potentiated by chlordiazepoxide (100 μM) and La3+ ions (100 μM). Responses of innervated granule neurons, on the other hand, are blocked more strongly by Zn2+ ions, are less affected by chlordiazepoxide and are equally potentiated by La3+ ions. Hence these cultures provide a source of identifiable, functionally innervated cells which express distinct types of GABAA receptors.
Implication of a Nitric Oxide Synthase Mechanism in the Action of Substance P: L‐NAME Blocks Thermal Hyperalgesia Induced by Endogenous and Exogenous Substance P in the Rat
Authors: Radhakrishnan V. , Yashpal K. , Hui‐Chan C. W. Y. , Henry J. L. 
Published: April 2006

AbstractThe effects of i.p. administration of the nitric oxide synthase inhibitor NG‐nitro‐L‐arginine methylester (L‐NAME) and its inactive isomer, D‐NAME, were tested in two nociceptive paradigms in the rat. In the first paradigm, rats were lightly anaesthetized with a mixture of chloral hydrate (120 mg/kg, i.p.) and sodium pentobarbital (20 mg/ kg, i.p.). Tail flick reaction times were monitored and thermal hyperalgesia was induced by immersion of the tail in hot water at 55°C for 1.5 min. In the groups of rats pretreated with saline (n= 5), 100 mg/kg D‐NAME (n= 6), 10 (n= 5) or 25 (n= 6) mg/kg L‐NAME, this thermal injury induced a transient reduction in the reaction time that was 54–59% of the baseline value. However, in the groups of rats pretreated with 50 (n= 6) or 100 (n= 7) mg/kg L‐NAME the reaction times were 73.9 ± 2.7% (P < 0.05) and 102.3 ± 0.9% (P < 0.001) of the baseline values respectively, indicating a block of the hyperalgesic responses seen in the other groups. As this hyperalgesia has been reported to be blocked by NK‐1 receptor antagonists, it is suggested that it is due to the action of endogenous substance P. In the second paradigm, tail flick responses were monitored in the awake rat and thermal hyperalgesia was induced by intrathecal administration of substance P (6.5 nmol) via a chronically implanted catheter. In the group of rats pretreated with saline (n= 5) or D‐NAME (n= 5; 100 mg/kg), substance P reduced the reaction time to 39.1 ± 9.9 and 45.5 ± 2.1% of the baseline value respectively. However, in the rats pretreated with L‐NAME (n= 6; 100 mg/kg), the reaction time following substance P administration was 108.8 ± 8.8% of the baseline value (P < 0.001), indicating a block of the hyperalgesic response induced by substance P. These data indicate that thermal hyperalgesia induced by endogenously released or exogenously administered substance P, are blocked by L‐NAME but not by its enantiomer, D‐NAME. Therefore an involvement of a nitric oxide synthase mechanism in the hyperalgesic responses to substance P is suggested.
Miniature Endplate Current Kinetics at the Mouse Neuromuscular Junction: Effects of Temperature and Medium Viscosity
Authors: Tanzi Franco , D'Angelo Egidio 
Published: April 2006

AbstractThe time course of miniature endplate currents (MEPCs), derived by extracellular focal recording, was studied in the mouse neuromuscular junction at different temperatures and medium viscosities, and in eserine‐treated endplates. At low temperatures (6–10°C), almost the whole MEPC decay is exponential and the rising phase is not significantly modified by the channel closing process. At physiological temperatures (38–40°C), the early part of the decay is much slower than the later part and the rising phase is made shorter and smaller by channel closing, showing that the channel opening and channel closing processes overlap remarkably. Even at physiological temperatures, however, the late part of MEPC decay shows an exponential time course. At high temperatures the channel opening process has low temperature sensitivity and slows down when bath solution viscosity is increased, suggesting that at high temperatures channel opening kinetics may mainly be controlled by the time course of acetylcholine diffusion. The lower limit of conformational change rate leading to channel opening was estimated at 10°C (4400 s‐1). Experimentally recorded MEPCs were mathematically simulated to obtain a quantitative description of the processes controlling MEPC generation. Mathematical simulation further suggests that (i) acetylcholine diffusion kinetics may affect the onset rate of MEPCs without, however, being rate‐limiting; and (ii) partial, transient acetylcholinesterase inhibition operated by acetylcholine may explain the low temperature sensitivity exhibited by the onset rate of MEPCs at high temperatures.
Somatosensory Activations of the Parietal Operculum of Man. A PET Study
Authors: Ledberg Anders , O'Sullivan Brendan T. , Kinomura Shigeo , Roland Per E. 
Published: April 2006

AbstractWe tested the hypothesis that somatosensory discrimination of roughness (microgeometry) but not of shape (macrogeometry) would activate the parietal operculum (PO) in man. It was also investigated whether a simple square pulse indentation of the skin on the index finger would activate the PO. Regional cerebral blood flow was measured with [15O]butanol and positron emission tomography in a total of 20 normal volunteers. Ten subjects used their right hand to discriminate objects that differed in roughness and similar smooth objects that differed in length. Ten other subjects pressed a button when they felt a square pulse indentation of the skin on their right index finger in a somatosensory reaction time task. Discrimination of roughness activated one field in the PO contralaterally and two fields ipsilaterally to the stimulated hand. The discrimination of length activated one field in the PO located ipsilaterally to the stimulated hand. The somatosensory reaction time task also activated one contralateral and two ipsilateral fields in the PO, and these fields partially overlapped the activated fields in the roughness discrimination task. Based on the extension of these fields and their overlaps we conclude that there exist at least one part of the contralateral PO and at least two parts of the ipsilateral PO that can be activated by somatosensory stimulation of the right hand. We argue further that the contralateral activated part contains a region that can be activated by roughness.
In Vivo Modulation of Sigma Receptor Sites by Calcitonin Gene‐related Peptide in the Mouse and Rat Hippocampal Formation: Radioligand Binding and Electrophysiological Studies
Authors: Bouchard Pascale , Monnet François , Bergeron Richard , Roman François , Junien Jean‐Louis , de Montigny Claude , Debonnel Guy , Quirion Rémi 
Published: April 2006

AbstractPossible interactions between sigma (σ) receptor sites and calcitonin gene‐related peptides (CGRP) were investigated using receptor subtype‐related analogues and fragments in in vivo [3H](+)SKF 10 047/σ binding in the hippocampus, and electrophysiological recording of the N‐methyl‐D‐aspartate (NMDA)‐induced activation of CA3 pyramidal neurons, two well‐established σ assays. In both paradigms, CGRP and the agonist [Cys(ACM)2,7]hCGRPα modulated σ systems. In vivo binding experiments demonstrated that CGRP and [Cys(ACM)2,7]hCGRPα inhibited 25–40% of specific [3H](+)SKF 10 047 labelling in the mouse hippocampal formation while the purported antagonist hCGRP8–37 was inactive. The specificity of this modulation was demonstrated further by the lack of effect of other vasoactive peptides, including the atrial natriuretic peptide, substance P, and its N‐terminal fragment, substance P1–7. In the CA3 subfield of the rat dorsal hippocampus, hCGRPα decreased (up to 61%) the NMDA‐induced activation of the pyramidal neurons. Conversely, the linear analogue [Cys(ACM)2,7]hCGRPα enhanced (by 85%) the NMDA‐induced activation of CA3 pyramidal neurons, while the antagonistic fragment hCGRP8–37 had no effect. Haloperidol, a high‐affinity σ receptor ligand, inhibited by 90% the in vivo [3H](+)SKF 10 047 labelling, and prevented the modulation of the NMDA‐induced activation by hCGRPα and [Cys(ACM)2,7]hCGRPα. It thus appears that CGRP can modulate σ‐related systems in the hippocampal formation.
Properties of unitary IPSPs evoked by anatomically identified basket cells in the rat hippocampus
Authors: Buhl E. H. , Cobb S. R. , Halasy K. , Somogyi P. 
Published: April 2006

AbstractHippocampal pyramidal cells receive GABA‐mediated synaptic input from several distinct interneurons. In order to define the effect of perisomatic synapses, intracellular recordings were made with biocytin‐containing microelectrodes from synaptically connected inhibitory and pyramidal cell pairs in subfields CA1 and CA3 of the rat hippocampus. Subsequent physiological analysis was restricted to the category of cells, here referred to as basket cells (n= 14), which had an efferent synaptic target profile (n= 282 synaptic contacts) of predominantly somatic (48.2%) and proximal dendritic synapses (45.0%). Electron microscopic analysis revealed that in two instances identified postsynaptic pyramidal cells received a total of 10 and 12 labelled basket cell synapses respectively. At an average membrane potential of ‐57.8 ± 4.6 mV, unitary inhibitory postsynaptic potentials (IPSPs; n= 24) had a mean amplitude of 450 ± 238 μV, a 10–90% rise time of 4.6 ± 3.2 ms and, measured at half‐amplitude, a mean duration of 31.6 ± 18.2 ms. In most instances (n= 19) the IPSP decay could be fitted with a single exponential with a mean time constant of 32.4 ± 18.0 ms. Unitary basket cell‐evoked IPSPs fluctuated widely in amplitude, ranging from the level of detectability to <2 mV. The response reversal of IPSPs (n= 5) was extrapolated to be at ‐74.9 ± 6.0 mV. Averages of unitary IPSPs had a mean calculated conductance of 0.95 ± 0.29 nS, ranging from 0.52 to 1.16 nS. Unitary basket cell IPSPs (n= 3) increased in amplitude by 26.3 ± 19.9% following bath application of the GABAB receptor antagonist CGP 35845A (1–4 μM), whereas subsequent addition of the GABAA receptor antagonist bicuculline (10–13 μM) reduced the IPSP amplitude to 13.5 ± 3.1% of the control response. Rapid presynaptic trains of basket cell action potentials resulted in the summation of up to four postsynaptic responses (n= 5). However, any increase in the rate of tonic firing (2‐ to 10‐fold) led to a <50% reduction of the postsynaptic response amplitude. At depolarized membrane potentials, averaged IPSPs could be followed by a distinct depolarizing overshoot or postinhibitory facilitation (n= 4). At firing threshold, pyramidal cells fired postinhibitory rebound‐like action potentials, the latter in close temporal overlap with the depolarizing overshoot. In conclusion, hippocampal basket cells have been identified as one source of fast, GABAA receptor‐evoked perisomatic inhibition. Unitary events are mediated by multiple synaptic release sites, thus providing an effective mechanism to avoid total transmission failures.
The Axonal Arborization of Single Thalamic Reticular Neurons in the Somatosensory Thalamus of the Rat
Authors: Pinault Didier , Bourassa Jacques , Deschênes Martin 
Published: April 2006

AbstractThis study describes the axonal projections of single neurons of the thalamic reticular complex within the somatosensory thalamic nuclei in rats. Experiments were performed under urethane anaesthesia and reticular cells were labelled by extracellular microiontophoretic applications of biocytin. The axonal arborization of 25 thalamic reticular cells projecting to the ventrobasal (VB) nucleus and/or to the posterior thalamic (PO) complex were reconstructed from serial horizontal sections. Reticular cells labelled with biocytin display somatodendritic features similar to those reported previously. Their cell body is fusiform and their dendrites bear few spines and show a high degree of streaming along the horizontal curved axis of the nucleus. In most cells, axon‐like beaded processes stem out from dendrites but, contrary to previous descriptions, no intrareticular axonal collateral was observed. The axonal arborization of most thalamic reticular cells is confined within the limits of a single thalamic nucleus; only two neurons were seen projecting to both the VB and the Po nuclei. In VB, termination fields form short rods (diameter ∼ 150 μm, length ∼ 200‐300 μm) densely packed with grape‐like boutons and varicosities; termination fields in Po are larger, much less dense, and they are contained within a horizontal slab of tissue (thickness ∼ 200 μm, mediolateral width ∼ 400 μm, rostrocaudal length ∼ 1 mm. By charting the position of all labelled cells within the thickness of the thalamic reticular complex, a strip‐like arrangement was revealed. Cells projecting to Po occupy the innermost portion of the nucleus whereas those projecting to the ventral‐posteromedial and ventral‐posterolateral nuclei are located respectively in the middle and in the outer tiers of the nucleus. This strip‐like reciprocity was confirmed by separate biocytin injections performed in VB and in Po. These results show that inhibition of reticular origin is distributed within the rat dorsal thalamus in a highly specific manner, most likely according to a principle of reciprocity within the somatotopic representation of the body.
Associative Synaptic Potentials in the Piriform Cortex of the Isolated Guinea‐pig Brain In Vitro
Authors: Biella Gerardo , de Curtis Marco 
Published: April 2006

AbstractThe involvement of local and remote associative fibres in the generation of piriform cortex synaptic potentials was investigated in the isolated guinea‐pig brain maintained in vitro by arterial perfusion by implementing current source density analysis (CSD) on cortical field potential profiles. Previous hypotheses were verified using acute surgical isolation of piriform cortical areas to study different synaptic events separately. Stimulation of the lateral olfactory tract activated associative potentials throughout the piriform cortex. In the anterior piriform cortex, the current sinks responsible for the generation of associative potentials were located in the superficial portion of layer lb and in layer III. In the posterior piriform cortex, two associative events were observed: an early sink located in the superficial part of layer Ib, followed by a sink in the deep part of the same layer. In the anterior piriform cortex, local associative synaptic potentials were separated from the component carried by long projective fibres by surgically isolating a small area of cortex monosynaptically activated by lateral olfactory tract stimulation. In this patch of lateral olfactory tract‐connected anterior piriform cortex, local associative sinks were observed in the superficial lb layer and in layer III. Monosynaptic activation of the isolated patch of anterior piriform cortex induced purely associative potentials throughout the piriform cortex. These potentials were mediated by the synaptic activation of apical dendrites in the superficial lb layer and selectively abolished by severing the long associative fibres. The anterior piriform cortex layer III sink and the posterior piriform cortex deep lb associative component were evoked by the activation of large population spikes in the monosynaptic anterior piriform cortex and the disynaptic posterior piriform cortex response respectively. These two sinks are presumably generated locally through a polysynaptic circuit, whose activation depends on the degree of cortical excitation. Olfactory signal processing in the guinea‐pig piriform cortex during states of normal excitability is supported by the interactions between associative inputs impinging on the synapses located separately on the dendrites of pyramidal neurons. An increase in the synchronization of piriform cortex neuron discharge activates usually silent local circuit synapses.
Effect of Collicular Proteoglycan on the Survival of Adult Rat Retinal Ganglion Cells Following Axotomy
Authors: Huxlin Krystel R. , Dreher B. , Schulz M. , Sefton A. Jervie , Bennett M. R. 
Published: April 2006

AbstractConsistent with numerous previous studies, we have found that in adult rats 29% of cells retrogradely prelabelled by injections into retino‐recipient nuclei are lost 1 week after intraorbital section of the optic nerve. This figure increases to 76% 2 weeks after axotomy. Intraocular injections of 150 ng of 480 kda chondroitin sulphate proteoglycan purified from the superior colliculi of neonatal rats were performed every third day after axotomy. This procedure resulted in the loss of only 3 and 28% of the axotomized retinal ganglion cells 7 and 14 days respectively after optic nerve section. Intraocular injections of chondroitin sulphate type C, one of the sugar types present on the collicular proteoglycan, also resulted in a significant saving of axotomized ganglion cells (with the loss of only 48% 14 days after optic nerve lesion). These findings suggest that the collicular proteoglycan, and to a lesser extent its sugar moieties, substantially slows down the degeneration of adult retinal ganglion cells following axotomy.
Quantitative Comparison of the Transient Rescue Effects of Neurotrophic Factors on Axotomized Motoneurons In Vivo
Authors: Vejsada R. , Sagot Y. , Kato A. C. 
Published: April 2006

AbstractA reproducible neuronal degeneration induced by nerve lesion in neonatal rats or mice provides a convenient in vivo assay for testing the survival‐promoting activity of putative growth factors on motoneurons. The goal of this study was to compare the rescue effects of the four known neurotrophins [nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3) and neurotrophin‐4 (NT‐4)] and two of the cytokines [ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF)] in one particular experimental model of spinal motoneuron degeneration at two different survival times. The sciatic nerve was cut in neonatal rats and the factors were applied onto the nerve stump; bovine serum albumin was used in controls. Simultaneous application of the retrograde tracer fluoro‐gold made it possible to count motoneurons specifically in the sciatic pool. One week after lesion, the neurotrophins BDNF, NT‐3 and NT‐4, but not NGF, equally enhanced motoneuron survival compared to controls; their effects were significantly better than those of the cytokines. However, the rescue from cell death was only transitory because a great number of the motoneurons died during the second week after nerve lesion. Additional BDNF and/or CNTF supplied by repeated subcutaneous injections (1 mg/ml) over 2 weeks could not prevent this delayed motoneuron loss. These results suggest that still other factors or alternative routes of administration may be required for permanent rescue of the lesioned immature motoneurons.