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Population Spike (population + spike)
Selected AbstractsElectrophysiological characterization of laminar synaptic inputs to the olfactory tubercle of the rat studied in vitro: modulation of glutamatergic transmission by cholinergic agents is pathway-specificEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2001G. S. Owen Abstract We have exploited the complementary arrangement of afferents in a coronal slice (300,400 µm) of the rat olfactory tubercle (OT) maintained in vitro to investigate transmission in two separate synaptic pathways. We recorded extracellular responses within the OT dense cell layer in slices and stimulated either the outermost layer to activate primary olfactory fibres or deeper to activate secondary input. Superficial stimulation produced a synaptic potential with superimposed population spike. This interpretation was based on blockade by calcium removal from the bathing medium and the use of the glutamate antagonist DNQX (10 µm); the spike was found to be selectively suppressed by tetrodotoxin applied near the cells. The spike, but not the synaptic wave, was depressed by 12 mm Ca2+ and enhanced by 1 mm Ba2+ in the bathing medium. Deep stimulation to activate association and intrinsic fibres elicited a nerve volley followed by a later response, also blocked by Ca2+ removal or 10 µm DNQX. It was unaffected by high Ca2+ or Ba2+, hence resulting from synaptic and not action current flow. Removal of Mg2+ from the bathing medium revealed an NMDA component of synaptic transmission at both loci that was selectively blocked by D-AP-5. The deep synaptic response, only, was depressed by carbachol IC50 7 µm or muscarine IC50 13 µm. This depression was also induced by AChE inhibitors eserine or tacrine and was antagonized by 1 µm atropine or 5,10 µm clozapine. These results characterize transmission in the OT and demonstrate a role for muscarinic modulation of deeper synapses in the OT that is influenced by psychotherapeutic drugs. [source] Parallel activation of field CA2 and dentate gyrus by synaptically elicited perforant path volleysHIPPOCAMPUS, Issue 8 2004Renata Bartesaghi Abstract Previous studies showed that dorsal psalterium (PSD) volleys to the entorhinal cortex (ENT) activated in layer II perforant path neurons projecting to the dentate gyrus. The discharge of layer II neurons was followed by the sequential activation of the dentate gyrus (DG), field CA3, field CA1. The aim of the present study was to ascertain whether in this experimental model field, CA2, a largely ignored sector, is activated either directly by perforant path volleys and/or indirectly by recurrent hippocampal projections. Field potentials evoked by single-shock PSD stimulation were recorded in anesthetized guinea pigs from ENT, DG, fields CA2, CA1, and CA3. Current source-density (CSD) analysis was used to localize the input/s to field CA2. The results showed the presence in field CA2 of an early population spike superimposed on a slow wave (early response) and of a late and smaller population spike, superimposed on a slow wave (late response). CSD analysis during the early CA2 response showed a current sink in stratum lacunosum-moleculare, followed by a sink moving from stratum radiatum to stratum pyramidale, suggesting that this response represented the activation and discharge of CA2 pyramidal neurons, mediated by perforant path fibers to this field. CSD analysis during the late response showed a current sink in middle stratum radiatum of CA2 followed by a sink moving from inner stratum radiatum to stratum pyramidale, suggesting that this response was mediated by Schaffer collaterals from field CA3. No early population spike was evoked in CA3. However, an early current sink of small magnitude was evoked in stratum lacunosum-moleculare of CA3, suggesting the presence of synaptic currents mediated by perforant path fibers to this field. The results provide novel information about the perforant path system, by showing that dorsal psalterium volleys to the entorhinal cortex activate perforant path neurons that evoke the parallel discharge of granule cells and CA2 pyramidal neurons and depolarization, but no discharge of CA3 pyramidal neurons. Consequently, field CA2 may mediate the direct transfer of ENT signals to hippocampal and extrahippocampal structures in parallel with the DG-CA3-CA1 system and may provide a security factor in situations in which the latter is disrupted. © 2004 Wiley-Liss, Inc. [source] Hierarchical model of the population dynamics of hippocampal dentate granule cellsHIPPOCAMPUS, Issue 5 2002G.A. Chauvet Abstract A hierarchical modeling approach is used as the basis for a mathematical representation of the population activity of hippocampal dentate granule cells. Using neural field equations, the variation in time and space of dentate granule cell activity is derived from the summed synaptic potential and summed action potential responses of a population of granule cells evoked by monosynaptic excitatory input from entorhinal cortical afferents. In this formulation of the problem, we have considered a two-level hierarchy: the synapses of entorhinal cortical axons define the first level of organization, and dentate granule cells, which include these synapses, define the second, higher level of organization. The model is specified by two state field variables, for membrane potential and for synaptic efficacy, respectively, with both evolving according to different time scales. The two state field variables introduce new parameters, physiological and anatomical, which characterize the dentate from the point of view of neuronal and synaptic populations: (1) a set of geometrical constraints corresponding to the morphological properties of granule cells and anatomical characteristics of entorhinal-dentate connections; and (2) a set of neuronal parameters corresponding to physiological mechanisms. Assuming no interaction between granule cells, i.e., neither ephaptic nor synaptic coupling, the model is shown to be mathematically tractable and allows solution of the field equations leading to the determination of activity. This treatment leads to the definition of two state variables, volume of stimulated synapses and firing time, which describe observed activity. Numerical simulations are used to investigate the populational characterization of the dentate by individual parameters: (1) the relationship between the conditions of stimulation of active perforant path fibers, e.g., stimulating intensity, and activity in the granule cell layer; and (2) the influence of geometry on the generation of activity, i.e., the influence of neuron density and synaptic density-connectivity. As an example application of the model, the granule cell population spike is reconstructed and compared with experimental data. Hippocampus 2002;12:698,712. © 2002 Wiley-Liss, Inc. [source] An improved brain slice model of nerve agent-induced seizure activityJOURNAL OF APPLIED TOXICOLOGY, Issue S1 2001Sebastien J. Wood Abstract A brain slice model was developed to investigate the mechanisms of seizure activity induced by soman and the effectiveness of potential anticonvulsant drugs. Unlike previously reported slice studies with nerve agents, this model contains the entorhinal cortex as well as the hippocampus. This allows the study of the spread of seizure discharges within the limbic system and the development of prolonged, sustained discharges that are rarely seen in the simple hippocampal slice preparation. Soman (1 µM) induced a second population spike in the evoked field potential in the CA1 or CA3 region within 15,20 min. In almost all the slices tested, this developed into spontaneous seizure activity within 30,40 min. As well as interictal bursts, many slices also showed longer periods of high-frequency bursting analogous to ictal seizure activity that originated in the entorhinal cortex. This activity appeared similar to that induced by the muscarinic agonist pilocarpine. Both the second population spike and the spontaneous discharges could be blocked by diazepam and by AMPA/kainate antagonists, but not by the NMDA antagonists AP5 and MK-801. This study confirms that the combined hippocampal,entorhinal cortex slice preparation is a suitable model for investigating the origin and propagation of nerve-agent-induced seizures within the limbic system. Copyright © 2001 John Wiley & Sons, Ltd. [source] Neuroprotection with caspase-9 inhbition against in vitro and in vivo traumaJOURNAL OF NEUROCHEMISTRY, Issue 2002R. A. Wallis Objective:, To evaluate the neuroprotective efficacy of the cell-permeable caspase-9 inhibitor, LEHD-CHO, against in vitro and in vivo traumatic neuronal injury. Methods:, The neuroprotective potential of LEHD-CHO was assessed in vitro using rat hippocampal slices. CA1 orthodromic and antidromic population spike (PS) amplitude was monitored before and after fluid percussion injury in slices treated with or without LEHD-CHO. Final recovery of PS amplitude was assessed 95 min after trauma. Studies of in vivo neuroprotection with LEHD-CHO utilized a model of controlled cortical impact (CCI). Rats were given either LEHD-CHO (10 nmol icv) or an equal volume of vehicle at 5 min following CCI. Rats were perfused 24 h after CCI and brains were processed for histological examination. Results:, LEHD-CHO provided significant protection against loss of CA1 evoked response after fluid percussion. The EC50 for LEHD-CHO protection of CA1 orthodromic and antidromic PS amplitude against trauma was 2.1 ,m and 2.3 ,m. Protection extended to preservation of LTP after trauma. In vivo treatment with LEHD-CHO significantly decreased the appearance of eosinophilic cells in the CA1 region after CCI from 131 ± 23 cells in vehicle-treated animals to 24 ± 5 in LEHD-CHO treated animals. Extensive labelling with TUNEL staining was seen in vehicle-treated animals, whereas sections from LEHD-CHO treated animals demonstrated little staining. Conclusions:, These findings indicate that the caspase 9 inhibitor LHED-CHO provides concentration-dependent protection against in vitro CA1 neuronal injury, which extends to protection against in vivo CA1 injury from CCI. They further suggest that inhibition of caspase 9 may be a useful treatment strategy for traumatic brain injury. Acknowledgement:, Supported by VA Research and UCLA BIRC. [source] Reduced signal transduction by 5-HT4 receptors after long-term venlafaxine treatment in ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2010R Vidal BACKGROUND AND PURPOSE The 5-HT4 receptor may be a target for antidepressant drugs. Here we have examined the effects of the dual antidepressant, venlafaxine, on 5-HT4 receptor-mediated signalling events. EXPERIMENTAL APPROACH The effects of 21 days treatment (p.o.) with high (40 mg·kg,1) and low (10 mg·kg,1) doses of venlafaxine, were evaluated at different levels of 5-HT4 receptor-mediated neurotransmission by using in situ hybridization, receptor autoradiography, adenylate cyclase assays and electrophysiological recordings in rat brain. The selective noradrenaline reuptake inhibitor, reboxetine (10 mg·kg,1, 21 days) was also evaluated on 5-HT4 receptor density. KEY RESULTS Treatment with a high dose (40 mg·kg,1) of venlafaxine did not alter 5-HT4 mRNA expression, but decreased the density of 5-HT4 receptors in caudate-putamen (% reduction = 26 ± 6), hippocampus (% reduction = 39 ± 7 and 39 ± 8 for CA1 and CA3 respectively) and substantia nigra (% reduction = 49 ± 5). Zacopride-stimulated adenylate cyclase activation was unaltered following low-dose treatment (10 mg·kg,1) while it was attenuated in rats treated with 40 mg·kg,1 of venlafaxine (% reduction = 51 ± 2). Furthermore, the amplitude of population spike in pyramidal cells of CA1 of hippocampus induced by zacopride was significantly attenuated in rats receiving either dose of venlafaxine. Chronic reboxetine did not modify 5-HT4 receptor density. CONCLUSIONS AND IMPLICATIONS Our data indicate a functional desensitization of 5-HT4 receptors after chronic venlafaxine, similar to that observed after treatment with the classical selective inhibitors of 5-HT reuptake. [source] Hippocampal synaptic transmission and LTP in vivo are intact following bilateral vestibular deafferentation in the ratHIPPOCAMPUS, Issue 4 2010Yiwen Zheng Abstract Numerous studies in animals and humans have shown that damage to the vestibular system in the inner ear results in spatial memory deficits, presumably because areas of the brain such as the hippocampus require vestibular input to accurately represent the spatial environment. Consistent with this hypothesis, studies in animals have demonstrated that complete bilateral vestibular deafferentation (BVD) causes a disruption of place cell firing as well as theta activity. The aim of this study was to investigate whether BVD in rats affects baseline field potentials (field excitatory postsynaptic potentials and population spikes) and long-term potentiation (LTP) in CA1 and the dentate gyrus (DG) of awake freely moving rats up to 43 days post-BVD and of anesthetized rats at 7 months post-BVD. Compared to sham controls, BVD had no significant effect on either baseline field potentials or LTP in either condition. These results suggest that although BVD interferes with the encoding, consolidation, and/or retrieval of spatial memories and the function of place cells, these changes are not related to detectable in vivo decrements in basal synaptic transmission or LTP, at least in the investigated pathways. © 2009 Wiley-Liss, Inc. [source] Fast Effects of Glucocorticoids on Memory-Related Network Oscillations in the Mouse HippocampusJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2008E. K. Weiss Transient or lasting increases in glucocorticoids accompany deficits in hippocampus-dependent memory formation. Recent data indicate that the formation and consolidation of declarative and spatial memory are mechanistically related to different patterns of hippocampal network oscillations. These include gamma oscillations during memory acquisition and the faster ripple oscillations (approximately 200 Hz) during subsequent memory consolidation. We therefore analysed the effects of acutely applied glucocorticoids on network activity in mouse hippocampal slices. Evoked field population spikes and paired-pulse responses were largely unaltered by corticosterone or cortisol, respectively, despite a slight increase in maximal population spike amplitude by 10 ,m corticosterone. Several characteristics of sharp waves and superimposed ripple oscillations were affected by glucocorticoids, most prominently the frequency of spontaneously occurring sharp waves. At 0.1 ,m, corticosterone increased this frequency, whereas maximal (10 ,m) concentrations led to a reduction. In addition, gamma oscillations became slightly faster and less regular in the presence of high doses of corticosteroids. The present study describes acute effects of glucocorticoids on sharp wave-ripple complexes and gamma oscillations in mouse hippocampal slices, revealing a potential background for memory deficits in the presence of elevated levels of these hormones. [source] Ethanol Attenuates the HFS-Induced, ERK-Mediated LTP in a Dose-Dependent Manner in Rat StriatumALCOHOLISM, Issue 1 2009Gui Qin Xie Background:, The striatum has been implicated to play a role in the control of voluntary behavior, and striatal synaptic plasticity is involved in instrumental learning. Ethanol is known to alter synaptic plasticity, in turn altering the behavior of human and animals. However, it remains unclear whether the striatum plays a role in the effects of ethanol on the central nervous system. The objective of this investigation was to study the effects of acute perfusion of ethanol on long-term potentiation (LTP) to elucidate the mechanisms of addictive drugs in the striatum. In addition, we investigated the contribution of intracellular extracellular signal regulated protein kinase (ERK) signaling pathway to corticostriatal LTP induction. Methods:, The stimulation evoked population spikes (PS) were recorded from the dorsomedial striatum (DMS) slices of rat using the extracellular recording technique. The LTP in DMS slices was induced by high-frequency stimulation (HFS). The ERK level of the DMS was assessed with the Western blot technique. Results:, U0126, the inhibitor of ERK, eliminated or significantly attenuated the LTP induced by HFS of the PS in the DMS. MK801 and APV, N -methyl- d -aspartic acid receptor (NMDAR) antagonists, inhibited the induction of striatal LTP, and HFS-induced ERK activation decreased in the slices treated with MK801 in the DMS. Clinically relevant concentrations of ethanol (22 to 88 mM) dose-dependently attenuated the HFS-induced striatal LTP and ERK activation in this brain region. Conclusions:, The LTP of the PS in the DMS is, at least partly, mediated by the ERK pathway coupling to NMDARs. Ethanol attenuated the HFS-induced, ERK-mediated LTP in a dose-dependent manner in this brain region. These results indicate that ethanol may change the synaptic plasticity of corticostriatal circuits underlying the learning of goal-directed instrumental actions, which is mediated by an intracellular ERK signaling pathway associated with NMDARs. [source] Alterations of Rat Corticostriatal Synaptic Plasticity After Chronic Ethanol Exposure and WithdrawalALCOHOLISM, Issue 5 2006Jian Xun Xia Background: The purpose of this study was to investigate the effects of chronic ethanol exposure (CEE) and withdrawal on corticostriatal plasticity in rats. Methods: We established an animal model of alcoholism using the method of Turchan et al. (1999). A synaptic model of long-term memory (long-term depression, LTD) was used as an index and the striatum, which is related to habit learning, was selected as a target region in the present study. The effects of CEE and withdrawal on the LTD were studied in striatal slices of ethanol-dependent rats using the extracellular recording method. Results: A stable LTD can be induced after high-frequency stimulation (HFS) in the slices of control rats. Chronic ethanol exposure and withdrawal suppressed the induction of corticostriatal LTD to different extents, with the strongest suppressive effects on LTD occurring in the slices of rats exposed to ethanol for 10 days and in those withdrawn from ethanol for 1 day. Notably, 3 days of withdrawal resulted in the shift of corticostriatal synaptic plasticity from LTD to long-term potentiation, and the peak latencies of the population spikes were obviously shortened compared with those of control rats. After 7 days of withdrawal, ethanol's effects tended to disappear. Conclusions: These results suggest that the alterations of corticostriatal synaptic plasticity produced by CEE and withdrawal may play a prominent role in alcohol abuse and alcoholism. [source] | |||||||||||||