bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somatostatin receptor subtypes 2 and 4 affect seizure susceptibility and hippocampal excitatory neurotransmission in mice
Authors: Moneta D. , Richichi C. , Aliprandi M. , Dournaud P. , Dutar P. , Billard J. M. , Carlo A. S. , Viollet C. , Hannon J. P. , Fehlmann D. , Nunn C. , Hoyer D. , Epelbaum J. , Vezzani A. 
Published: March 2003

AbstractWe have investigated the role of somatostatin receptor subtypes sst2 and sst4 in limbic seizures and glutamate‐mediated neurotransmission in mouse hippocampus. As compared to wild‐type littermates, homozygous mice lacking sst2 receptors showed a 52% reduction in EEG ictal activity induced by intrahippocampal injection of 30 ng kainic acid (P < 0.05). The number of behavioural tonic–clonic seizures was reduced by 50% (P < 0.01) and the time to onset of seizures was doubled on average (P < 0.05). Seizure‐associated neurodegeneration was found in the injected hippocampus (CA1, CA3 and hilar interneurons) and sporadically in the ipsilateral latero‐dorsal thalamus. This occurred to a similar extent in wild‐type and sst2 knock‐out mice. Intrahippocampal injection of three selective sst2 receptor agonists in wild‐type mice (Octreotide, BIM 23120 and L‐779976, 1.5–6.0 nmol) did not affect kainate seizures while the same compounds significantly reduced seizures in rats. L‐803087 (5 nmol), a selective sst4 receptor agonist, doubled seizure activity in wild‐type mice on average. Interestingly, this effect was blocked by 3 nmol octreotide. It was determined, in both radioligand binding and cAMP accumulation, that octreotide had no direct agonist or antagonist action at mouse sst4 receptors expressed in CCl39 cells, up to micromolar concentrations. In hippocampal slices from wild‐type mice, octreotide (2 µm) did not modify AMPA‐mediated synaptic responses while facilitation occurred with L‐803087 (2 µm). Similarly to what was observed in seizures, the effect of L‐803087 was reduced by octreotide. In hippocampal slices from sst2 knock‐out mice, both octreotide and L‐803087 were ineffective on synaptic responses. Our findings show that, unlike in rats, sst2 receptors in mice do not mediate anticonvulsant effects. Moreover, stimulation of sst4 receptors in the hippocampus of wild‐type mice induced excitatory effects which appeared to depend on the presence of sst2 subtypes, suggesting these receptors are functionally coupled.
Speech processing activates visual cortex in congenitally blind humans
Authors: Röder Brigitte , Stock Oliver , Bien Siegfried , Neville Helen , Rösler Frank 
Published: March 2003

AbstractNeurophysiological recordings and neuroimaging data in blind and deaf animals and humans suggest that perceptual functions may be organized differently after sensory deprivation. It has been argued that neural plasticity contributes to compensatory performance in blind humans, such as faster speech processing. The present study employed functional magnetic resonance imaging (fMRI) to map language‐related brain activity in congenitally blind adults. Participants listened to sentences, with either an easy or a more difficult syntactic structure, which were either semantically meaningful or meaningless. Results show that blind adults not only activate classical left‐hemispheric perisylvian language areas during speech comprehension, as did a group of sighted adults, but that they additionally display an activation in the homologueous right‐hemispheric structures and in extrastriate and striate cortex. Both the perisylvian and occipital activity varied as a function of syntactic difficulty and semantic content. The results demonstrate that the cerebral organization of complex cognitive systems such as the language system is significantly shaped by the input available.
The integrative role of the rat medullary subnucleus reticularis dorsalis in nociception
Authors: Monconduit L. , Desbois C. , Villanueva L. 
Published: March 2003

AbstractNeurons within the medullary subnucleus reticularis dorsalis (SRD) of the rat convey selectively nociceptive information from all parts of the body. We have sought to define the neuronal networks that convey information from widespread noxious stimuli to the diffuse thalamocortical system and also modulate spinal outflow. The experiments, which were performed in rats, were designed to determine whether efferents from the SRD issue collaterals to the thalamus and spinal cord. Injections of the tracers fluorogold and tetramethylrhodamine‐labelled dextran were centred stereotaxically in two areas that receive dense projections from the SRD: the cervical spinal cord and the lateral ventromedial thalamus (VMl), respectively. In other experimental series, SRD neurons were characterized electrophysiologically and individually labelled in a Golgi‐like manner following juxtacellular iontophoresis of biotin–dextran. More than half reticulothalamic neurons within the SRD provided monosynaptic connections to the spinal cord. SRD neurons that responded to Aδ‐ or Aδ‐ and C‐fibre activation from any area of the body had axons that gave both ascending and descending collaterals. Because the SRD innervates several areas involved in motor processing and receives strong, direct influences from several cortical regions, it could provide a structural basis for the processing of nociceptive and motor activities.
Connexin29 expression, immunocytochemistry and freeze‐fracture replica immunogold labelling (FRIL) in sciatic nerve
Authors: Li Xinbo , Lynn B. D. , Olson C. , Meier C. , Davidson K. G. V. , Yasumura T. , Rash J. E. , Nagy J. I. 
Published: March 2003

AbstractThe recently discovered connexin29 (Cx29) was reported to be present in the central and peripheral nervous systems (CNS and PNS), and its mRNA was found in particular abundance in peripheral nerve. The expression and localization of Cx29 protein in sciatic nerve were investigated using an antibody against Cx29. The antibody recognized Cx29 in HeLa cells transfected with Cx29 cDNA, while nontransfected HeLa cells were devoid of Cx29. Immunoblotting of sciatic nerve homogenate revealed monomeric and possibly higher molecular weight forms of Cx29. These were distinguished from connexin32 (Cx32), which also is expressed in peripheral nerve. Double immunofluorescence labelling for Cx29 and Cx32 revealed only partial colocalization of the two connexins, with codistribution at intermittent, conical‐shaped striations along nerve fibers. By freeze‐fracture replica immunogold labelling (FRIL), Cx32 was found in gap junctions in the outermost layers of myelin, whereas Cx29‐immunogold labelling was found only in the innermost layer of myelin in close association with hexagonally arranged intramembrane particle (IMP) ‘rosettes’ and gap junction‐like clusters of IMPs. Although both Cx32 and Cx29 were detected in myelin of normal mice, only Cx29 was present in Schwann cell membranes in Cx32 knockout mice. The results confirm that Cx29 is a second connexin expressed in Schwann cells of sciatic nerve. In addition, Cx29 is present in distinctive IMP arrays in the inner most layer of myelin, adjacent to internodal axonal plasma membranes, where this connexin may have previously unrecognized functions.
5‐HT4 receptors exert a frequency‐related facilitatory control on dorsal raphé nucleus 5‐HT neuronal activity
Authors: Lucas Guillaume , Debonnel Guy 
Published: March 2003

AbstractWe investigated, using single‐unit recordings in chloral hydrate‐anaesthetized rats, the role of serotonin4 (5‐HT4) receptors in the control of dorsal raphé nucleus (DRN) 5‐HT neuron activity. About one‐half (36) of the 76 neurons recorded were affected by either the preferential 5‐HT4 agonist cisapride (500 and 1000 µg/kg, i.v.) or the selective 5‐HT4 antagonist, GR 125487 (200– 2000 µg/kg, i.v.). Responding neurons displayed a significantly higher mean basal firing rate (1.93 ± 0.1 Hz) than non‐responders (1.31 ± 0.1 Hz). The firing rate of responding 5‐HT neurons was enhanced dose‐dependently by cisapride (+47 and +94% at 500 and 1000 µg/kg, respectively), an effect abolished by GR 125487 (500 µg/kg) and reduced by the 5‐HT4 antagonist, SDZ 205557 (500 µg/kg, i.v). Conversely, GR 125487 induced a dose‐dependent inhibition of responders activity, which was almost completely suppressed at the dose of 2000 µg/kg. In a separate set of experiments, the selective 5‐HT4 agonist, prucalopride (500 µg/kg, i.v), increased the firing activity (+35%) of 5‐HT neurons displaying a high basal firing rate; subsequent injection of GR 125487 (500 µg/kg, i.v.) suppressed this effect. These results indicate that 5‐HT4 receptors exert both a tonic and a phasic, positive, frequency‐related control on DRN 5‐HT neuronal activity. The existence of such a control might open new avenues for therapeutic research in the antidepressant field.
Functional anatomy of chemical senses in the alert monkey revealed by positron emission tomography
Authors: Kobayashi Masayuki , Sasabe Tetsuya , Takeda Masaki , Kondo Yusuke , Yoshikubo Shin‐ichi , Imamura Kazuyuki , Onoe Hirotaka , Sawada Tohru , Watanabe Yasuyoshi 
Published: March 2003

AbstractFunctional imaging technique using positron emission tomography (PET) has made it possible to localize functional brain regions in the human brain by detecting changes in regional cerebral blood flow (rCBF). Performing PET studies in the monkey will aid in integrating monkey electrophysiological research with human PET studies. We examined changes in rCBF during olfactory or combined olfactory and gustatory (flavour) stimulation using PET in the alert rhesus monkey. Olfactory or flavour stimulation with acetic acid or apple increased rCBF in the prepyriform area, substantia innominata and amygdala. Besides these areas, flavour stimulation increased rCBF in the anterior insula and frontal operculum, orbitofrontal cortex, inferior frontal gyrus and cerebellum. Apple odour or flavour stimuli increased rCBF in the inferior occipital gyrus in addition to the above areas. These findings suggest that the increases of rCBF in response to neural activities in the primary olfactory and gustatory cortices are detectable by the use of PET. In addition, regions activated by apple stimuli suggest that higher brain function might be detected with PET in the alert monkey.
Kindling enhances kainate receptor‐mediated depression of GABAergic inhibition in rat granule cells
Authors: Behr Joachim , Gebhardt Christine , Heinemann Uwe , Mody Istvan 
Published: March 2003

AbstractSeveral lines of evidence indicate a substantial contribution of kainate receptors to temporal lobe seizures. The activation of kainate receptors located on hippocampal inhibitory interneurons was shown to reduce GABA release. A reduced GABA release secondary to kainate receptor activation could contribute to an enhanced seizure susceptibility. As the dentate gyrus serves a pivotal gating function in the spread of limbic seizures, we tested the role of kainate receptors in the regulation of GABA release in the dentate gyrus of control and kindled animals. Application of glutamate (100 µm) in the presence of the NMDA receptor antagonist d‐APV and the AMPA receptor antagonist, SYM 2206 caused a slight depression of evoked monosynaptic inhibitory postsynaptic currents (IPSCs) in control, but a substantial decrease in kindled dentate granule cells. The observation that kainate receptor activation altered paired‐pulse depression and reduced the frequency of TTX‐insensitive miniature IPSCs without affecting their amplitude is consistent with a presynaptic action on the inhibitory terminal to reduce GABA release. In kindled preparations, neither glutamate (100 µm) nor kainate (10 µm) applied in a concentration known to depolarize hippocampal interneurons led to an increase of the TTX‐sensitive spontaneous IPSC frequency nor to changes of the postsynaptic membrane properties. Consistently, the inhibitory effect on evoked IPSCs was not affected by the presence of the GABAB receptor antagonist, CGP55845A, thus excluding a depression by an enhanced release of GABA acting on presynaptic GABAB receptors. The enhanced inhibition of GABA release following presynaptic kainate receptor activation favours a use‐dependent hyperexcitability in the epileptic dentate gyrus.
Selective lesions of basal forebrain cholinergic neurons produce anterograde and retrograde deficits in a social transmission of food preference task in rats
Authors: Vale‐Martínez Anna , Baxter Mark G. , Eichenbaum Howard 
Published: March 2003

AbstractWe examined the performance of Long‐Evans rats with 192 IgG‐saporin lesions of the medial septum/vertical limb of the diagonal band (MS/VDB) or nucleus basalis magnocellularis/substantia innominata (NBM/SI), which removed cholinergic projections mainly to hippocampus or neocortex, respectively. We studied the effects of these lesions on anterograde and retrograde memory for a natural form of hippocampal‐dependent associative memory, the social transmission of food preference. In a study of anterograde memory, MS/VDB lesions did not affect the immediate, 24‐h or 3‐week retention of the task. In contrast, NBM/SI lesions severely impaired immediate and 24‐h retention. In a study of retrograde memory in which rats acquired the food preference 5 days or 1 day before surgery and they were tested 10–11 days after surgery, MS/VDB‐lesioned rats showed striking memory deficits for the preference acquired at a long delay (5 days) before surgery, although all lesioned rats exhibited poorer retention on both retest sessions than on their pretest performance. Subsequent testing of new anterograde learning in these rats revealed no disrupting effects of lesions on a standard two‐choice test. When rats were administered a three‐choice test, in which the target food was presented along with two more options, NBM/SI‐lesioned rats were somewhat impaired on a 24‐h retention test. These results provide evidence that NBM/SI and MS/VDB cholinergic neurons are differentially involved in a social memory task that uses olfactory cues, suggesting a role for these neurons in acquisition and consolidation/retrieval of nonspatial declarative memory.
Properties of place cell firing after damage to the visual cortex
Authors: Paz‐Villagràn Vietminh , Lenck‐Santini Pierre‐Pascal , Save Etienne , Poucet Bruno 
Published: March 2003

AbstractHippocampal place cells were recorded while rats with lesions of the striate visual cortex foraged for food pellets in a cylindrical arena. Compared to control rats, rats with striate damage had place cells whose firing was less well organized in space, according to a measurement of spatial coherence. More importantly, the spatial location of firing fields in rats with striate lesions was poorly controlled by three‐dimensional objects, unlike the fields of either normal sighted rats or early blind rats. These findings suggest a possible contribution of the striate visual cortex to the selection of cues used for anchoring place cell firing fields in space.
SHORT COMMUNICATION Learning‐induced reduction in post‐burst after‐hyperpolarization (AHP) is mediated by activation of PKC
Authors: Seroussi Yaron , Brosh Inbar , Barkai Edi 
Published: March 2003

AbstractWe studied the role of protein kinase C (PKC) and protein kinase A (PKA) in mediating learning‐related long lasting reduction of the post‐burst after‐hyperpolarization (AHP) in cortical pyramidal neurons. We have shown previously that pyramidal neurons in the rat piriform (olfactory) cortex from trained (TR) rats have reduced post‐burst AHP for 3 days after odour‐discrimination learning, and that this reduction is due to decreased conductance of calcium‐dependent potassium current. In the present study, we examined whether this long‐lasting reduction in AHP is mediated by second messenger systems. The broad‐spectrum kinase inhibitor, H7, increased the AHP in neurons from TR rats, but not in neurons from pseudo‐trained (pseudo‐TR) and naive rats. Consequently, the difference in AHP amplitude between neurons from TR and control animals was diminished. This effect was also obtained by application of the specific PKC inhibitor, GF‐109203x. The PKC activator, 1‐Oleoyl‐2‐acetyl‐sn‐glycerol (OAG), significantly reduced the AHP in neurons from naive and pseudo‐TR rats, but not in neurons from TR rats, so that the difference between the groups was abolished. The PKA‐specific inhibitor, H‐89, increased the AHP in neurons from all groups to a similar extent, and the difference in AHP amplitude between neurons from TR rats and neurons from controls was maintained. We suggest that while the post‐burst AHP in piriform cortex pyramidal neurons is modulated by both PKC and PKA, a PKC‐dependent process maintains the learning‐related reduction of the AHP in these cells.
Homeostatic sleep regulation is preserved in mPer1 and mPer2 mutant mice
Authors: Kopp Caroline , Albrecht Urs , Zheng Binhai , Tobler Irene 
Published: March 2003

AbstractA limited set of genes, Clock, Bmal1, mPer1, mPer2, mCry1 and mCry2, has been shown to be essential for the generation of circadian rhythms in mammals. It has been recently suggested that circadian genes might be involved in sleep regulation. We investigated the role of mPer1 and mPer2 genes in the homeostatic regulation of sleep by comparing sleep of mice lacking mPER1 (mPer1 mutants) or a functional mPER2 (mPer2 mutants), and wild‐type controls (WT) after 6 h of sleep deprivation (SD). Our main result showed that after SD, all mice displayed the typical increase of slow‐wave activity (SWA; EEG power density between 0.75 and 4 Hz) in nonREM sleep, reflecting the homeostatic response to SD. This increase was more prominent over the frontal cortex as compared to the occipital cortex. The genotypes did not differ in the effect of SD on the occipital EEG, while the effect on the frontal EEG was initially diminished in both mPer mutants. Differences between the genotypes were seen in the 24‐h distribution of sleep, reflecting especially the phase advance of motor activity onset observed in mPer2 mutants. While the daily distribution of sleep was modulated by mPer1 and mPer2 genes, sleep homeostasis reflected by the SWA increase after 6‐h SD was preserved in the mPer mutants. The results provide further evidence for the independence of the circadian and the homeostatic components underlying sleep regulation.
Selective GABAergic innervation of thalamic nuclei from zona incerta
Authors: Barthó P. , Freund T. F. , Acsády L. 
Published: March 2003

AbstractThalamocortical circuits that govern cortical rhythms and ultimately effect sensory transmission consist of three major interconnected elements: excitatory thalamocortical and corticothalamic neurons and GABAergic cells in the reticular thalamic nucleus. Based on the present results, a fourth component has to be added to this scheme. GABAergic fibres from an extrareticular diencephalic source were found to selectively innervate relay cells located mainly in higher‐order thalamic nuclei. The origin of this pathway was localized to zona incerta (ZI), known to receive collaterals from corticothalamic fibres. First‐order nuclei were innervated only in zones showing a high density of calbindin‐positive neurons. The large GABA‐immunoreactive incertal terminals established multiple contacts preferentially on the proximal dendrites of relay cells via symmetrical synapses with multiple release sites. The distribution, ultrastructural characteristics and postsynaptic target selection of extrareticular terminals were similar to type II muscarinic acetylcholine receptor‐positive boutons, which constituted up to 49% of all GABAergic terminals in the posterior nucleus. This suggests that a significant proportion of the GABAergic input into certain thalamic territories involved in higher‐order functions may have extrareticular origin. Unlike the reticular nucleus, ZI receives peripheral and layer V cortical input but no thalamic feedback; it projects to brainstem centres and has extensive intranuclear recurrent collaterals. This indicates that ZI exerts a conceptually new type of inhibitory control over the thalamus. The proximally situated, multiple active zones of ZI terminals indicate a powerful influence on the firing properties of thalamic neurons, which is conveyed to multiple cortical areas via relay cells which have widespread projections to neocortex.
Differential effects of acute and chronic exercise on plasticity‐related genes in the rat hippocampus revealed by microarray
Authors: Molteni Raffaella , Ying Zhe , Gómez‐Pinilla Fernando 
Published: March 2003

AbstractStudies were performed to determine the effects of acute and chronic voluntary periods of exercise on the expression of hippocampal genes. RNAs from rodents exposed to a running wheel for 3, 7 and 28 days were examined using a microarray with 1176 cDNAs expressed primarily in the brain. The expression of selected genes was quantified by Taqman RT‐PCR or RNase protection assay. The largest up‐regulation was observed in genes involved with synaptic trafficking (synapsin I, synaptotagmin and syntaxin); signal transduction pathways (Ca2+/calmodulin‐dependent protein kinase II, CaM‐KII; mitogen‐activated/extracellular signal‐regulated protein kinase, MAP‐K/ERK I and II; protein kinase C, PKC‐δ) or transcription regulators (cyclic AMP response element binding protein, CREB). Genes associated with the glutamatergic system were up‐regulated (N‐methyl‐d‐aspartate receptor, NMDAR‐2A and NMDAR‐2B and excitatory amino acid carrier 1, EAAC1), while genes related to the gamma‐aminobutyric acid (GABA) system were down‐regulated (GABAA receptor, glutamate decarboxylase GAD65). Brain‐derived neurotrophic factor (BDNF) was the only trophic factor whose gene was consistently up‐regulated at all timepoints. These results, together with the fact that most of the genes up‐regulated have a recognized interaction with BDNF, suggest a central role for BDNF on the effects of exercise on brain plasticity. The temporal profile of gene expression seems to delineate a mechanism by which specific molecular pathways are activated after exercise performance. For example, the CaM‐K signal system seems to be active during acute and chronic periods of exercise, while the MAP‐K/ERK system seems more important during long‐term exercise.
Hippocampal long‐term depression as an index of spatial working memory
Authors: Nakao Kazuhito , Ikegaya Yuji , Yamada Maki K. , Nishiyama Nobuyoshi , Matsuki Norio 
Published: March 2003

AbstractLong‐term potentiation (LTP), a form of synaptic plasticity in the hippocampus, is a cellular model for the neural basis of learning and memory, but few studies have investigated the contribution of long‐term depression (LTD), a counterpart of LTP. To address the possible relationship between hippocampal LTD and spatial performance, the spatial cognitive ability of a rat was assessed in a spontaneous alternation test and, thereafter, LTD in response to low‐frequency burst stimulation (LFBS) was monitored in the dentate gyrus of the same rat under anaesthesia. To enhance a divergence in the ability for spatial performance, some of the animals received fimbria–fornix (FF) transection 14 days before the experiments. LTD was reliably induced by application of LFBS to the medial perforant path of intact rats, while no apparent LTD was elicited in rats with FF lesions. The behavioural parameters of spatial memory showed a significant correlation with the magnitude of LTD. We found no evidence that the cognitive ability correlated with other electrophysiological parameters, e.g. basal synaptic responses, stimulus intensity to produce half‐maximal responses, paired‐pulse facilitation or paired‐pulse depression. These results suggest that the magnitude of LTD in the dentate gyrus serves as a reliable index of spatial cognitive ability, providing insights into the functional significance of hippocampal LTD.