bluuebunny/crossref_metadata_2025_split huggingface dataset:
Muscarinic and GABAA receptors modulate acetylcholine release in feline basal forebrain
Authors: Vazquez Jacqueline , Baghdoyan Helen A. 
Published: March 2003

AbstractAcetylcholine (ACh) release within the basal forebrain changes significantly as a function of sleep and wakefulness, hence identifying the neurochemical modulators of basal forebrain ACh release will contribute to a mechanistic understanding of sleep cycle regulation. This study tested the hypothesis that muscarinic and gamma aminobutyric acidA (GABAA) receptors modulate basal forebrain ACh release. Cats were anaesthetized with halothane to hold arousal state constant and a microdialysis probe was aimed stereotaxically for the substantia innominata region of the basal forebrain. Four concentrations of the muscarinic antagonist scopolamine (0.1, 0.3, 1.0, and 10 nm) and five concentrations of the GABAA antagonist bicuculline (3, 10, 30, 100, and 300 µm) were delivered by reverse dialysis from the same probes used to collect ACh. These results are based on 27 experiments in nine animals. Scopolamine and bicuculline each caused a concentration dependent enhancement of ACh release. Scopolamine increased ACh by 118% above control levels whereas bicuculline was more effective, causing a 287% increase in ACh release. Scopolamine was more potent (EC50 = 0.16 nm) than bicuculline (EC50 ≥ 90 µm) for increasing ACh release. The results support the hypothesis that substantia innominata ACh release is modulated by muscarinic autoreceptors and inhibited by GABAA receptors. These findings are consistent with the interpretation that inhibition of basal forebrain cholinergic neurotransmission by GABA contributes to the generation of sleep.
Cellular mechanisms of Δ9‐tetrahydrocannabinol behavioural sensitization
Authors: Rubino T. , Viganò D. , Massi P. , Parolaro D. 
Published: March 2003

AbstractWe investigated the cellular events linked to the induction of cannabinoid behavioural sensitization. In sensitized rats, autoradiographic binding studies with [3H]CP‐55,940 showed a significant increase in cannabinoid receptor binding, specifically in the cerebellum, with no changes in the other brain areas where basal CB1‐receptor expression is observed. In vitro autoradiography of CP‐55,940‐stimulated [35S]GTPγS binding provided a picture of cannabinoid receptor‐mediated G protein activation. Basal [35S]GTPγS binding was not affected, whereas sensitized rats showed a significant increase of net [35S]GTPγS binding in the caudate putamen and cerebellum. Autoradiographic studies suggested that only these two areas had altered receptor functionality. We therefore focused our intracellular investigations only there, first surveying the responsiveness of the cAMP system to cannabinoids. CP‐55,940 was unable to inhibit forskolin‐induced cAMP accumulation in the cerebellum of sensitized animals, but no difference was observed between groups in the caudate putamen. Finally, we surveyed the levels of CREB and AP‐1 binding activity, in the same two areas and found no difference in sensitized rats. The intracellular picture in sensitized rats suggests that besides the cAMP cascade, other signalling pathways may participate in the development of cannabinoid sensitization.
Substance induced plasticity in noradrenergic innervation of the paraventricular hypothalamic nucleus
Authors: Jansen Arthur S. P. , Schmidt E. Donné , Voorn Pieter , Tilders Fred J. H. 
Published: March 2003

AbstractSingle administration of the cytokine interleukin‐1α (IL‐1), or the psychostimulant amphetamine, enhanced adrenocorticotropin hormone and corticosterone responses to a stress challenge weeks later. This long‐lasting hypothalamic‐pituitary‐adrenal (HPA)‐sensitization is paralleled by an increase in electrically evoked release of noradrenaline in the paraventricular hypothalamic nucleus (PVN). We hypothesized that these functional changes may be associated with morphological plasticity of noradrenergic projections to the PVN, a parameter that shows high reproducibility. Specific alterations in relative (nor)adrenergic innervation density were studied by using dopamine‐α‐hydroxylase (DBH) as a marker. An image analysis system was used to detect changes in the relative DBH innervation density of the PVN. Groups of adult male rats were given IL‐1 (10 µg/kg i.p.), amphetamine (5 mg/kg i.p.), or saline. Three weeks later, IL‐1 and amphetamine primed rats showed enhanced adrenocorticotropin hormone and corticosterone responses to an amphetamine challenge. In another set of experiments, the relative DBH innervation density was measured in different PVN subnuclei at four rostro‐caudal levels. Single administration of either IL‐1 or amphetamine causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin‐releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN. We conclude that (1) long‐lasting sensitization induced by single exposure to IL‐1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH‐rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
Attention‐dependent coupling between beta activities recorded in the cat's thalamic and cortical representations of the central visual field
Authors: Bekisz Marek , Wróbel Andrzej 
Published: March 2003

AbstractWe have previously proposed that enhanced 16–24 Hz (beta) local field potential activity in the primary visual cortex and lateral geniculate nucleus may be an electrophysiological correlate of the attentional mechanism that increases the gain of afferent visual information flow to the cortex. In this study, we measured coupling between beta signals recorded in the thalamic (i.e. lateral geniculate or perigeniculate) and cortical representations of the central visual field (within 5° fromarea centralis), during visual and auditory attentive situations. Signal coupling was calculated in two ways: (i) by means of crosscorrelation between raw beta activities, which depends primarily on phase coherence, and (ii) by phase‐independent crosscorrelation between amplitude envelopes of beta activities. Mean amplitudes of raw signal crosscorrelations obtained for thalamo‐cortical recording pairs were not significantly different when calculated during behavioural demands for either visual or auditory attention. In contrast, amplitudes of envelope crosscorrelations obtained during behaviour requiring visual attention were, on average, two times higher than those calculated during the auditory task. This attention‐related coupling emerged from synchronized amplitude modulation of beta oscillatory activity that occurs within the cortico‐thalamic circuit involved in central vision.
Localization of a FMRFamide‐related peptide in efferent neurons and analysis of neuromuscular effects of DRNFLRFamide (DF2) in the crustacean Idotea emarginata.
Authors: Weiss Torsten , Kreissl Sabine , Rathmayer Werner 
Published: March 2003

AbstractIn the ventral nerve cord of the isopod Idotea emarginata, FMRFamide‐immunoreactive efferent neurons are confined to pereion ganglion 5 where a single pair of these neurons was identified. Each neuron projects an axon into the ipsilateral ventral and dorsal lateral nerves, which run through the entire animal. The immunoreactive axons form numerous varicosities on the ventral flexor and dorsal extensor muscle fibres, and in the pericardial organs. To analyse the neuromuscular effects of a FMRFamide, we used the DRNFLRFamide (DF2). DF2 acted both pre‐ and postsynaptically. On the presynaptic side, DF2 increased transmitter release from neuromuscular endings. Postsynaptically, DF2 depolarized muscle fibres by approximately 10 mV. This effect was not observed in leg muscles of a crab. The depolarization required Ca2+, was blocked by substituting Ca2+ with Co2+, but not affected by nifedipine or amiloride. In Idotea, DF2 also potentiated evoked extensor muscle contractions. The amplitude of high K+ contractures was increased in a dose dependent manner with an EC50 value of 40 nm. In current‐clamped fibres, DF2 strongly potentiated contractions evoked by current pulses exceeding excitation‐contraction threshold. In voltage‐clamped fibres, the inward current through l‐type Ca2+ channels was increased by the peptide. The observed physiological effects together with the localization of FMRFamide‐immunoreactive efferent neurons suggest a role for this type of peptidergic modulation for the neuromuscular performance in Idotea. The pre‐ and postsynaptic effects of DF2 act synergistically and, in vivo, all should increase the efficacy of motor input to muscles resulting in potentiation of contractions.
Long‐term striatal overexpression of GDNF selectively downregulates tyrosine hydroxylase in the intact nigrostriatal dopamine system
Authors: Rosenblad Carl , Georgievska Biljana , Kirik Deniz 
Published: March 2003

AbstractSustained neurotrophic factor treatment in neurodegenerative disorders such as Parkinson's disease is likely to affect both degenerating and intact neurons. To investigate the effect of long‐term glial cell line‐derived neurotrophic factor (GDNF) overexpression on intact nigrostriatal dopamine neurons, we injected a recombinant lentiviral vector encoding GDNF, or green fluorescent protein, in the right striatum of young adult rats. Thirteen months after viral injection GDNF levels were 4.5 ng/mg tissue in the striatum and 0.9 ng/mg in the substantia nigra as measured by ELISA, representing a 25–100‐fold increase above control vector‐ or nontransduced tissue. GDNF overexpression significantly reduced tyrosine hydroxylase mRNA levels (by 39–72%) in the substantia nigra and ventral tegmental area neurons, and the optical density of tyrosine hydroxylase‐immunoreactive innervation in the striatum was reduced by 25–52% with the most prominent reductions appearing caudally. No significant reduction was seen in striatal vesicular monoamine transporter 2‐immunoreactivity or [3H]mazindole binding autoradiography to dopamine uptake sites, two other presynaptic markers in dopamine axon terminals. The striatal D1 and D2 receptor binding as determined by [3H]SCH23390 and [3H]spiperone binding, respectively, was unaltered relative to the intact side in both treatment groups. Preproenkephalin mRNA levels in postsynaptic striatal neurons, which increase upon removal of striatal dopamine, were also unaffected by the GDNF treatment. Taken together our findings indicate that sustained GDNF administration to intact nigrostriatal dopamine neurons selectively reduces tyrosine hydroxylase expression, without altering striatal dopamine transmission to the extent that compensatory changes in several other components related to dopamine storage and signalling occur.
Odorant specificity of three oscillations and the DC signal in the turtle olfactory bulb
Authors: Lam Ying‐Wan , Cohen Lawrence B. , Zochowski Michal R. 
Published: March 2003

AbstractThe odour‐induced population response in the in vivo turtle (Terepene sp.) olfactory bulb consists of three oscillatory components (rostral, middle and caudal) that ride on top of a DC signal. In an initial step to determine the functional role of these four signals, we compared the signals elicited by different odorants. Most experiments compared isoamyl acetate and cineole, odorants which have very different maps of input to olfactory bulb glomeruli in the turtle and a different perceptual quality for humans. We found substantial differences in the response to the two odours in the rise‐time of the DC signal and in the latency of the middle oscillation. The rate of rise for cineole was twice as fast as that for isoamyl acetate. Similarly, the latency for the middle oscillation was about twice as long for isoamyl acetate as it was for cineole. On the other hand, a number of characteristics of the signals were not substantially different for the two odorants. These included the latency of the rostral and caudal oscillation, the frequency and envelope of all three oscillations and their locations and spatial extents. A smaller number of experiments were carried out with hexanone and hexanal; the oscillations elicited by these odorants did not appear to be different from those elicited by isoamyl acetate and cineole. Qualitative differences between the oscillations in the turtle and those in two invertebrate phyla suggest that different odour processing strategies may be used.
Long‐term potentiation in the hippocampal CA1 area and dentate gyrus plays different roles in spatial learning
Authors: Okada Takashi , Yamada Nobuaki , Tsuzuki Keisuke , Horikawa Hiroshi P. M. , Tanaka Kohichi , Ozawa Seiji 
Published: March 2003

AbstractNMDA receptor‐dependent long‐term potentiation (LTP) at hippocampal synapses has been considered a crucial component of the cellular basis for learning and memory. This form of LTP occurs in excitatory synapses in both the CA1 area and the dentate gyrus in the hippocampus. However, differential roles of LTP in these areas have not yet been identified. To address this issue, we enhanced the degree of LTP by expressing Ca2+‐permeable AMPA receptors at either hippocampal CA1 or dentate gyrus synapses using Sindbis viral vectors (SINs) encoding both green fluorescent proteins and unedited GluR2 (GluR2Q) subunits, and examined their effects on rat spatial learning. The viral vectors were locally injected into the 8‐week‐old‐rat brain in vivo bilaterally. The postsynaptic expression of Ca2+‐permeable AMPA receptors enhanced the degree of LTP, and induced NMDA receptor‐independent LTP in the presence of the NMDA receptor antagonist in SIN‐infected regions in both CA1 and dentate gyrus in hippocampal slice preparations. However, the regional expression of Ca2+‐permeable AMPA receptors caused opposite behavioural consequences on the Morris water maze task: rats with SIN‐infected CA1 pyramidal cells showed shorter escape latency and better probe test performance, whereas those with SIN‐infected dentate gyrus granule cells showed impaired performance. Thus, it was demonstrated that CA1 and dentate gyrus synapses play different functional roles in spatial learning despite their similar mechanism for LTP induction.
Induction of bilateral plasticity in sensory cortical maps by small unilateral cortical infarcts in rats
Authors: Reinecke S. , Dinse H. R. , Reinke H. , Witte O. W. 
Published: March 2003

AbstractBehavioural impairments caused by brain lesions show a considerable, though often incomplete, recovery. It is hypothesized that cortical and subcortical plasticity of sensory representations contribute to this recovery. In the hindpaw representation of somatosensory cortex of adult rats we investigated the effects of focal unilateral cortical lesions on remote areas. Cortical lesions with a diameter of ≈ 2 mm were induced in the parietal cortex by photothrombosis with the photosensitive dye Rose Bengal. Subsequently, animals were kept in standard cages for 7 days. On day seven, animals were anaesthetized and cutaneous receptive fields in the cortical hindpaw representations ipsi‐ and contralateral to the lesion were constructed from extracellular recordings of neurons in layer IV using glass microelectrodes. Receptive fields in the lesioned animals were compared to receptive fields measured in nonlesioned animals serving as controls. Quantitative analysis of receptive fields revealed a significant increase in size in the lesioned animals. This doubling in receptive field size was observed equally in the hemispheres ipsi‐ and contralateral to the lesion. The results indicate that the functional consequences of restricted cortical lesions are not limited to the area surrounding the lesion, but affect the cortical maps on the contralateral, nonlesioned hemisphere.
Activation of the phasic pontine‐wave generator enhances improvement of learning performance: a mechanism for sleep‐dependent plasticity
Authors: Mavanji Vijayakumar , Datta Subimal 
Published: March 2003

AbstractThe aim of this study was to test the hypothesis that supplementary activation of the phasic pontine wave (P‐wave) generator during rapid eye movement (REM) sleep enhances consolidation and integration of memories, resulting in improved learning. To test this hypothesis, two groups of rats were trained on a two‐way active avoidance learning task in the morning. Immediately after training, one group of rats received a carbachol microinjection into the P‐wave generator and the other group was microinjected with control saline into the same target area. After training trials and microinjections, rats were allowed a 6‐h period of undisturbed sleep in the polygraphic recording chamber. At the end of 6 h of undisturbed sleep–wake recordings, rats were retested in a session of avoidance learning trials. After learning trials, the total percentage of time spent in REM sleep was significantly increased in both saline (15.36%)‐ and carbachol (17.70%)‐microinjected rats. After learning trials, REM sleep P‐wave density was significantly greater throughout the 6‐h period of recordings in carbachol treated rats than in the saline treated rats. In the retrial session, the improvement in learning task performance was 22.75% higher in the carbachol‐microinjected rats than in the saline‐microinjected rats. These findings show that the consolidation and integration of memories create a homeostatic demand for P‐waves. In addition, these findings provide experimental evidence, for the first time, that activation of the P‐wave generator may enhance consolidation and integration of memories, resulting in improved performance on a recently learned task.
cDNA profiling of epileptogenesis in the rat brain
Authors: Lukasiuk Katarzyna , Kontula Laura , Pitkänen Asla 
Published: March 2003

AbstractSymptomatic temporal lobe epilepsy typically develops in three phases: brain insult → latency period (epileptogenesis) → recurrent seizures (epilepsy). We hypothesized that remodeling of neuronal circuits underlying epilepsy is associated with altered gene expression during epileptogenesis. Epileptogenesis was induced by electrically triggered status epilepticus (SE) in rats. Animals were continuously monitored with video‐EEG, and the hippocampus and temporal lobe were collected either during epileptogenesis (1, 4 and 14 days) or after the first spontaneous seizures (14 days) for cDNA array analysis. Altogether, 282 genes had altered expression, from which 87 were in the hippocampus and 208 in the temporal lobe (overlap in 13). Assessment of hippocampal gene expression during epileptogenesis indicated that 37 genes were altered in the 1‐day group, 12 in the 4‐day group and 14 in the 14‐day epileptogenesis group. There were 42 genes with altered expression in the 14‐day epilepsy group. In the temporal lobe, the number of genes with altered expression was 29 in the 1‐day group, 155 in the 4‐day group, 32 in the 14‐day epileptogenesis group and 62 in the 14‐day epilepsy group. Products of the altered genes are involved in neuronal plasticity, gliosis, organization of the cytoskeleton or extracellular matrix, cell adhesion, signal transduction, regulation of cell cycle, and metabolism. As most of these genes have not previously been implicated in epileptogenesis or epilepsy, these data open new avenues for understanding the molecular basis of epileptogenesis and provide new targets for rational development of antiepileptogenic treatments for patients with an elevated risk of epileptogenesis after brain injury.
LTP but not seizure is associated with up‐regulation of AKAP‐150
Authors: Génin A. , French P. , Doyère V. , Davis S. , Errington M. L. , Maroun M. , Stean T. , Truchet B. , Webber M. , Wills T. , Richter‐Levin G. , Sanger G. , Hunt S. P. , Mallet J. , Laroche S. , Bliss T. V. P. , O'Connor V. 
Published: March 2003

AbstractWe have used differential display to profile and compare the mRNAs expressed in the hippocampus of freely moving animals after the induction of long‐term potentiation (LTP) at the perforant path–dentate gyrus synapse with control rats receiving low‐frequency stimulation. We have combined this with in situ hybridization and have identified A‐kinase anchoring protein of 150 kDa (AKAP‐150) as a gene selectively up‐regulated during the maintenance phase of LTP. AKAP‐150 mRNA has a biphasic modulation in the dentate gyrus following the induction of LTP. The expression of AKAP‐150 was 29% lower than stimulated controls 1 h after the induction of LTP. Its expression was enhanced 3 (50%), 6 (239%) and 12 h (210%) after induction, returning to control levels by 24 h postinduction. The NMDA receptor antagonist CPP blocked the tetanus‐induced modulation of AKAP‐150 expression. Interestingly, strong generalized stimulation produced by electroconvulsive shock did not increase the expression of AKAP‐150. This implies that the AKAP‐150 harbours a novel property of selective responsiveness to the stimulation patterns that trigger NMDA‐dependent LTP in vivo. Its selective up‐regulation during LTP and its identified functions as a scaffold for protein kinase A, protein kinase C, calmodulin, calcineurin and ionotropic glutamate receptors suggest that AKAP‐150 encodes is an important effector protein in the expression of late LTP.
Dopamine gating of forebrain neural ensembles
Authors: O'Donnell Patricio 
Published: March 2003

AbstractDopamine may exert different actions depending on a number of factors. A common view is that D1 receptors may be responsible for excitatory actions whereas D2 receptors are involved in inhibitory actions. However, this position cannot be reconciled with several findings indicating otherwise. The role of dopamine on forebrain neural ensembles may be better understood in the light of functional states of the system. Pyramidal cortical neurons and striatal medium spiny neurons alternate between two membrane potential states (‘up’ and ‘down’) that could shape dopamine actions. It is proposed that D1 receptors can act as state‐stabilizers by sustaining up states and thereby facilitating plasticity mechanisms by providing postsynaptic depolarization and increasing NMDA function. In this way, dopamine can sustain activity in depolarized units. This action is accompanied by a decrease in cell firing (perhaps mediated by D2 receptors), which renders the cells responsive only to strong stimuli. The result would be a net increase in signal‐to‐noise ratio in a selected assembly of neurons.