bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spatio‐temporal Distribution of Epileptiform Potentials in the Hippocampal Slice: Recordings with Voltage‐sensitive Dyes
Authors: Albowitz Birgit , Kuhnt Ulrich 
Published: April 2006

AbstractVoltage‐sensitive dyes and fast optical recording techniques were used to monitor the spatio‐temporal activity pattern of epileptiform potentials in hippocampal slices from guinea pigs. Epileptiform potentials were induced by adding 4‐aminopyridine to the bath solution and applying single pulse stimulation either to the stratum pyramidale of area CA3 or to the stratum radiatum of area CA1. Optical activity as well as intra‐ or extracellular electrical activity were recorded from area CA1. There was a good correlation between optical and intracellular records from the same site. The spatio‐temporal activity pattern of control and epileptiform potentials elicited by stimulation of CA1 was similar for the initial part of the potential. Then, epileptiform changes became apparent throughout the vertical extent of pyramidal neurons. Qualitative changes occurred in the stratum moleculare, reflecting activity of apical dendrites, such changes occurred even more strongly in the stratum oriens, reflecting activity of basal dendrites. The activity in the stratum oriens occurred relatively late, so that it cannot account for the initiation of epileptic discharges. It might, however, play an important role in the synchronization and spread of epileptiform potentials. The investigation of the horizontal distribution of potentials throughout the entire area CA1 indicates that different mechanisms are involved in the spread of epileptiform activity elicited by stimulation of CA1 and stimulation of CA3.
Mediodorsal Thalamic Lesions Impair Long‐Term Visual Associative Memory in Macaques
Authors: Gaffan D. , Watkins S. 
Published: April 2006

AbstractSix cynomolgus monkeys (Macaca fascicularis) were trained to associate visual stimuli with the delivery of various amounts of food reward. The animals had to choose correctly between pairs of stimuli drawn from a population of 16. Four of these stimuli were associated with 0 reward pellets, four with 1 pellet, four with 2 pellets and four with 4 pellets. Mediodorsal thalamic lesions including the medial part of the mediodorsal nucleus, similar to those which are frequently seen in Korsakoff amnesia, produced a severe impairment in this task. The impairment was seen both in memory for the quantity of reward, as expressed in choices between 1‐pellet and 2‐pellet stimuli or choices between 2‐pellet and 4‐pellet stimuli, and also in memory for the qualitative absence or presence of reward, as expressed in choices between 0‐pellet and 1‐pellet stimuli. The deficit in this task establishes that mediodorsal thalamic lesions in monkeys can impair long‐term memory tasks, in addition to their known effects on several short‐term memory tasks. The contrast between the present results and those of previous experiments on visual long‐term memory in the monkey following mediodorsal thalamic lesions can be related to similar contrasts in studies of lesions in the amygdala, suggesting that the functions of these two structures are related.
NMDA Actions on Rat Abducens Motoneurons
Authors: Durand Jacques 
Published: April 2006

AbstractIntracellular recordings were made from rat abducens motoneurons in vivo during local extracellular micro‐ionophoretic application of N‐methyl‐d‐aspartate (NMDA) and NMDA receptor antagonists. Typical NMDA responses, at a resting potential of –60 mV, consisted of a slow depolarization with an apparent increase in membrane resistance, bursts of action potentials followed by stable repetitive firing, lonophoretic applications of aminophosphonovalerate (APV), kynurenate or MK801 reduced or blocked the NMDA‐induced responses. The NMDA responses were voltage‐dependent. NMDA responses induced by short (< 30 s) NMDA application pulses were blocked by hyperpolarizing the neuron. Long duration (> 30 s) NMDA applications induced rhythmic plateau potentials in hyperpolarized abducens motoneurons. The rhythmic depolarizations (15–30 mV) were modulated in both frequency and duration by current injection. They were abolished by further hyperpolarization or replaced by stable repetitive firing when hyperpolarization was removed. Our data show that NMDA receptors are present in rat abducens motoneurons and may be involved in the induction of rhythmic activities. The voltage‐dependent blockade of somatic NMDA receptor‐associated ion channels by cell hyperpolarization may be important for these oscillations. It is suggested that the rhythmic behaviour is due to the activation of dendritic NMDA receptors.
Innervation of Entorhinal Principal Cells by Neurons of the Nucleus Reuniens Thalami. Anterograde PHA‐L Tracing Combined with Retrograde Fluorescent Tracing and Intracellular Injection with Lucifer Yellow in the Rat
Authors: Wouterlood Floris G. 
Published: April 2006

AbstractThe innervation of dendrites of identified entorhinal principal cells by fibres originating in the nucleus reuniens thalami was studied in the rat. The lectin Phaseolus vulgaris‐leucoagglutinin (PHA‐L, anterograde tracer) was injected into the nucleus reuniens and the fluorescent dye Fast Blue (retrograde tracer) into the hippocampus. After survival, perfusion‐fixation and the preparation of brain slices, entorhinal neurons retrogradely labelled with Fast Blue were intracellularly injected with the dye Lucifer yellow to introduce a specific marker into their dendrites. The transported PHA‐L and the injected Lucifer yellow were visualized through dual peroxidase immunohistochemistry. Varicosities on PHA‐L labelled reuniens fibres abut ascending and descending Lucifer yellow‐filled secondary dendrites of multipolar and pyramidal principal entorhinal neurons that possess either spiny or sparsely spiny dendrites, but they do not appose the perikarya of these cells. In the electron microscope, PHA‐L labelled boutons in the entorhinal cortex were observed forming asymmetrical synaptic contacts with dendritic spines (50%) or shafts (50%). The results indicate that direct thalamic input occurs on dendrites of neurons in the entorhinal cortex which project to the hippocampus.
Immunohistochemistry of c‐fos in Mouse Brain During Postnatal Development: Basal Levels and Changing Response to Metrazol and Kainate Injection
Authors: Sakurai‐Yamashita Yasuko , Sassone‐Corsi Paolo , Gombos Giorgio 
Published: April 2006

AbstractLevels and cellular distribution of FOS, the product of c‐fos (onco)gene, were studied by immunohistochemistry during the development of mouse brain at rest and after the administration of convulsants. Basal FOS immunoreactivity became detectable only after postnatal day 20 (P20). Metrazol and kainate at the appropriate doses induced convulsions at all ages but, in both cases, FOS accumulated in limbic areas (particularly in the dentate gyrus) only after a certain age: P20 for kainate and P30 for Metrazol. Surprisingly, considering the different molecular targets of Metrazol and kainate, respectively, and the different type of convulsions elicited, the cell groups in the limbic areas in which FOS increased were the same in the two cases. These results suggest that both drugs produced FOS increase by finally activating the same circuit. During ontogeny, the ability to accumulate FOS, which appears after P20, could be the sign of the attained maturity of signal transduction mechanisms in the cells of the hippocampal formation; endogenous signals originating from the activity of the nervous system increase the basal FOS levels and exogenous signals (i.e. like those given, probably locally, by kainate) further increase these levels. Metrazol manifests its capability to induce FOS accumulation only at later ages. We suggest that this occurs because the Metrazol target is probably distant from the hippocampal region and thus the maturity of a nerve pathway(s) is also required for c‐fos induction.
Properties of a High‐threshold Voltage‐activated Calcium Current in Rat Cerebellar Granule Cells
Authors: De Waard M. , Feltz A. , Bossu J. L. 
Published: April 2006

AbstractPostmitotic cerebellar granule cells, maintained for 5–6 days in Dulbecco's modified essential medium supplemented with 25 mM KCl, have been studied in whole‐cell recording conditions to characterize calcium currents. With 10 mM Ba2+ as the divalent charge carrier, and using a pipette solution highly buffered for Ca2+ (30 mM EGTA, 100 mM HEPES–Tris, pH 7.2), only a high‐threshold voltage‐activated barium current was recorded from a holding potential of – 90 mV. The addition of 1 mM ATP to the pipette medium allowed stable recording for an average duration of 10 min, compatible with pharmacological studies of the barium current. Ninety‐six per cent of the current was half‐inactivated at low negative holding potential (‐76 mV). A total block of current was obtained with 1 μM Cd2+. Sixty‐three per cent of the mean current was abolished by 3 μM ω‐conotoxin (ω‐CgTx; Ki= 10 nM for a 15 min application), but individual cells showed either full sensitivity to this toxin or incomplete sensitivity. Seventy‐eight per cent of the mean current was also abolished by 10 μM nicardipine but with a higher Ki, of 0.5 μM. After exposure to ω‐CgTx, BAY K 8644 had no effect on the remaining current, though it was suppressed by nicardipine. No sensitivity to diltiazem, desmethoxyverapamil or flunarizine could be detected. Our major conclusion is that at least half of the channels have a mixed pharmacology, showing sensitivity to both ω‐CgTx and dihydropyridine antagonists.
Activation of a Large‐conductance Ca2+‐Dependent K+ Channel by Stimulation of Glutamate Phosphoinositide‐coupled Receptors in Cultured Cerebellar Granule Cells
Authors: Fagni L. , Bossu J. L. , Bockaert J. 
Published: April 2006

AbstractTrans‐1‐amino‐cyclopentyl‐1,3‐dicarboxylic acid (trans‐ACPD), a specific agonist of the glutamate phosphoinositide‐coupled receptor (Qp receptor), increased the amplitude of the outward K+ current recorded in the whole‐cell configuration of the patch‐clamp technique in mouse cultured cerebellar granule cells. This effect was abolished by buffering internal Ca2+ with BAPTA [1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid]. Activation of a large‐conductance K+ channel was observed when trans‐ACPD or quisqualic acid (QA), another Qp receptor agonist, was applied outside the cell‐attached patch pipettes. No activation was observed with alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA), a specific agonist of ionotropic non‐N‐methyl‐d‐aspartate (non‐NMDA) receptors. The effects of trans‐ACPD or QA were potentiated in the presence of external Ca2+. The channel was also directly activated by both micromolar concentrations of internal Ca2+ and membrane depolarization. Its unitary conductance was 100–115 pS under asymmetrical K+ and 195–235 pS under high symmetrical K+ conditions. In the absence of agonist, the channel was blocked by 1 mM external tetraethylammonium. This is the first description of a large conductance Ca2+‐activated K+ channel in cultured cerebellar granule cells. It possesses properties similar to those of the so‐called ‘big K+ channel’ described in other preparations. Our cell‐attached experiments demonstrated an indirect coupling between Qp receptors and this channel. The most likely hypothesis is that the second messenger system inositol 1,4,5‐triphosphate (IP3)‐Ca2+ was involved in the coupling process. This hypothesis was further strengthened by our whole‐cell experiments. On the basis of the voltage‐ and Ca2+‐sensitivities of the studied channel, we estimated an increase of 350 to 570 nM in internal Ca2+ concentration when Qp receptors were stimulated by 100 μM trans‐ACPD. Under physiological conditions, stimulation of Qp receptors by the endogenous neurotransmitter should lead to similar K+ channel activation and therefore would tend to reduce the efficacy of ionotropic glutamate synaptic receptor stimulation responsible for cell excitation.
Single Channel Recording from Glial Cells on the Untreated Surface of the Frog Optic Nerve
Authors: Marrero Hector , Orkand Paula M. , Kettenmann Helmut , Orkand Richard K. 
Published: April 2006

AbstractThe patch clamp technique has been used to record single channel currents from the untreated surface of the intact frog optic nerve after the meninges and basal lamina have been mechanically removed. Cells filled via dialysis with Lucifer yellow (LY) from the patch pipette had a typical astrocyte morphology and were dye‐coupled to adjacent astrocytes. This is consistent with the electron‐microscopic observation that all the cells on the surface of this nerve are astrocytes. Two types of ion channels were studied in detached patches. One, identified as a K+ channel, had a conductance of 88±4 (S.E.) n= 9 pS and an equilibrium potential of −59±8 mV in physiological K+ solutions. The steady‐state open probability was not significantly altered by changing the membrane potential. A second channel had a large conductance of 300–1200 pS, a reversal potential of ∼ 0 mV in symmetrical and non‐symmetrical solutions, and was open only in the voltage range of ±20 mV. These are the characteristics of a large anionic channel described in other preparations including cultured astrocytes.
High‐Resolution Light and Electron Microscopic Immunocytochemistry of Colocalized GABA and Calbindin D‐28k in Somata and Double Bouquet Cell Axons of Monkey Somatosensory Cortex
Authors: DeFelipe J. , Jones E. G. 
Published: April 2006

AbstractA simple method for high‐resolution immunocytochemical colocalization of different antigens in semithin sections 1 ‐ 3 μm thick was used to study the colocalization of the calcium binding protein calbindin D‐28k (calbindin) with γ‐aminobutyric acid (GABA) in double bouquet cells of monkey (Macaca fuscata) somatosensory cortex. Double bouquet cells were first visualized in vibratome sections by pre‐embedding immunocytochemical staining for calbindin. Sections containing calbindin‐immunoreactive somata and double bouquet cell axons were then osmicated, embedded in Araldite, resectioned at 1–3μm and stained for GABA by postembedding immunocytochemistry after elution of the bound anti‐calbindin antibodies. Other semithin sections adjacent to those eluted and still containing calbindin immunoreactive somata and processes were resectioned at 60–70 nm for electron microscopy and stained immunocytochemically for GABA by the postembedding immunogold procedure. Calbindin‐positive cells are most numerous in layer II and upper layer III, where they outnumber those in all other layers combined. In layers II and upper III, ‐30% of the stained cells are pyramidal and do not colocalize GABA. Only approximately two‐thirds of the calbindin‐stained nonpyramidal cells in these layers colocalize GABA, but among these virtually all the calbindin‐positive double bouquet cells and their axons are GABA‐immunoreactive. In deeper layers all calbindin‐positive cells are nonpyramidal and all colocalize GABA. At the electron microscopic level, however, significant numbers of calbindin‐positive axon terminals making symmetrical synapses are not GABA‐immunoreactive. These results suggest the calbindin cells of monkey somatosensory cortex are a heterogeneous population that includes GABAergic and non‐GABAergic cell types.
Accelerated Differentiation in Response to Retinoic Acid After Retrovirally Mediated Gene Transfer of GAP‐43 into Mouse Neuroblastoma Cells
Authors: Morton A. Jennifer , Buss Timothy N. 
Published: April 2006

AbstractAlthough substantial evidence exists for the involvement of growth‐associated protein‐43 (GAP‐43) in neuronal development and regeneration, the precise role of this protein in neurite outgrowth is currently debated. To investigate the role of GAP‐43 in the initiation of neurite outgrowth, we transfected a full‐length cDNA coding for GAP‐43 into a mouse neuroblastoma cell line (Neuro‐2a) which can be differentiated to a neuronal phenotype using retinoic acid (RA). We show that the consequent overexpression of GAP‐43 results in a change in the basic morphology of these cells, but is not in itself sufficient to induce the extension of neurites. However, overexpression of GAP‐43 results in a marked acceleration of neurite formation in response to RA. We propose that while GAP‐43 does not trigger the initiation of neurite extension, its expression is rate‐limiting for neurite outgrowth in response to differentiation agents such as RA.
Long‐term Potentiation in the Striatum is Unmasked by Removing the Voltage‐dependent Magnesium Block of NMDA Receptor Channels
Authors: Calabresi P. , Pisani A. , Mercuri N. B. , Bernardi G. 
Published: April 2006

AbstractWe have studied the effects of tetanic stimulation of the corticostriatal pathway on the amplitude of striatal excitatory synaptic potentials. Recordings were obtained from a corticostriatal slice preparation by utilizing both extracellular and intracellular techniques. Under the control condition (1.2 mM external Mg2+), excitatory postsynaptic potentials (EPSPs) evoked by cortical stimulation were reversibly blocked by 10 μM 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), an antagonist of dl‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) ionotropic glutamate receptors, while they were not affected by 30–50 μM 2‐amino‐5‐phosphonovalerate (APV), an antagonist of N‐methyl‐d‐aspartate (NMDA) glutamate receptors. In the presence of 1.2 mM external Mg2+, tetanic activation of cortical inputs produced long‐term depression (LTD) of both extracellularly and intracellularly recorded synaptic potentials. When Mg2+ was removed from the external medium, EPSP amplitude and duration increased. In Mg2+‐free medium, cortically evoked EPSPs revealed an APV‐sensitive component; in this condition tetanic stimulation produced long‐term potentiation (LTP) of synaptic transmission. Incubation of the slices in 30–50 μM APV blocked striatal LTP, while it did not affect LTD. In Mg2+‐free medium, incubation of the slices in 10 μM CNQX did not block the expression of striatal LTP. Intrinsic membrane properties (membrane potential, input resistance and firing pattern) of striatal neurons were altered neither by tetanic stimuli inducing LTD and LTP, nor by removal of Mg2+ from the external medium. These findings show that repetitive activation of cortical inputs can induce long‐term changes of synaptic transmission in the striatum. Under control conditions NMDA receptor channels are inactivated by the voltage‐dependent Mg2+ block and repetitive cortical stimulation induces LTD which does not require activation of NMDA channels. Removal of external Mg2+ deinactivates these channels and reveals a component of the EPSP which is potentiated by repetitive activation. Since the striatum has been involved in memory and in the storage of motor skills, LTD and LTP of synaptic transmission in this structure may provide the cellular substrate for motor learning and underlie the physiopathology of some movement disorders.
The Effect of Kainic Acid Lesions of the Cerebellar Cortex on the Conditioned Nictitating Membrane Response in the Rabbit
Authors: Hardiman M. J. , Yeo C. H. 
Published: April 2006

AbstractIn previous studies we have shown that aspiration lesions centred on lobule HVI in the cerebellar cortex of rabbits produce a profound loss of conditioned nictitating membrane (NM) responses. Because aspiration lesions of the cerebellar cortex cause retrograde degeneration in precerebellar nuclei we tested in rabbits whether excitotoxic lesions of the cerebellar cortex that spare these precerebellar nuclei also cause a loss of conditioned NM responses. Following discrete injections of kainic acid into HVI and rostral regions of the adjacent folia of crus I and crus II, we observed an immediate loss of conditioned NM responses. Following extensive retraining several subjects showed a gradual recovery of conditioned responses. But subjects with the most complete lesions never recovered more than a few conditioned responses. Kainic acid lesions did not change ipsilateral unconditioned reflex responses to a range of stimulus intensities. The kainic acid injections caused obvious degeneration of Purkinje and granule cells but not of the precerebellar nuclei. We conclude that HVI and parts of crus I and crus II are essential for normal retention of conditioned NM responses.
Endothelin‐evoked Release of Arachidonic Acid from Mouse Astrocytes in Primary Culture
Authors: Tencé Martine , Cordier Jocelyne , Glowinski Jacques , Prémont Joël 
Published: April 2006

AbstractIn striatal astrocytes, receptors for the vasoactive peptide endothelin (ET) are associated with several intracellular signalling pathways: ET‐1 increases the breakdown of phosphoinositides, induces a sustained influx of Ca2+ and inhibits the isoproterenol‐induced formation of cAMP (Marin et al., J. Neurochem., 56, 1270–1275, 1991). In the present study, it will be shown that ET‐1 and ET‐3 markedly stimulate the release of arachidonic acid (AA) from cultured astrocytes from the mouse striatum (EC50= 3 and 7 nM for ET‐1 and ET‐3, respectively), mesencephalon and cerebral cortex. The ET‐1‐evoked release of AA probably resulted from the activation of a phospholipase A2, since it required extracellular Ca2+ and was prevented by mepacrine but not by RHC 80267, an inhibitor of diacylglycerol lipase. The ET‐1‐induced release of AA was shown to be partially mediated by a guanine nucleotide‐binding protein sensitive to pertussis toxin but not to cholera toxin. A cAMP‐dependent process is not involved since the ET‐1‐evoked release of AA was not affected when cells were incubated with either isoproterenol or 8‐bromo‐cAMP. The ET‐1‐evoked release of AA could be mimicked by the co‐application of a calcium ionophore and a protein kinase C activator. However, staurosporine, a potent inhibitor of protein kinase C, which blocked the release of AA induced by the combined application of ionomycin and phorbol 12‐myristate 12‐acetate (PMA), was without effect on the ET‐1‐evoked response, indicating that protein kinase C is not directly involved in the ET‐1‐induced release of AA. Furthermore, the responses induced by ET‐1 and by PMA were found to be additive. These results suggest that (1) ET‐1 receptors are coupled to the release of AA by a mechanism independent of both protein kinase C activation and the adenylate cyclase pathway, possibly via the activation of phospholipase A2, (2) different mechanisms (or different phospholipase A2 subtypes) are involved in the control of AA release in astrocytes.