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C Batini

Publications and source records attributed to C Batini.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Transfer of photosensitive epilepsy of genetic origin by selective grafts of brain vesicles in chick embryo].

We transferred the avian photosensitive genetic epilepsy to normal chicken by transplanting at least prosencephalic and mesencephalic vesicles from epileptic to normal chick embryos at day 2 of incubation. Chimeras showed typical interictal EEG and developed, under intermittent light stimulation, seizures phenotypically and electrically similar to the epileptic strain seizures.

Animals↗
PubMed1993

Transfer of a genetic form of epilepsy in the chicken by embryonic brain grafts.

The genetic photosensitive epilepsy of the Fayoumi chickens was transferred to normal chickens by grafting, in situ, on the 2nd day of incubation, the prosencephalic and mesencephalic vesicles from epileptic embryos. Such chimeras displayed typical interictal EEG and developed intermittent light stimulation-induced seizures phenotypically and electrically similar to the epileptic strain seizures.

Animals↗
PubMed1992

Pattern of electroencephalographic activity during light induced seizures in genetic epileptic chicken and brain chimeras.

Genetic epilepsy was studied in Fayoumi epileptic (F.Epi) chickens and in neural chimeras obtained by selective substitution of embryonic brain vesicles of F.Epi donors in normal recipient chickens. Typical motor seizures accompanied by convulsions were evoked by intermittent light stimulation in F.Epi and in chimeras having embryonic substitution of the prosencephalon and the mesencephalon. The motor seizure was less severe in chimeras receiving only the prosencephalon. In the F.Epi, as well as in all the chimeras, the EEG during seizures was characterized by a desynchronized (or a flattening) pattern of activity. F.Epi and chimeras had a lower threshold to Metrazol induced seizures than control chickens. The experimental animals show that, in this model, large prosencephalic and mesencephalic areas are involved in the epileptic disease. The epileptic character of this genetic dysfunction is discussed.

Animals↗
PubMed1992

Cerebellar nuclei and the nucleocortical projections in the rat: retrograde tracing coupled to GABA and glutamate immunohistochemistry.

The amino acids GABA and glutamate (Glu) are thought to be the principal substances in the central nervous system responsible for neuronal inhibition and excitation. Their distributions among the different neurons in a defined pathway may thus be indicative of the contributions of the cells to pathway function. Examples of such neurons are those of the cerebellar nuclei which, while regulating output from the Purkinje cells of the cerebellar cortex, are also found to project back to the cerebellar cortex. Immunohistochemical experiments were done to identify GABA and glutamate (Glu) containing cells in the adult rat cerebellar nuclei. Consecutive semithin and serial vibratome sections were incubated with antisera raised in rabbit against GABA and Glu. In semithin sections, only small neurons were intensely GABA immunoreactive (GABA-IR) (31.7%), and the majority (80.5%) were Glu immunoreactive (Glu-IR) of different sizes. Consistent with Glu being a metabolic precursor for GABA, 75.4% of the GABA-IR population colocalized Glu. In vibratome sections GABA-IR neurons showed some local differences in number, whereas the Glu-IR were uniformly distributed in the three nuclei studied. Measured mean diameters for these neurons showed a distinct size difference for the GABA- and Glu-IR with little overlap. Cerebellar nuclei neurons projecting to the cortex (nucleocortical neurons, NCN) were identified by locally preinjecting the retrograde transported WGA-apoHRP-colloidal gold complex in the cerebellar cortex. Vibratome sections of these cerebellar were silver intensified for the retrograde tracer and double labeled for GABA and Glu. Of the total number of identified NCN, 8.7% were GABA-IR (10 animals) and 47.7% Glu-IR (5 animals). Many retrograde labeled NCN in the core of the thick sections were immunonegative for both amino acids due to poor antibody penetration, thus underestimating the proportions of cells containing GABA and Glu. The size distributions for the GABA-IR and Glu-IR NCN were similar to those measured in non-retrograde labeled nuclei in thick sections. The conclusions reached are that GABA-IR neurons of the cerebellar nuclei, including the NCN, use GABA as the presumed inhibitory neurotransmitter and that Glu-IR neurons may use Glu or another excitatory neurotransmitter.

Afferent Pathways↗
PubMed1992

Divalent cation changes in cerebellar Purkinje cells after climbing fiber deafferentation.

A secondary ion mass spectrometry (SIMS) microscope was used to detect intracellular stores of calcium, magnesium, sodium and potassium. Measurements were made in semithin sections of fixed tissues of normal and climbing fiber deafferented cerebellar cortex. Quantitative data were collected from 150 microns diameter image fields in the molecular and granule layers. The results indicate smaller quantities of both calcium and magnesium in the deafferented cerebellar cortex compared to the normals, the molecular as well as the granule layer being affected. The results are discussed in terms of the usefulness and limitations of the SIMS microscope for histological preparations.

Afferent Pathways↗
PubMed1991

The immunocytochemical distribution of calbindin-D28k and parvalbumin in identified neurons of the pulvinar-lateralis posterior complex of the cat.

The calbindin-D28k and parvalbumin immunoreactivities of the neurons of the pulvinar-lateral posterior complex (Pul-LP) were studied in the cat. The neurons of the Pul-LP projecting to the cerebral cortex were identified by a retrogradely transported tracer injected in the suprasylvian gyrus. Two populations of cells were found, a calbindin-D28k-immunoreactive, large-diameter population and a parvalbumin-immunoreactive, small-diameter group. The two kinds of cells are closely intermingled. The former includes the neurons retrogradely marked, and therefore projecting to the suprasylvian gyrus. The latter includes neurons which were not retrogradely marked, and therefore presumably intrinsic elements.

Animals↗
PubMed1991

Tetrodotoxin induced calcium spikes: in vitro and in vivo studies of normal and deafferented Purkinje cells.

Tetrodotoxin (TTX) is widely used to block the sodium dependent action potential in excitable cells to study their other ionic properties. TTX applied outside, selectively blocks voltage dependent sodium channels and is thought to have no other effects. We report here that TTX, applied to slices of rat cerebellum, suppressed sodium spikes of the Purkinje cells and induced firing in bursts of slower spikes. This activity was blocked by cobalt (2 mM) or cadmium (0.2 mM) in the medium as well as by hyperpolarizing currents showing that the slow spikes were due to voltage dependent calcium channels. The membrane potential was not significantly changed by TTX and the spikes during the bursts had the same threshold potentials and peak spike amplitudes as the voltage and Ca2+ dependent dendritic spikes evoked by injected current before adding TTX. This indicated that no marked changes in the membrane conductances were produced by the TTX. Unlike the burst firing induced by removing extracellular sodium, the TTX induced bursts were not followed by a large hyperpolarization. The same kind of results were obtained with extracellular recording in the in-vivo preparation with TTX applied topically or by pressure near the recording sites. TTX induced burst firing was not due to blocking afferent inhibitory input to the PC, since bicuculline (10(-6) M) applied without TTX, produced only increased firing of fast action potentials and no bursts. The bursts could be arrested within 1 to 2 min by intravenously administering 2 mg/kg sodium pentobarbital, the blockage lasted from 5 to 15 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1991

Decreased sensitivity of cerebellar nuclei neurons to GABA and taurine: effects of long-term inferior olive destruction in the rat.

The effects of iontophoretically applying the presumed Purkinje cell inhibitory neurotransmitters, GABA and taurine, were tested on neurons of the cerebellar nuclei in normal and in climbing-fiber-deafferented cerebella. Rats treated with 3-acetylpyridine to totally destroy the inferior olive were used for acute experiments 105-185 days after treatment. In controls, nearly all neuronal firing was dose-dependently depressed by both inhibitory amino acids. The depression in firing for both were antagonized by bicuculline and picrotoxin but not by strychnine while TAG specifically antagonized only responses to taurine. At sufficient doses, bicuculline and TAG induced disinhibitory responses (significant release of neuron discharge) in the absence of applied antagonist. In deafferented animals, the inhibitory efficacy of GABA and taurine were drastically reduced; most of the neurons failed to respond to these amino acids at the same iontophoretic parameters as for the control rats. Moreover, high doses of bicuculline and TAG did not induce any disinhibitory response (no significant increase in discharge rate) in most of the neurons tested. These results clearly demonstrate that climbing fiber deafferentation reduces postsynaptic sensitivity of the cerebellar nuclei neurons for the presumed Purkinje cell inhibitory neurotransmitters.

Action Potentials↗
PubMed1990

Colocalization of calbindin and GABA in medial nucleus of the trapezoid body of the rat.

Using immunocytochemical methods, both calbindin and GABA were found to be colocalized in the somas of all the cells of the medial nucleus of the trapezoid body (NMTB) of the rat auditory system. In the lateral superior olive (LSO), calbindin was also found in the terminals but not in the cells. Some terminal labelling was found in the medial superior olive (MSO). GABA was also found in the somas of some cells in both LSO and MSO, but most of the labelling was in terminals. In the rat, calbindin appears to be more involved in a pathway that detects interaural intensity differences.

Animals↗
PubMed1990

Cerebellar localization and colocalization of GABA and calcium binding protein-D28K.

Immunocytochemical studies using antibodies raised against the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA) and against the 28 Kd vitamin D dependent calcium binding protein (calbindin) in the cerebellum, are reviewed. The GABA immunoreactive neurones found in the cerebellar cortex were the Purkinje cell (PC), the three classes of intrinsic inhibitory interneurones, stellate, basket and Golgi cells and the cells of Lugaro. Some of the neurons of the cerebellar nuclei were also found to be GABA immunoreactive. A part of these could be identified as extrinsic neurones projecting either back to the cerebellar cortex, or to the inferior olive, both these pathways being topographically highly organized but arising from independent parent neurons. The presumed inhibitory function of these two pathways are discussed. Calbindin immunoreactivity in the cerebellum was confined to the PCs, staining concerned the whole cell including soma, branching dendrites, axons and axons terminals. The antibody, which appears to be tightly bound to the PC in vivo, failed to stain some of the PC when cerebellar slices maintained in vitro were studied. The stability of the antigen-antibody binding and the use of calbindin as a marker specific for the PC in the cerebellum, is discussed. Co-localization of GABA with calbindin as well as with other calcium binding proteins are reported to be found in the PCs. While these co-localizations have led to much speculation, conclusive functional roles for them have not been identified at present.

Animals↗
PubMed1989

The GABAergic neurones of the cerebellar nuclei in the rat: projections to the cerebellar cortex.

The presence of gamma-aminobutyric acid (GABA) in the neurones of the cerebellar nucleocortical pathway is here reported. The pathway was identified by retrograde tracer and the GABA content was revealed immunohistochemically. It was found that most of the neurones giving rise to the reciprocal, non-reciprocal and symmetrical projections are indeed GABA-immunoreactive. They were observed in all the subdivisions of the nucleus medialis, of the nucleus interpositus and of the nucleus lateralis sending axons respectively to the sagittal zones A, C1-3 and D of the cerebellar cortex. The nucleus vestibularis lateralis and the related sagittal zone B were devoid of such projections.

Animals↗
PubMed1987

Release of cerebellar inhibitory activity by partial destruction of the inferior olive with kainic acid in rat.

Partial destruction of the neurones of the inferior olive was obtained by local ionophoretic injection of kainic acid. Complex spike discharges of the Purkinje cells are suppressed 2-3 h after application of the drug. The metabolic activity increases in the region of the cerebellar nuclei within 2 h and persists for 3 days following the kainic acid injection. The increase is only observed in those parts of the cerebellar nuclei receiving terminals from the Purkinje cells deafferented of the climbing fibres. No changes were detected when the injection affected only the underlying reticular formation.

Action Potentials↗
PubMed1987

The interposito-rubrospinal system. Anatomical tracing of a motor control pathway in the rat.

The cerebello-rubromotor pathway, impinging on both spinal and facial motor nuclei, has been traced in the rat, using the bidirectional transport of horseradish peroxidase-wheat germ agglutinin conjugate. After injection of the tracer in the red nucleus (NR), retrograde labelling shows a topical arrangement of the cerebellorubral connection. The nucleus lateralis projects to the parvocellular NR (NRp) and the nucleus interpositus to the magnocellular NR (NRm). The nucleus interpositus anterior (NIA) reaches the entire NRm and this projection is topographically arranged: the medial NIA sends fibres ventrally, the lateral NIA dorsally. The medial two-thirds of the nucleus interpositus posterior (NIP) project only to the medial aspect of the NRm, with no apparent organization. No connection has been found between the lateral third of NIP and the NRm. After injection of the tracer in the spinal cord or the nucleus of the facial nerve, retrograde labelling is observed almost throughout the entire caudorostral extent of the NR, although labelling is more scant in NRp than in NRm. Rubrospinal and rubrofacial projections are somatotopically arranged in the dorsoventral direction: ventrolateral regions of NR reach the lumbar cord, medioventral regions the lower cervical levels, intermediary regions the upper cervical levels and finally the dorsalmost part of the NR projects to the nucleus of the facial nerve. After injection of the tracer in the cerebellar nuclei, anterograde labelling in the NR shows that interpositorubral connections determine two subregions in the NR: a lateral one under the exclusive control of the NIA, and a medial one under the control of both NIA-NIP afferents. It confirms in addition the topography of the NIA-NRm projection and shows the preponderant participation of the NIA afferents to the interpositorubral connection. Thus, it appears from our results that the cerebellorubral arrangement matches, to a great extent, the "rubromotor" efferent organization.

Animals↗
PubMed1986

The cerebellorubral projection in the rat: retrograde anatomical study.

The cerebellorubral projections have been studied in the rat using the retrograde transport of horseradish peroxidase-wheat germ agglutinin conjugate. The lateral cerebellar nucleus projects to the parvocellular red nucleus (RN), the anterior (NIA) and posterior (NIP) interposed nuclei project to the magnocellular RN. Whereas the projections from the NIP are limited to the medial aspect of the RN, those from the NIA extend throughout the magnocellular RN. NIA-RN projections are topographically arranged: the medial NIA projects ventrally, the lateral NIA projects dorsally. Functionally, this differential distribution seems to fit the hindlimb-forelimb areas of origin of the rubrospinal tract.

Animals↗
PubMed1985

Long term modification of cerebellar inhibition after inferior olive degeneration.

The long term effects of inferior olive destruction on the activities of the Purkinje cells and their target neurones in the cerebellar nuclei were studied in the rat. Careful observations were also made of motor behaviour throughout the study. Albino rats were injected with 3-acetylpyridine to produce a neurotoxic destruction of the inferior olive and then were used for acute recording experiments at 1-2 days, 5-7 days, 12-18 days, 35-38 days, 75-97 days and 230-252 days. After degeneration of the inferior olive, there was an initial period lasting for a few days, characterized by a high firing frequency of Purkinje cells associated with a very low level of activity of the neurones in the cerebellar nuclei. During this period, there was a deep depression of motor activity. A period of adaptation follows during the first month, characterized by a slow recovery of the initial firing frequency of the cerebellar units and a gradual recovery of spontaneous locomotion; nevertheless the firing pattern and motor behaviour remain abnormal. From one month on the unit activities disturbances and the motor deficiencies stabilize. The hypothesis is advanced that Purkinje cell inhibition on their target neurones, which increases during the initial period, gradually diminishes during the adaptation time, and then stabilizes to a subnormal state.

Aging↗
PubMed1985

Release of cerebellar inhibition by climbing fiber deafferentation.

Cerebellar units were recorded extracellularly in rats before and after an intraveinous injection of 3-acetylpyridine destroying selectively the IO. All the Purkinje cells show a loss of the complex discharge between 2 h 15 min and 2 h 45 min after treatment. This time, called the "critical period" corresponds to the degeneration of the neurons of the inferior olive as revealed by the decrease of their metabolic activity. The simple spikes of the Purkinje cells increase their discharge frequency soon after the climbing fibers cease firing. On the contrary the firing frequency of the inhibitory interneurons does not show significant changes after degeneration of the inferior olive. The efferent cerebellar neurons, including cells of the cerebellar and vestibular nuclei receiving the axon terminals of the Purkinje cells, decrease their discharge rate up to thirty times during and after the critical period. It is demonstrated that this effect is due to the increased inhibitory activity of the Purkinje cells deafferented from the climbing fibers, whereas the deafferentation of the efferent cerebellar neurones from the collaterals of the olivary cells has little impact.

Animals↗
PubMed1985

[Does proprioception of the extrinsic eye muscles participate in equilibrium, vision and oculomotor action?].

Extrinsic eye muscles respond to both proprioceptive and visual impulses. Histology of ocular proprioceptive receptors shows them to be qualitatively and original, neuromuscular bundles are found in primates, and so called "palisade sensory nerve endings" in felines. Golgi's osteotendinous receptors are apparently absent. The number of muscle receptors is high and their proportion in relation to muscle weight even more so. The afferent pathway for this sensory system initially accompanies the motor fibers of oculomotor III, IV, ans VI nerves. Some fibers continue with these nerves to the brain stem while others join the ophthalmic branch of the trigeminal nerve (probably in the cavernous sinus). Cell bodies of proprioceptive fibers are located either in the mesencephalic root of the trigeminal nerve and in the Gasserian ganglion. The superior colliculus, center of eye-head coordination integration, also receives proprioceptive data. Proprioceptive afferent signals also project on two cerebellar cortex regions, one in the VI th and VII th lobules of the posterior lobe vermis, the other in the flocculus, all major centers for control and interaction of visuocervicovestibular activity. Extraocular proprioceptive impulses play an important role as do visual influx, in the maturation of the visual cortex in mammalia. Moreover, maintenance of binocular integration appears to require both coherent binocular vision and balanced bilateral, extraocular afferent impulses. Clinical consequences are multiple. Proprioceptive imbalance due to oculomotor dysfunction could explain the attendant visual deficit, which is reversible after correction of they motor disorder. Forced excentration of gaze provokes equilibrium disturbances in normal subjects. In cases of oculomotor palsy, the accompanying vertigo often observed could thus be due à lack of coordination between the intention of movement and its execution. Many oculomotor signs are dependent on the position of gaze alone, in the absence of any visual guide: end-position nystagmus gaze nystagmus, rebound nystagmus, gaze drift, periodic alternating and vertical superior nystagmus, ocular flutter and opsoclonus, nystagmus retractorius, etc. Proprioceptive impulses from extrinsic eye muscles are probably necessary for assessment of orbital coordinates of the ocular globe position during target fixation: this emphasizes the importance of this proprioceptive factor in the origin of ocular jerks. Proprioceptive impulses may play a crucial role in the triggering of the rapid phase of nystagmus, thus conditioning the variations in amplitude seen in provoked nystagmus tests.

Afferent Pathways↗