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Results for “CEREBELLAR CORTEX”

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PubMed1995

Distribution of six transplasma membrane NADH-dehydrogenases in rat brain tissue.

Transplasma membrane redox plays a significant role in cellular activation and growth. Six isoenzymes could be prepared from purified rat brain synaptic plasma membrane. Polyclonal antibodies have been prepared against six transplasma membrane oxydoreductases (PMO-I to PMO-VI) and the tissue distribution of the various iso-enzymes have been investigated in adult rat brains by means of immunohistochemistry. PMO-I is densely observed in layers I, IV and V of the parietal cortex, in CA1 of the hippocampus (except for the molecular layer), in the caudate putamen, in the dorsal, granular and ventral parts of the auditory nuclei, in some loci of the vestibular nuclei as well as in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-II is mainly located in the polymorphic layer of the dentate gyrus and in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-III is abundant in the piriform cortex, in the pyramidal layers of both CA1 and CA2, in the diagonal band of the basal ganglia, in the supraoptic nucleus and in various loci of the magnetocellular paraventricular nucleus of the hippothalamus as well as in the vestibular nuclei from the brain stem. In addition PMO-III is also densely present in motor nuclei (oculomotor, facial, hypoglossal and ambiguus nuclei), in the reticular formation and in the deep cerebellar nucleus as well as in the Purkinje layer of the cerebellar cortex. PMO-IV has a similar location but is less abundant in the vestibular nuclei of the sensory brain stem and in the motor nucleus. PMO-V in contrast is poorly present in most brain areas compared to the other iso-enzymes, apart of the Purkinje layer of the cerebellar cortex. Finally PMO-VI is mainly present in the oriens layer and in the stratum radiatum of the hippocampus formation, in the supraoptic and lateral magnocellular nucleus of the hypothalamus, in the mesencephalic trigeminal nucleus, in the ventral auditory nucleus and in the facial nucleus of the brain stem as well as in red nucleus of the reticular formation and in the Purkinje layer of the cerebellar cortex. These data show that the iso-enzymes are located in specific brain nuclei. The significance of the results in respect to the yet very poorly defined function of PMO's is discussed.

Animals↗

PubMed2003

Human cerebellum: surface-assisted cortical parcellation and volumetry with magnetic resonance imaging.

We describe a system of surface-assisted parcellation (SAP) of the human cerebellar cortex derived from neural systems functional and behavioral anatomy. This system is based on MRI and preserves the unique morphologic and topographic features of the individual cerebellum. All major fissures of the cerebellum were identified and traced in the flattened representation of the cerebellar cortex using the program "FreeSurfer." Parcellation of the cerebellar cortex followed using the fissure information in conjunction with landmarks using the program "Cardviews" to create 64 gyral-based cerebellar parcellation units. Computer-assisted algorithms enable the execution of the cerebellar parcellation procedure as well as volumetric measurements and topographic localization. The SAP technique makes it possible to represent multimodal structural and functional imaging data on the flattened surface of the cerebellar cortex as illustrated in one functional MRI experiment.

Adult↗

PubMed1998

Cerebellar contributions to motor timing: a PET study of auditory and visual rhythm reproduction.

The perception and production of temporal patterns, or rhythms, is important for both music and speech. However, the way in which the human brain achieves accurate timing of perceptual input and motor output is as yet little understood. Central control of both motor timing and perceptual timing across modalities has been linked to both the cerebellum and the basal ganglia (BG). The present study was designed to test the hypothesized central control of temporal processing and to examine the roles of the cerebellum, BG, and sensory association areas. In this positron emission tomography (PET) activation paradigm, subjects reproduced rhythms of increasing temporal complexity that were presented separately in the auditory and visual modalities. The results provide support for a supramodal contribution of the lateral cerebellar cortex and cerebellar vermis to the production of a timed motor response, particularly when it is complex and/or novel. The results also give partial support to the involvement of BG structures in motor timing, although this may be more directly related to implementation of the motor response than to timing per se. Finally, sensory association areas and the ventrolateral frontal cortex were found to be involved in modality-specific encoding and retrieval of the temporal stimuli. Taken together, these results point to the participation of a number of neural structures in the production of a timed motor response from an external stimulus. The role of the cerebellum in timing is conceptualized not as a clock or counter but simply as the structure that provides the necessary circuitry for the sensory system to extract temporal information and for the motor system to learn to produce a precisely timed response.

Adult↗

PubMed1991

Organization of the cerebellum in the pigeon (Columba livia): I. Corticonuclear and corticovestibular connections.

The projections of the cerebellar cortex upon the cerebellar nuclei and the vestibular complex of the pigeon have been delineated using WGA-HRP as an anterograde and retrograde tracer. Injections into individual cortical lobules (II-IXa) produce a pattern of ipsilateral terminal labeling of both the cerebellar and vestibular nuclei. The pattern of corticonuclear projections indicates both a rostrocaudal and a mediolateral organization with respect to the lobules and is consistent with a division of the cerebellar nuclei into a medial (CbM) and a lateral (CbL) nucleus. The retrograde experiments indicate that these nuclei receive projections, respectively, from Purkinje cells within medial (A) and lateral (C) longitudinal zones, which alternate with longitudinal zones (B, E) projecting upon the vestibular complex. Purkinje cells in (vestibulocerebellar) lobules IXb-X show only limited projections upon the cerebellar nuclei, but do project extensively upon the cerebellovestibular process (PCV), as well as upon the medial, superior, and descending vestibular nuclei. As the injection site shifts from medial to lateral, there is a corresponding shift in focus of the projection within PCV from areas bordering CbM to those abutting CbL. The topographic organization of corticovestibular projections is less clear-cut than those of the corticonuclear projections. Lobules II-X project upon the lateral vestibular nucleus (anterior lobe) or the dorsolateral vestibular nucleus (posterior lobe). These projections originate from either side of the lateral (C) zone. Projections originating from the medialmost (B) zone are interrupted in lobules VI and VII. The anterior and posterior portions of the lateralmost (E) zone overlap along lobules VI and VII. In addition, the E zone of the anterior lobe is the source of projections upon the medial, the descending, and the superior vestibular nuclei. Projections from the auricle and adjacent lateral unfoliated cortex (F zone) focus upon the infracerebellar nucleus, the medial tangential nucleus, and the medial division of the superior vestibular nucleus. The data suggest that the cerebellar cortex of the pigeon, like that of mammals, may be subdivided into a mediolaterally oriented series of longitudinal zones, with Purkinje cells in each zone projecting ipsilaterally to specific cerebellar nuclei or vestibular regions. For cortical regions exclusive of the auricle and lateral unfoliated cortex, three such zones (A, B, and C) are defined that are comparable in their efferent targets with the A, B, and C zones of mammals. There does not appear to be a D zone in the pigeon. The results are discussed in relation to comparative data on amphibians, reptiles, and mammals.

Animals↗

PubMed1980

Acetylcholinesterase activity and its molecular forms in selected regions of the dog's nervous system.

Acetylcholinestrase (AChE, EC 3.1.1.7) activity and its molecular forms were studied in the cerebral cortex, basal ganglia, thalamus, cerebellar cortex, medulla oblongata, the various parts of spinal cord, the spinal ganglia and the sciatic nerve in intact adult dogs. The number and the proportion of different molecular forms of AChE in these regions of the dog's nervous system varied considerably. The highest AChE activity was found in the basal ganglia, where only one molecular forms was detected. Activity was also high in the cerebellar cortex (2 isoenzymes), the thalamus (4 isoenzymes) and the medulla oblongata (5 isoenzymes), and was lower in the cerebral cortex (3 isoenzymes). AChE activity in the spinal cord was highest in the sacral part (4 isoenzymes); in the other parts (3 isoenzymes) it was equal. Five molecular forms were found in the spinal ganglia and two in the sciatic nerve. The significance of the multiple molecular forms of AChE is discussed.

Acetylcholinesterase↗

PubMed2005

[Nervous component of mature cystic ovarian teratomas].

In 30-50 percent of cases mature cystic ovarian teratomas contain a nervous tissue which can be highly differentiated. This study was focused on research of the nervous component of mature cystic ovarian teratomas with generally available methods to pathologists, including impregnation techniques, immunohistochemistry and electron microscopy. From the total number of 212 mature cystic ovarian teratomas, the nervous tissue was found in 72 cases (34%), which corresponds to the literature data. According to its differentiation, it was possible to distinguish five categories of nervous tissue by light microscopy: 0 peripheral nervous tissue only, 1--solid glial nodules, 2--glial cysts, 3--glial tissue with abundant scattered neurons and, finally, 4--organoid nervous tissue similar to certain CNS structures. Apart from the foci similar to grey matter of the spinal cord and cerebral cortex, those of differentiated cerebellar cortex were present as well. Astrocytes mostly predominated in the nervous tissue, and they sometimes showed reactive changes including gemistocytes and formation of Rosenthal fibres. Neuronal elements also showed degenerative changes quite frequently, especially in a less differentiated nervous component. These changes might have developed due to an abnormal location of the nervous tissue or its hypoxia in the teratoma. Contrary to some literature data, oligodendrocytes and myelin were present in the nervous tissue of most of our cases. Ultrastructurally, neurons with fully developed synapses were observed in the nervous component, and dendritic spines were present on dendrites of Purkinje cells of cerebellar cortex. The results obtained from the examination of teratomas in this study confirmed and enriched the literature data concerning the high degree of differentiation of their nervous components. We suggest that the differentiated nervous tissue of teratoma represents a unique natural model suitable for research of some aspects of neurohistology and neuropathology, e.g. synaptogenesis or myelinogenesis.

Adolescent↗

PubMed1992

Age-related changes in binding to excitatory amino acid uptake sites in human cerebellum.

In vitro autoradiography and test-tube assay of the sodium-dependent binding of D-[3H]aspartate were used to localize and quantify the uptake site for the excitatory amino acid neurotransmitters glutamate and aspartate in the cerebellar cortex of human cerebellar hemispheres. Autoradiograms revealed a pronounced heterogeneity in the distribution of D-[3H]aspartate binding in cortex from adult brains, with the highest binding density corresponding to the Purkinje cell layer, high binding in molecular layer and low binding in granule cell layer. In contrast, cerebellar cortex from infants at term (40 weeks gestation) had only low binding of the ligand in both the molecular and the Purkinje cell layers. Both methods employed for measuring D-[3H]aspartate binding showed that the number of binding sites in Purkinje and molecular layers increased rapidly from term to 20 weeks postnatal age and achieved levels higher than those found in adult cerebellum. It is concluded that a substantial increase in the numbers of glutamate/aspartate uptake sites takes place in the human cerebellum during the early postnatal period. It is deduced that the excess uptake sites are eliminated as the cerebellum matures.

Aged↗

PubMed1996

Ultrastructural localization of glycogen phosphorylase predominantly in astrocytes of the gerbil brain.

The localization of glycogen phosphorylase in gerbil brain was determined by immunoelectron microscopy using the pre-embedding peroxidase technique. Electron-dense granular reaction product of peroxidase activity was observed in astrocytes of all brain regions examined (cerebral cortex, striatum, cerebellar cortex, hippocampal formation, corpus callosum, mesencephalic trigeminal nucleus). The reaction product was distributed in a diffuse pattern throughout the cytoplasmic matrix of perikarya and processes; sometimes the nucleus of labeled astrocytes also contains immunopositive material. The light microscopically visible glycogen phosphorylase immunoreactivity associated with capillaries could be characterized as a staining of astrocytic endfeet ensheathing capillaries. Endothelial cells and pericytes were never labeled. In addition to astrocytes, ependymal cells also presented immunopositive material in their cytoplasm. On the other hand, no reaction product was observed in cells identified as oligodendroglia or microglia. Neurons (with the exception of neurons of the mesencephalic trigeminal nucleus), their processes, and their synaptic endings were free of reaction product. In the neuropil we frequently observed immunopositive glial processes adjacent to synaptic structures. This intimate spatial relationship may be interpreted as a morphological sign of a metabolic interaction. The data support the hypothesis that astroglia play a key role in glycogen metabolism and energization of the brain.

Animals↗

PubMed1994

Histological and ultrastructural localization of the kainate receptor subunits, KA2 and GluR6/7, in the rat nervous system using selective antipeptide antibodies.

Kainate receptors are found throughout many regions of the brain and presumably contribute to responses of neurons to glutamate and other excitatory amino acids. Two affinity-purified polyclonal antibodies that recognize the kainate binding subunits, KA2 and GluR6, were made using C-terminus peptides. A previous study demonstrated that each antibody is specific for its subunit, although antibody to GluR6 recognizes GluR7 to some extent (hence the designation GluR6/7). Vibratome sections immunostained with either antibody showed light to moderate staining in many structures in the brain as well as in cervical spinal cord, dorsal root and vestibular ganglia, and pineal and pituitary glands. Moderate levels were seen in the olfactory bulb, cerebral cortex, caudate/putamen, and hypothalamus, whereas much of the thalamus was stained lightly. In the hippocampus, CA3 pyramidal cells were stained more densely than CA1 pyramidal cells--the difference more evident with antibody to GluR6/7. In addition, neuropilar staining was densest in the stratum lucidum of the CA3 region. In the brainstem, staining was moderate to moderately dense in a number of sensory, motor, and reticular nuclei. The moderately dense staining in the reticulothalamic nucleus and pontine nuclei with antibody to GluR6/7 may represent its recognition of GluR7. In the cerebellum, staining was moderate in granular and molecular layers with antibody to KA2 and in the molecular layer with antibody to GluR6/7, whereas it was moderately dense to dense in the granular layer with the GluR6/7 antibody. Outside of the brain, densest staining was seen with antibody to KA2 in the intermediate lobe of the pituitary gland. Ultrastructural localization of immunostaining was examined in the hippocampus, cerebral cortex, and cerebellar cortex. Typically, major staining was in postsynaptic densities apposed by unstained presynaptic terminals with round or mainly round vesicles and in associated dendrites. The light microscope pattern of staining was fairly similar to that of previous [3H]kainate binding and in situ hybridization studies. In addition, comparison with previous studies on distribution of other types of glutamate receptors indicates that KA2 and GluR6/7 are found with various other subunits in many of the same cell populations throughout the nervous system.

Amino Acid Sequence↗

PubMed2001

Distribution of intraventricularly administered antiamyloid-beta peptide (Abeta) antibody in the mouse brain.

There is considerable interest in utilizing the intracerebroventricular (icv) route of administration of antibodies in the brain for various studies and for the therapy of malignancies, but very little is known about the anatomic extent of distribution of the antibody in brain after injection into the third ventricle. To explore the potential for icv administration of antiamyloid-beta peptide (Abeta) in reducing Abeta toxicity in brain in Alzheimer's disease, we first mapped the time course and path of transit of horseradish peroxidase (HRP)-labeled antibody. The results show that, after a single injection into the mouse third venticle, the HRP-labeled antibody is localized within the microvasculature, first that of the corticohippocampal region close to the site of injection at 3 hr. By 24 hr, the antibody is distributed throughout the hippocampus and frontoparietal cortex close to the injection site, as well as in the deep and outer cerebral cortex and cerebellar cortex remote from the injection site. The injected antibody is almost entirely removed by 4 days. Therefore, the antibody had diffused throughout all the brain by 24 hr, showing the feasibility of small quantities of anti-Abeta antibody infused into the third ventricle to reach extracellular epitopes throughout the brain parenchyma rapidly.

Alzheimer Disease↗

PubMed2000

Measurement of extrastriatal D2-like receptor binding with [11C]FLB 457--a test-retest analysis.

[11C]FLB 457 is a radioligand for positron emission tomography (PET) that possesses high affinity to D2/D3 receptors. It has been suggested to be useful for quantification of low-density dopamine D2 receptor populations, e.g. in cortical and limbic brain areas. We explored the reproducibility of five methods for measuring extrastriatal D2-like receptor binding potential with [11C]FLB 457. Seven healthy male volunteers were examined twice with [11C]FLB 457 (high specific radioactivity) on the same day, at least 3 h apart. Four brain areas, frontal cortex, nucleus thalamus, temporal cortex and cerebellar cortex, were examined. Binding potentials (BPs) were derived from (1) a target to cerebellum distribution volume ratio, (2/3) two reversible reference tissue compartment models and (4) a transient equilibrium approach. For comparison, BP values were also calculated with the standard three-compartment kinetic model that does not assume a receptor-free reference region. The use of the standard three-compartment model did not result in reproducible BP estimates. The distribution volume (DV) ratio, reference tissue compartment models and the transient equilibrium method all had good to excellent intraclass correlation coefficients (ICCs) in the studied brain areas ranging from 0.56 to 0.93. Absolute variability was also relatively low, ranging from 5.3% to 10.4%. There were no marked differences in the ICC or absolute and relative variability between the four methods based on a reference tissue (cerebellum). In addition, we did not observe systematic differences in the BP between the first and the second scan. These data indicate that the reproducibility of the DV ratio, reference tissue models and the transient equilibrium method is good or excellent. However, each of these methods includes assumptions affecting their validity. Thus, the choice of method will be critically dependent on the purpose of the study.

Adult↗

PubMed1994

Autoradiographic distribution of D3-type dopamine receptors in human brain using [3H]7-hydroxy-N,N-di-n-propyl-2-aminotetralin.

The regional distribution of D3 dopamine receptors was studied in human brain by quantitative autoradiography with [3H]7-hydroxy-N,N-di-n-propyl-2-aminotetralin ([3H]7-OH-DPAT). The highest densities were found in the ventral striatum/nucleus accumbens, followed by the remainder of the neostriatum, cerebral cortex, and cerebellar cortex. Moderate amounts were found in the substantia nigra. Low densities of D3 dopamine receptors were visualized in pituitary gland (posterior lobe > anterior lobe), amygdala, and hippocampus. The globus pallidus and thalamus contained lower densities. The distribution pattern is much more widespread as detected by in situ hybridisation histochemistry for D3 mRNA in human and in rat brain. Our data confirm a predilection of D3 receptors in brain areas involved in cognitive and emotional functions. The presence of D3 receptors in non-limbic parts of the neostriatum and substantia nigra suggests that they also play a role in the dopaminergic control of motor processes. Its precise function in cerebellum and pituitary gland is at present uncertain.

Aged↗

PubMed1994

Rapid potentiation of DNA binding activities of particular transcription factors with leucine-zipper motifs in discrete brain structures of the gerbil with transient forebrain ischemia.

Binding of radiolabeled double stranded oligonucleotide probes for nuclear transcription factors with leucine-zipper motifs, such as activator protein-1 (AP1), cyclic AMP response element binding protein (CREB) and Myc, was unevenly distributed in gerbil brain in a manner peculiar to each factor. Among 3 different hippocampal subfields examined, the dentate gyrus had the highest basal DNA binding activities of AP1 with progressively less potent binding in the CA3 and CA1 subfields. Similarly, the dentate gyrus was highest in the basal binding of probes for both CREB and Myc among the 3 distinct hippocampal subregions. However, transient forebrain ischemia for 5 min induced more potent enhancement of the AP1 binding in the CA1 subfield 4 h after the insult than in the CA3 subfield and dentate gyrus. In contrast, the ischemic injury similarly tripled DNA binding activities of CREB without markedly affecting those of Myc in hippocampal CA1 and CA3 subfields. Binding of the probe for AP1 was also markedly potentiated following ischemia in the thalamus, caudate putamen, frontal cortex and cerebellar cortex in a rank order of decreasing magnitude, while the ischemic insult induced slight but statistically significant potentiation of both CREB and Myc binding in the thalamus without affecting that in other discrete brain regions. These results suggest that expression of AP1 may be a determinant of unique vulnerability and/or resistance to an ischemic insult in the gerbil hippocampus.

Animals↗

PubMed1996

Central benzodiazepine receptor occupancy by zolpidem in the human brain as assessed by positron emission tomography.

The central benzodiazepine receptor occupancy by zolpidem in man is unknown. The present study used positron emission tomography (PET) and [11C]flumazenil to assess in five healthy volunteers, central benzodiazepine receptor occupancy in brain regions with high receptor densities 1 h following an acute oral administration of twice the usual hypnotic dose of zolpidem (20 mg). Receptor occupancy was measured in five discrete structures (middle frontal gyrus, middle temporal gyrus, posterior occipital cortex, lateral parietal cortex, and cerebellar cortex) and in a large neocortical area as the fractional change in the [11C]flumazenil bound/free ratio for the interval 15-40 min post-administration of the radiotracer. The free-radioligand concentration was estimated from the pons, a reference structure virtually devoid of central benzodiazepine receptor. With individual pons values, mean occupancy was about 21% but with spurious inter-subject variability. With pons values averaged across the five subjects and separately for control and treated condition, the occupancy was (mean +/- S.D.) 27 +/- 11% for the whole neocortex, and ranged from 26 to 29% in the five discrete structures (P < 0.01). By showing hypnotic effect at moderate occupancies, this study directly provides evidence for the full-agonist properties of zolpidem in human.

Adult↗

PubMed1992

Ontogenesis of cerebellar afferents identified by cholecystokinin-like immunoreactivity.

The present account provides a developmental timetable for the maturation of cholecystokinin (CCK)-positive fibers in the cerebellar cortex and cerebellar nuclei of the opossum. CCK-positive fibers are in the cerebellar peduncle by postnatal day (PD) 1, however they wait until PD 7 to penetrate the cerebellar anlage. Between PD 7 and PD 20 the fibers wait again in the medullary core of the cerebellum. After PD 20, there are 2 distinct patterns of CCK localization within the overlying cortical layers. The first pattern develops between PD 20-26 when CCK puncta are present in restricted foci within the Purkinje cell layer of the anterior lobe vermis. They distribute in 4 parasagittal bands, 2 on either side of the midline, that extend from the primary fissure rostrally into the anterior lobe of the cerebellum. By PD 33 two additional parasagittal bands are present in the posterior lobe vermis. The vast majority of these CCK puncta are transient in nature as all but a few disappear by PD 84. Those that remain progress through a series of developmental stages characteristic of climbing fiber ontogeny. These climbing fibers persist in lobules V, VII and VIII of the adult cerebellum. Further, there is a transient expression of CCK-immunoreactivity within inferior olivary neurons. These observations support the interpretation that the transient population of CCK-IR puncta are immature climbing fiber axons derived from the inferior olive. The second pattern of CCK localization is evident between PD 30-33, the time when granule cells first can be recognized in a histologically distinct internal granule cell layer (IGL). Between PD 30 and PD 68 there is a differential pattern of distribution of CCK-IR profiles within the lobules of the cerebellum. Initially, CCK-IR axons are only present in the anterior vermis where they are aligned in register with the bands of CCK puncta in the Purkinje cell layer. CCK-IR puncta are not present in the posterior lobe vermis or hemispheres until later stages of development. Further, a sagittal organization is not evident in either of these latter 2 areas. Initially, CCK-IR profiles in the IGL cannot be identified as mossy fibers based on their terminal morphology. When they first enter the IGL they appear as punctate elements. Over time they become increasingly more complex in shape and between PD 68-84 develop morphological characteristics of adult mossy fiber rosettes. The cerebellar nuclei can be distinguished histologically by PD 18, but CCK-IR fibers are not evident among these neurons until PD 36 which corresponds to about the time they can be visualized in the IGL. In addition, CCK-IR cell bodies first appear in the cerebellar nuclei between PD 26-30; these are present in the adult.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed1993

The cerebellum as a predictor of neural messages--I. The stable estimator hypothesis.

To describe how the central nervous system combines sensory messages, the hypothesis of a "stable estimator" is proposed: the central nervous system would construct internal estimates of the physical variables characterizing the body movements (e.g. head rotational velocity in space), while a regulating circuit would optimize the process of estimation of each variable, according to the available information and the overall performances of the sensorimotor reactions. The stable estimator of each variable would be embedded in a definite folium of the cerebellar cortex and the related cerebellar and brainstem nuclei. It would be controlled by the related part of the inferior olive. The estimate of each physical variable would be constructed by complementing the message from a dedicated sensory system (e.g. the semi-circular canals, which measure head rotational velocity in space) by neural messages related to the same variable (e.g. eye velocity in the head and retinal slip). Thus, the estimate would be accurate over the widest possible physiological ranges of frequency and velocity. The complementing signals would result from combining estimates of other variables (such as gaze velocity and eye velocity in the orbit), according to rules reproducing the relationships between physical variables. From the same complementing signals, the message from the dedicated sensory system would be predicted, and it is argued that this predictive function resides in the cerebellar cortex. The inferior olive would compare an actual signal about the performance of a sensorimotor reaction to signals of expected performance, computed from the various internal estimates of the variables which determine this performance. Any erroneous setting in a stable estimator would cause differences between the actual and the expected values. Then the inferior olive would compute an error signal directing compensatory functional plasticity. Finally, the whole estimating circuit would be regulated so that the internal coherence between neural messages and the performance of sensorimotor reactions would be achieved. Anatomical identifications and rules of functional plasticity are proposed.

Adaptation, Psychological↗

PubMed1996

Distribution of glycine-immunoreactive cell bodies and fibers in the rat brain.

To localize glycinergic cell bodies and fibers in the rat brain, we developed a sensitive immunohistochemical method combining the use of specific glycine antibodies (Campistron G. et al. (1986) Brain Res. 376, 400-405; Wenthold R. J. et al. (1987) Neuroscience 22, 897-912) with the streptavidin-horseradish peroxidase technique and 3,3'-diaminobenzidine.4HCl-nickel intensification. We confirmed the presence of numerous glycine-immunoreactive cell bodies and fibers in the cochlear nuclei, superior olivary complex, nucleus of the trapezoid body, cerebellar cortex, deep cerebellar nuclei and area postrema. For the first time in rats, we described a large to very large number of cell bodies in the medial vestibular ventral part, prepositus hypoglossal, gracile, raphe magnus and sensory trigeminal nuclei. A large number of cells was also observed in the oral and caudal pontine, parvocellular, parvocellular pars alpha, gigantocellular and gigantocellular pars alpha reticular nuclei. In addition, glycine-immunoreactive cells were seen in the ambiguous and subtrigeminal nuclei, the lateral habenula and the subfornical organ. We also provide the first evidence in rats for a very large number of fibers in the trigeminal, facial, ambiguous and hypoglossal motor nuclei, all nuclei of the medullary and pontine reticular formation, and the raphe and trigeminal sensory nuclei. We further revealed the presence of a substantial number of fibers in regions where glycine was not considered as a main inhibitory neurotransmitter, such as the pontine nuclei, the periaqueductal gray, the mesencephalic reticular formation, the anterior pretectal nucleus, the intralaminar thalamic nuclei, the zona incerta, the fields of Forel, the parvocellular parts of the paraventricular nucleus, the posterior hypothalamic areas, the anterior hypothalamic area, and the lateral and medial preoptic areas. These results indicate that, in contrast to previous statements, glycine may be an essential inhibitory neurotransmitter not only in the lower brainstem and spinal cord, but also in the upper brainstem and the forebrain.

Animals↗

PubMed2005

Ethanol-induced neuroapoptosis in the developing rodent cerebellum and related brain stem structures.

For three decades since the fetal alcohol syndrome (FAS) was first described, researchers have been keenly interested in understanding the mechanism(s) by which ethanol damages or disrupts development of the human fetal brain. It has been reported repeatedly that exposure of infant rats to ethanol causes a reduction in brain mass and loss of cerebellar Purkinje cells, but the mechanisms underlying these effects have remained elusive. In a recent series of studies, we have demonstrated that exposure of infant rats or mice to ethanol on a single occasion during the synaptogenesis period of development causes neurons in many regions of the developing central nervous system to commit suicide (die by apoptosis), but the cerebellum was not among the brain regions focused upon in these studies. Here we show in infant rats and mice that one-time exposure to ethanol triggers acute neurodegeneration of Purkinje cells and other neurons in the cerebellar cortex, deep cerebellar nuclei, and two related brainstem nuclei (nucleus pontis, inferior olivary complex). We also describe the time course of neurodegeneration and window of vulnerability for each of these neuronal cell types and demonstrate that the cell death process in each case is unequivocally apoptotic. We conclude that exposure of infant rats or mice to ethanol on a single occasion during synaptogenesis can kill Purkinje cells, and many other neuronal populations at all levels of the developing neuraxis, and in each case the mechanism of cell death is apoptosis.

Alcohol-Induced Disorders, Nervous System↗