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PubMed1982

Changing patterns of single-stranded-DNA-binding proteins in differentiating brain cortex and cerebellar neurons.

Single-stranded-DNA-binding proteins were analyzed in nuclei of differentiating rat cortex and cerebellar neurons. The developmental period investigated ranged from gestational day 19 (i.e. 3 days before term) to postnatal day 30. During this time both types of neurons undergo transition from proliferating, undifferentiated precursor cells to non-proliferating, terminally differentiated neurons. For comparison, nuclei from mature cortex glia and liver were also examined. Nuclei were isolated according to cell type, the proteins were 14C-labeled in vitro by reductive methylation and were fractionated by affinity chromatography on tandemly arranged columns of double-stranded and single-stranded DNA-cellulose. The columns were uncoupled and the proteins adsorbed to the single-stranded DNA were eluted with salt. They were then analyzed by high resolution two-dimensional gel electrophoresis followed by fluorography. This strategy ensured the selective detection of proteins that recognize single-stranded DNA specifically, and eliminated interference by proteins binding to DNA by simple ionic interaction as well as by proteins with affinity for double-stranded DNA. Many single-stranded-DNA-binding proteins showed conspicuous developmental fluctuations. In cortex neurons these took place around the time of birth and the first postnatal week, whereas in cerebellar neurons they occurred later and in a more protracted fashion. Thus, in both cortex and cerebellar neurons the protein changes followed a time course closely paralleling the arrest of cell division and the beginning of terminal differentiation. It is suggested that this approach may lead to the detection of putative regulatory proteins of the cell nucleus.

Animals↗

PubMedDate not supplied

Pharmacological analysis of cerebellar contributions to the timing and expression of conditioned eyelid responses.

Contradictory results have been reported regarding the effects of cerebellar cortex lesions on the expression of conditioned eyelid responses--either no effect, partial to complete abolition of responses, or disruption of response timing. This uncertainty is increased by debates regarding the region(s) of cerebellar cortex that are involved, by the likelihood that cortex lesions can inadvertently include damage to the interpositus nucleus or other pathways necessary for response expression, and by potential confounds from the degeneration of climbing fibers produced by cerebellar cortex lesions. We have addressed these issues by reversibly blocking cerebellar cortex output via infusion of the GABA antagonist picrotoxin into the interpositus nucleus. After picrotoxin infusion, conditioned responses are spared but their timing is disrupted and their amplitude diminished. In the same animals, conditioned responses were abolished by infusion of the GABA agonist muscimol and were unaffected by infusion of saline vehicle. These results are consistent with the hypothesis that (i) plasticity in the interpositus nucleus contributes to the expression of conditioned responses, as suggested by the responses seen with the cortex disconnected, and (ii) plasticity in the cerebellar cortex also contributes to conditioned response expression, as suggested by disruption of response timing.

Animals↗

PubMed1997

Pathology and immunocytochemistry of a kuru brain.

We report here results of modern staining techniques including anti-prion protein (PrP) immunocytochemistry to a set of archival brain specimens of a 16 year-old male who died from kuru in 1967. Brain suspensions transmitted disease to chimpanzees and New World monkeys. The PrP gene is homozygous for valine at the polymorphic codon 129. Histology shows neuronal loss, spongiform change, and astrogliosis. Lesions are maximal in parasagittal and interhemispheric areas of frontal, central and parietal cortex, cingulate cortex, striatum, and thalamus, and are accentuated in middle and deep cerebral cortical layers. PrP accumulates as diffuse synaptic type deposits and mostly unicentric plaques. PrP deposition is maximal in parasagittal and interhemispheric areas of frontal, central and parietal cortex, cingulate cortex, basal ganglia, and cerebellar cortex. Plaques are prominent in the striatum, thalamus, and granular layer of cerebellar cortex. Meticulous examination reveals only rare "florid" plaques with surrounding vacuolation. We conclude that 1) pathology including immunomorphology of PrP deposition in this kuru brain is within the lesion spectrum of Creutzfeldt-Jakob disease although plaques are unusually prominent and widespread; 2) kuru does not share the neuropathological hallmarks of the new Creutzfeldt-Jakob disease variant recently reported in the UK and France; 3) topographic prominence of PrP deposition parallels that of spongiform change and/or astrogliosis.

Adolescent↗

PubMed1994

Distribution of cholecystokinin binding sites in the North American opossum cerebellum.

Previous studies in our laboratory have reported on the differential distribution of several neuropeptides, including the octapeptide cholecystokinin (CCK8), in the cerebellar cortex and nuclei of the North American opossum (Didelphis marsupialis virginiana). The present account reports on the distribution of CCK8 binding sites as determined from serial autoradiographic images of the cerebellum which were labelled by using [125I]Bolton Hunter sulfated CCK8. Evidence for the limited presence of CCK8-like immunoreactivity and CCK8 binding sites in several other species suggests that the distribution of this peptide and its receptor(s) may be species specific. In the opossum, CCK8-like immunoreactivity is present in mossy fiber terminals that distribute throughout the cerebellar cortex; it has a very limited distribution in climbing fibers (King and Bishop (1990) J. Comp. Neurol. 238, 373-384. CCK8 binding sites are present throughout all lobules of the cerebellar cortex and the cerebellar nuclei, which correlates well with the distribution of the peptide. CCK8-like immunoreactivity is located primarily in the granule cell layer, although the greatest density of binding sites is in the molecular layer. The presence of CCK8 is mossy fiber terminals, coupled with the presence of CCK8 binding sites in the cerebellar cortex, and the fact that CCK8 alters the firing rate of Purkinje cells (Madtes et al. (1992) Neurosci. Abstr. 18, 853) indicate this peptide may function as a neuromodulator in the cerebellum of the North American opossum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

Central trigeminal and posterior eighth nerve projections in the turtle Chrysemys picta studied in vitro.

Recent electrophysiological studies in the turtle Chrysemys picta have suggested that a neural correlate of the eye-blink reflex can be evoked in an in vitro brain-stem-cerebellum preparation by electrical rather than natural stimulation of the cranial nerves. Discharge recorded in the abducens nerve, which is similar to EMG recordings from extraocular muscles during eye retraction, is triggered by a brief electrical stimulus applied to the ipsilateral trigeminal nerve. Evidence also suggests that pairing a one-second electrical stimulus applied to the posterior eighth nerve immediately prior to a single shock to the trigeminal nerve results in classically conditioned abducens nerve discharge in response to the previously neutral eighth nerve stimulus. In view of these physiological findings, the aim of the present study was to examine the central projections of trigeminal and posterior eighth nerve inputs to elucidate the anatomical substrates that may underlie the in vitro eye-blink reflex and possible pathways involved in reflex conditioning. Neurobiotin (NB) or fluorescein dextran (FD) was pressure injected into the cut end of either the trigeminal or posterior eighth nerve of the in vitro brainstem-cerebellum. Following trigeminal nerve injections, both tracers showed label in the ipsilateral trigeminal nuclear complex. Direct projections to the ipsilateral principal and accessory abducens motor nuclei were observed, suggesting that the eye-blink reflex is monosynaptic. Trigeminal nerve axons were also observed to terminate in the ipsilateral cerebellar cortex. The results of the posterior eighth nerve injections showed axonal projections and terminals in the cochlear, vestibular and principal sensory trigeminal nuclei. Terminal label was also observed in the ipsilateral cerebellar cortex, deep cerebellar nuclei, and in the principal and accessory abducens motor nuclei. Results from the NB cases suggested transneuronal transport of this tracer substance, whereas the FD cases did not. The present findings suggest that convergence of trigeminal and posterior eighth nerve inputs occurs in the ipsilateral cerebellar cortex, the principal sensory trigeminal nucleus, and the principal and accessory abducens motor nuclei. These regions of convergence may therefore be considered as potential sites of synaptic modification during in vitro studies of the conditioned abducens nerve reflex.

Animals↗

PubMed1986

The organization of hypothalamocerebellar cortical fibers in the squirrel monkey (Saimiri sciureus).

The organization and distribution of hypothalamocerebellar cortical fibers in squirrel monkey were investigated by using horseradish peroxidase (HRP, WGA-HRP) and 3H-leucine as anterograde tracers. Following hypothalamic injections, anterogradely labeled fibers coursed bilaterally through the periventricular gray (ipsilateral preponderance) and into the cerebellar white matter. Sparse numbers of labeled fibers appeared to descend into the reticular formation and enter the cerebellum via the brachium pontis. The pattern of cerebellar cortical labeling does not conform to that of mossy or climbing fibers. Labeled axons enter and branch within the granular layer, proceed around Purkinje cell somata, and enter the molecular layer. Within the latter some labeled fibers branch outwardly in a fanlike manner whereas others ascend before branching. Many fibers within the molecular layer ultimately assume an orientation that is similar to that of parallel fibers. The distribution patterns of hypothalamocerebellar cortical axons resemble those reported for monoaminergic fibers in the cerebellar cortex. Afferent fibers to the cerebellar cortex (including hypothalamocerebellar) that do not terminate as mossy or climbing fibers may collectively constitute a third general category of cerebellar afferent axons. On the basis of their distribution within all cortical layers these fibers are designated as multilayered fibers. The morphology of multilayered fibers stands in contrast to the presumptive mossy fiber labeling seen in lobules IX and X following large injections. Such labeling may represent a subpopulation of hypothalamocerebellar fibers or result from enzyme deposition in areas bordering the hypothalamus that project to cerebellar structures.

Animals↗

PubMed2005

Time course and sequence of pathological changes in the cerebellum of microsphere-embolized rats.

Ischemia is a major cause of damage to the central nervous system as a consequence of stroke or trauma. Here, we analyzed with high temporal resolution the time course of pathological changes in the neurons (granule and Purkinje cells) and glia (Bergmann and astroglia cells) in the cerebellar cortex and white matter. The period studied ranged from 30 min to 7 days after a microsphere-induced embolism used as a model of stroke and multi-infarct dementia. Some pathological changes in the neurons in the cerebellar cortex were identified early, that is, beginning at 3 h after the microsphere-induced embolism, and glial pathology appeared only later. The pathological changes in the white matter also appeared slightly later, that is, 6 h after embolism and were less pronounced than those in the cerebellar cortex. This suggests that neuronal pathology is induced more rapidly and/or more easily than the glial pathology. In addition, BrdU staining shows that cell proliferation is limited to a 1-day period beginning about 1 day after the embolism. These data demonstrate that changes after an ischemic lesion of the cerebellum proceeds from upper cerebellar cortex to deeper cerebellar cortex or white matter and also that microsphere-induced changes proceed from neuronal to glial pathology.

Animals↗

PubMed1993

GABA, THIP and baclofen inhibition of Purkinje cells and cerebellar nuclei neurons.

The sensitivity of Purkinje cells (PCs) and neurons of the cerebellar nuclei (NCNs) to iontophoretic application of gamma-aminobutyric acid (GABA), 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP) and baclofen, i.e., GABAA and GABAB agonists respectively, have been studied in anesthetized rats. All the agonists produced dose-dependent firing rate depression of the PCs but with different potencies. The inhibitory actions of both GABA and THIP were specifically antagonized by bicuculline (Bic) and the baclofen-induced responses by 2-hydroxysaclofen. GABA and THIP also depressed the spontaneous activity of NCNs while baclofen was ineffective. The present results therefore suggest that GABAA receptors are involved in the GABA-induced inhibition in the cerebellar cortex and in the cerebellar nuclei and GABAB receptors are involved only in the cerebellar cortex.

Animals↗

PubMed1977

The cerebellar projection from the raphe nuclei in the cat as studied with the method of retrograde transport of horseradish peroxidase.

Following injections of horseradish peroxidase (HRP) in the cerebellar cortex and nuclei of the cat, the distribution of labeled cells in the raphe nuclei was mapped. The findings confirm those made previously in studies of retrograde cell degeneration following cerebellar ablations (Brodal et al., 1960a), and in addition reveal new details in the projection of the raphe nuclei onto the cerebellar cortex and nuclei. All the raphe nuclei except nucleus linearis intermedius and nucleus linearis rostralis project onto the cerebellar cortex. The nuclei raphe obscurus and pontis contribute the greatest number of afferents to the cerebellum. With the exception of lobule VI which probably is the recipient of a weak projection, all parts of the cerebellar cortex receive afferents from the raphe nuclei. The heaviest projection is to the vermis of lobules VIIA and X, and to crus II. The afferents to the cerebellar nuclei are few in number (Tables 2-6). The observations indicate that each raphe neuron probably projects to more than one terminal site in the cerebellum. The findings are discussed with reference to other efferent and afferent studies of the raphe nuclei. All these studies indicate that the raphe nuclei have widespread efferent and afferent connections, making them capable to participate in a variety of regulatory functions.

Animals↗

PubMed1993

Developmental cues modulate GABAA receptor subunit mRNA expression in cultured cerebellar granule neurons.

The developmental expression of mRNAs encoding the GABAA receptor was analyzed in the rat cerebellar cortex and in cultured cerebellar granule neurons. Our studies in vivo reveal that the alpha 1-, beta 2-, and gamma 2-subunit mRNA levels in the cerebellar cortex rise dramatically during the second post-natal week, a period temporally correlated with extensive cerebellar maturation. To determine if these increases were preprogrammed or dependent on extrinsic factors, we examined subunit mRNA expression in granule cell cultures prepared at embryonic day 19 (E19) and postnatal day 10 (P10), immature and mature stages of cerebellar development, respectively. In E19 cultures, the alpha 1, beta 2, and gamma 2 GABAA receptor subunit mRNAs were present and their levels remained constant over the 21 d culture period. These results suggest that GABAA receptor gene expression is not intrinsic to the immature granule cells. A different pattern was found in P10 cultures where the three subunit mRNAs were initially present at levels approximately sixfold higher than those found at E19. The beta 2- and gamma 2-subunit mRNAs remained constant for 4 d and then increased sixfold between 4 and 7 d in culture. The magnitude and time course of these increases were similar to the developmental changes that occurred in vivo. Thus, our findings raise the possibility that signals encountered during development are necessary to induce GABAA receptor subunit mRNA expression. Moreover, these cues have been received by granule neurons prior to P10.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗

PubMed1993

2-deoxyglucose enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced ATP loss in the mouse brain.

The effects of 2-deoxyglucose (2-DG), an inhibitor of the uptake and use of glucose, on ATP loss caused by the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were determined in the mouse brain. 2-DG alone had no effect on brain ATP levels, but when administered 30 min before MPTP exposure, 2-DG significantly enhanced MPTP-induced ATP reduction. This was reflected as an increase in ATP loss in the striatum (from 15 to 27%) as well as a significant decrease in ATP in the cerebellar cortex, an area of the brain that was not affected after exposure to MPTP alone. In mice pretreated with 2-DG, striatal ATP levels remained significantly decreased for > 8 h after MPTP administration. In contrast, ATP levels in the cerebellar cortex returned to normal values within 4 h from MPTP exposure. Mazindol, a catecholamine uptake blocker, completely protected against MPTP-induced loss of striatal ATP in the absence of 2-DG, but it only partially prevented striatal ATP decrease after administration of both 2-DG and MPTP; mazindol was also ineffective in protecting against ATP loss caused by 2-DG and MPTP in the cerebellar cortex. 2-DG/MPTP-induced ATP loss appeared to be associated with the presence of the 1-methyl-4-phenylpyridinium (MPP+) metabolite because (1) the pattern of ATP recovery in the striatum and cerebellar cortex appeared to reflect the pattern of MPP+ clearance from these areas of the brain (i.e., significant MPP+ levels persisted longer in the striatum than in the cerebellar cortex), and (2) ATP decrease was completely prevented by blocking the conversion of MPTP to MPP+ with the monoamine oxidase B inhibitor deprenyl.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1988

Cerebellar benzodiazepine receptors: cellular localization and consequences of neurological mutations in mice.

The distribution of cerebellar [3H]flunitrazepam binding sites was studied autoradiographically in Purkinje cell degeneration (pcd/pcd), weaver (wv/wv), staggerer (sg/sg) and reeler (rl/rl) mutant mice. In the normal 78-day-old C57BL/6J mouse cerebellum, the highest concentration of [3H]flunitrazepam binding sites was observed over the molecular layer. Intermediate grain density was present over the Purkinje cell layer and intermediate to high density over the deep cerebellar nuclei. Low labeling was observed over the granule cell layer. Negligible concentrations of binding sites were seen in the white matter. In 45-49-day-old Purkinje cell degeneration mutants, where essentially all Purkinje cells have disappeared by day 45, there was a small decrease in grain density over the cerebellar cortex. Concomitantly, a substantial increase in grain density was observed over the deep cerebellar nuclei of the pcd/pcd mutants when compared to littermate controls. A significant increase in [3H]flunitrazepam labeling was observed over the cerebellar cortex of 81-86-day-old wv/wv mutants; this was most pronounced in the vermis where the granule cell loss was greatest. Over the hemispheres, where fewer granule cells degenerate, a lower density of binding sites was seen. Grain density over the wv/wv deep cerebellar nuclei was comparable to that of littermates. Substantially lower [3H]flunitrazepam labeling was detected over the cerebellar cortex of 25-27-day-old sg/sg mutants in which the number of granule, Purkinje and Golgi cells is greatly reduced; the labeling over the deep nuclei, however, was significantly increased. In 27-29-day-old rl/rl mutant cerebella, where all classes of cells are malpositioned, labeling density over all areas of the cerebellar cortex, including the Purkinje cell masses, was increased. Our autoradiographic data suggest that a proportion of cerebellar cortical benzodiazepine receptors are associated with Purkinje cells; we propose that the remainder of the receptors are localized on Golgi cells, while granule cells are devoid of receptors. In the deep cerebellar nuclei, the observed increase in benzodiazepine receptors in the pcd/pcd and sg/sg mutants may be a manifestation of denervation supersensitivity subsequent to the loss of innervation by Purkinje cell axon terminals. The finding of a high receptor density in the Purkinje cell masses of the rl/rl mutant, where Purkinje cells are devoid of afferent basket cell input, suggests that benzodiazepine receptors are expressed and maintained in the absence of a full complement of GABAergic afferents.

Animals↗

PubMed1999

Cerebellar cortical AMPA-kainate receptor blockade prevents performance of classically conditioned nictitating membrane responses.

Classical conditioning of the nictitating membrane-eye blink response of rabbits is a simple form of associative motor learning. Lesion studies have shown that performance of learned responses is dependent on the cerebellum, but they have not shown whether there is storage of memories within the cerebellum or distinguished the roles of the cerebellar cortex and nuclei. Reversible inactivations of the cerebellar nuclei have directly implicated the cerebellum in the acquisition of nictitating membrane conditioning, but previously the cerebellar cortex has not been reversibly inactivated to assess its contribution to the performance or acquisition of conditioned responses. Here we use the water-soluble disodium salt of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) reversibly to block cerebellar cortical AMPA-kainate receptors in lobule HVI and quantitative autoradiography to map its distribution. Conditioned responses are completely, but reversibly, abolished for 10-60 min depending on the concentration of the CNQX infusion and its location within HVI. Zebrin immunohistochemistry was used to define the optimal cortical infusion site that, we suggest, corresponds to the location of the eye blink control regions. We confirm that areas in HVI are essential for the expression of classically conditioned nictitating membrane responses, and we establish a method to analyze the role of cerebellar cortex in the acquisition of this form of motor learning.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2005

Oxidative DNA damage in relation to neurotoxicity in the brain of mice exposed to arsenic at environmentally relevant levels.

To clarify the association between oxidative DNA damage and the neurotoxicity of arsenic, the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) as an index of oxidative DNA damage in the brain was examined in mice fed with drinking water containing 1 or 2 ppm arsenic, using an HPLC-electrochemical detector and immunohistochemical method. 8-OHdG levels were significantly increased in the brain of mice given arsenic and its immunoreactivity was distributed in the cerebral and cerebellar cortexes. Cerebral cortex neurons and Purkinje cells in the cerebellar cortex showed degenerative changes in accordance with the distribution of 8-OHdG immunoreactivity. The levels of arsenic in this study were lower than those reported in epidemiological studies. Thus, we conclude that environmentally relevant levels of arsenic induce pathological changes through oxidative DNA damage in the brain tissues in vivo and that cerebral and cerebellar cortex neurons seem to be the major targets of arsenic neurotoxicity.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1999

Cerebellar atrophy in Alzheimer's disease-clinicopathological correlations.

Morphometry of the cerebellum of 11 subjects who died in the severe, final stage of Alzheimer's disease (AD) and of five age-matched subjects without dementia revealed significant atrophy in the AD group, with a decrease in the volume of the molecular layer by 24% and of the granular layer by 22% in comparison with controls. The 32% decrease in the total number of Purkinje cells that was observed correlates with the atrophy of the molecular layer, whereas the 30% reduction in the total number of granule cells correlates with the atrophy of the molecular and granular layers. A unique pattern of Alzheimer-type pathology was observed in the cerebellum: (1) there were no neurofibrillary changes in the cerebellum of either the control or the AD subjects, (2) there was almost the same extent of leptomeningeal and cortical amyloid angiopathy in the normal aged subjects and in the AD patients, and (3) the presence of plaques was noted in the AD group, but not in the control group. This pattern of pathology suggests that two factors might be considered in the etiopathogenesis of cerebellar atrophy: (1) transneuronal degeneration and neuronal loss resulting from primary pathologic changes in cerebral structures and (2) parenchymal cerebellar ss-amyloidosis. The correlation between the temporal duration of AD and both the decrease of the total number of granule cells (r=0.86, p<0.01) and the volumetric loss of the molecular (r=0.73, p<0.05) and granular (r=0.93, p<0.001) layers of the cerebellar cortex indicates that these cerebellar atrophic changes are likely to be related to the basic pathologic process of AD. Similarly, the correlation between the most complex parameter the atrophy of the cerebellar cortex and the Functional Assessment Staging (FAST) measure of the clinical severity of AD at the time of demise (r=0.63, p<0.05) as well as with the duration of AD (r=0.78, p<0.01) indicates that cerebellar pathology, when viewed holistically, evolves continuously in association with clinical changes throughout the clinically manifest course of AD.

Aged↗

PubMed1997

[Assessment of cerebral benzodiazepine receptor distribution in epilepsy by 123I-iomazenil-SPECT].

123I-Iomazenil (123I-IMZ) and 123I-IMP imaging were performed in 8 epileptic patients (EP) in the interictal phase and 6 normal volunteers (NV). On 123I-IMZ delayed imaging, the 8 EP showed abnormally decreased findings. Two EP showed decreased perfusion in the same region on 123I-IMP imaging. 123I-IMZ imaging for the detection of epileptic foci showed relatively high specificity compared with EEG recording. On 123I-IMZ early images, the count ratio of the right lower frontal cortex was lower the cerebellar cortex in EP was lower than that in NV. On 123I-IMZ delayed images, the count ratio of the bilateral occipital and the right upper and lower frontal cortices to the cerebellar cortex in EP was lower than that in NV. On 123I-IMZ delayed images, the count ratio of the right upper frontal cortex to the occipital cortex in EP was lower than that in NV. On 123I-IMZ delayed images, the count ratio of the left lower frontal cortex to the occipital cortex in EP was higher than that in NV. These results pointed to the involvement of the benzodiazepine receptor complex in epilepsy.

Adult↗

PubMed2000

Cerebellar cortical degeneration disrupts discrimination learning but not delay or trace classical eyeblink conditioning.

The authors investigated classical eyeblink conditioning in a relatively rare patient, B.R., with extensive cerebellar cortical atrophy and marked sparing of the dentate nucleus. Patient B.R.'s ability to acquire and extinguish simple associations (delay and trace conditioning tasks) as well as her ability to acquire more complex associations (temporal and simple discrimination tasks) were examined. There are 2 primary findings from this study. First, B.R. showed normal acquisition and extinction in delay and trace conditioning. Second, she demonstrated a complete inability to learn associative discriminations, even in the case of a simple 2-tone discrimination within the context of a delay paradigm. The latter finding was unexpected because of the sparing of her deep cerebellar nuclei. These data suggest that the cerebellar cortex, or pathways traversing cerebellar cortex, play an important role in classical eyeblink discrimination learning.

Adult↗