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PubMed1982

[Analysis of the population of Purkinje's cells in the cerebellar cortex of dogs subjected to heart arrest].

The population of Purkinje's cells (PC) was studied in the cerebellum cortex of 5 mongrel dogs that suffered 12-minute circulatory arrest caused by electric trauma followed by complete external recovery of the neurological status. Morphometric analysis revealed that 2 weeks after resuscitation the total number of PC per mm of their layer length remains unchanged, while the composition of the population drastically changes. In all the zones of the cerebellum studied, the number of PC having different morphological changes increases, whereas the number of light PC was significantly decreased. The result of the changes was that 2 weeks after clinical death, dark cells constituted half the normal (morphologically unchanged) population of PC. Meanwhile in the control group, dark PC constituted 1/3 of the population. Cytophotometry revealed that in both groups of animals (the intact and with a history of clinical death) the dark PC are characterized by the increased content of nucleic acid, as compared to that of the light PC. It is suggested that the increase in the relative number of the dark PC in the cerebellum cortex of dogs after systemic circulation arrest is related to the transition of intracellular physiological regeneration to the reparative one. Therefore, both pathological and compensatory processes are seen in the dog cerebellum cortex 2 weeks after resuscitation. It was disclosed that PC of the lateral zone of the cerebellum hemisphere are most vulnerable, while those of the medial zone (vermis cerebelli) are most viable.

Animals↗

PubMed1980

Application of cryofracture and SEM to the study of human cerebellar cortex.

The SEM and cryofracture methods were used to study neuronal architecture and some synaptic connections of human cerebellum. Samples were processed according to the technique of Humphreys et al. (1975) with minor modifications. The granule cells, arranged in groups or randomly distributed, appeared as spheroidal, rough surfaced microneurons with unbranched filiform axons and coniform dendritic processes. The mossy fibers were observed as thick axons showing the rosette expansions covered by numerous granule cell dendritic processes at the glomerular regions. The mossy glomeruli were seen as round or ovoid clews or balls of yarn separating the granule cell groups. The uncovered mossy rosettes, devoid of the postsynaptic granule cell dendritic digits, unattached by the cryofracture technique appear as solid club-like structures. the climbing fibers were characterized by their thick collaterals. Some fractographs exhibited isolated Golgi cells showing the entire ascending and horizontal dendrites and their beaded shape axonal plexus. At the Purkinje layer, the surface fracture was produced at the level of Bergmann glial cells, which are selectively removed, thus allowing us to visualize the rough surface of purkinje cell soma and the supra and infraganglionic plexuses of basket cell axons. At the molecular layer the stellate neurons were characterized with their horizontal short axons and the Bergmann fiber ends were seen attached to the surface of the folia forming the external glial limiting membrane.

Adolescent↗

PubMed1987

Thyrotropin-releasing hormone reduces myo-inositol content in rat cerebellum pretreated with lithium.

The effect of thyrotropin-releasing hormone (TRH) and lithium on myo-inositol metabolism has been assessed in rat cerebral cortex, cerebellar cortex, and sciatic nerves. Sprague-Dawley male rats were injected subcutaneously with 10 mEq/kg of LiCl and intraperitoneally with 10 mg/kg of TRH-tartrate, alone or in combination. Either lithium or TRH alone had little effect on the myo-inositol concentration in cerebellar cortex, whereas the combination of lithium and TRH significantly lowered the level. The myo-inositol level of cerebellar cortex reached its nadir (70% of values in untreated control rats) 30 min after addition of TRH and then returned to the control level at 90 min. In cerebral cortex, both lithium alone and lithium plus TRH significantly reduced the myo-inositol level. No effect was seen on the myo-inositol concentration in sciatic nerves with these regimens. These results suggested that the pharmacological dose of TRH activated phosphatidylinositol turnover in rat cerebellar cortex and subsequently reduced the myo-inositol level in the presence of lithium.

Animals↗

PubMed2000

Broadly altered expression of the mRNA isoforms of FE65, a facilitator of beta amyloidogenesis, in Alzheimer cerebellum and other brain regions.

FE65 is a key "adapter" protein that links a multiprotein complex to an intracellular domain of beta-amyloid precursor protein (betaPP). Its overexpression modulates the trafficking of betaPP and facilitates the generation of beta-amyloid (Abeta). FE65 is predominantly expressed in brain tissues. An exon 9-inclusive isoform is exclusively expressed in neurons, and an exon 9-exclusive isoform is only expressed in non-neuronal cells. We quantitated the two isoforms in middle temporal cortex, middle frontal cortex, cerebellar cortex and caudate nucleus of 17 Alzheimer disease (AD) patients, 12 normal controls and 9 non-AD neurodegenerative disease controls by reverse transcription-competitive polymerase chain reaction (RT-cPCR). Expression of the two isoforms was significantly and differentially altered, with a 30-57% decrease in levels of the neuronal form (P < 0.05-0.002) and a 73-135% increase in levels of non-neuronal form (P < 0.02-0.001), in the temporal and frontal cortex of AD brains. These alterations presumably reflect advanced neurodegenerative processes of these regions. Surprisingly, expression of both isoforms was significantly up-regulated by 42-66% in the cerebellar cortex and caudate nucleus of AD brains when compared to normal brains (P < 0.05-0.005). Diffuse Abeta-positive plaques were observed in the cerebellum of these AD subjects but not in the normal controls. Selective up-regulation of only the FE65 neuronal isoform was seen in the cerebellar cortex in association with other neurodegenerative diseases (largely Parkinson's disease). Because FE65 modulates trafficking of betaPP toward the production of Abeta, the up-regulation of FE65 in AD cerebellum may be relevant to the genesis of diffuse plaques. Thus, early biochemical alterations in AD, not complicated by advanced pathology, may be beneficially investigated in the less-affected regions of the brain, such as the cerebellum.

Alzheimer Disease↗

PubMed1994

Localization of a novel pathway for the liberation of GABA in the human CNS.

Serum carnosinase is a dipeptidase, which is synthesized in human brain, where it hydrolyzes homocarnosine to release free GABA. Immunohistochemical procedures were used to demonstrate the presence of this enzyme in several layers of the retina and in certain neuronal tracts of the cerebral cortex, cerebellar cortex, olfactory bulb, hippocampus, and in disseminated tracts presumably from the internal capsule, interspersed among the basal ganglia. The enzyme was also present in the epithelial cells of the choroid plexus and in corpora amylacea, which were seen in many regions of the CNS. Homocarnosine was localized either in the same tracts or in nearby neurons. For example, the Purkinje cells of the cerebellar cortex contained homocarnosine, whereas serum carnosinase was localized in adjacent neuronal projections apparently originating from outside the cerebellar cortex and having probable synaptic contact with the Purkinje cells. These findings suggest that in addition to glutamate decarboxylation, a second metabolic reaction for the formation of free GABA exists in specific neuronal tracts of the human CNS where GABA is released from homocarnosine by the action of serum carnosinase.

Animals↗

PubMed1998

Uneven regional distribution of nucleotide metabolism in human brain.

Adenine and uridine nucleotides and adenosine are proposed to act as neuromodulators and other nucleotides and nucleosides are also suggested to be involved in brain function. A following major step towards the verification of the functional role of nucleotides and nucleosides in the brain would be the examination of regional distribution of purines, pyrimidines and the enzymes involved in their metabolism. Using our recently developed chromatography-based assay for nucleosides from tissue homogenates, we analysed nucleosides in microdissected samples derived from various regions of human brain. Marked differences in the levels of nucleosides were measured in the cerebral cortex, cerebellar cortex, thalamus and white matter. The greatest levels of most nucleosides were found in the cerebral cortex, followed by the cerebellar cortex and the white matter while the smallest concentrations were found in the thalamus, although adenosine and xanthine showed a different distribution pattern in these brain areas. Within the cerebral cortex, the measured substances showed little variations except certain high levels in the cingulate and low levels in the frontal cortex. Even distribution of nucleosides was found in the thalamic nuclei while relative high values were measured in the medial geniculate body. Since a dramatic change in nucleoside concentrations occurs after death, the measured nucleoside concentrations are an interplay of original nucleotide and nucleoside concentrations and enzyme reactions following death. Thus our results suggest regional differences in nucleotide and nucleoside composition and nucleotide metabolising enzyme activities between brain areas.

Adenosine↗

PubMed2002

Neural responses during Valsalva maneuvers in obstructive sleep apnea syndrome.

The repetitive upper airway muscle atonic episodes and cardiovascular sequelae of obstructive sleep apnea (OSA) suggest dysfunction of specific neural sites that integrate afferent airway signals with autonomic and somatic outflow. We determined neural responses to the Valsalva maneuver by using functional magnetic resonance imaging. Images were collected during a baseline and three Valsalva maneuvers in 8 drug-free OSA patients and 15 controls. Multiple cortical, midbrain, pontine, and medullary regions in both groups showed intensity changes correlated to airway pressure. In OSA subjects, the left inferior parietal cortex, superior temporal gyrus, posterior insular cortex, cerebellar cortex, fastigial nucleus, and hippocampus showed attenuated signal changes compared with controls. Enhanced responses emerged in the left lateral precentral gyrus, left anterior cingulate, and superior frontal cortex of OSA patients. The anterior cingulate, cerebellar cortex, and posterior insula exhibited altered response timing patterns between control and OSA subjects. The response patterns in OSA subjects suggest deficits in particular neural pathways that normally mediate the Valsalva maneuver and compensatory actions in other structures.

Adult↗

PubMed1975

Water contents of various regions of the feline nervous system.

A systematic analysis of the regional water content of the feline nervous system was made. In general, areas rich in grey matter contained about 10-15% more water than white matter areas. Percentage water values were lowest for cranial and peripheral nerves and highest for cerebral cortex, cerebellar cortex, olfactory bulb and other grey matter regions. Values for cerebral cortex varied from about 81.5% for suprasplenic gyrus to over 84% for frontal gyrus. It is suggested that the effective concentrations of dissolved substances in various regions of the nervous system might be influenced greatly by these differences in water content.

Animals↗

PubMed1971

The uptake of [14C]glycine by slices of mammalian spinal cord.

1. The accumulation of [(14)C]glycine by slices of mammalian spinal cord has been measured.2. When slices of rat cord were incubated at 37 degrees C in a medium containing [(14)C]glycine, tissue:medium ratios of about 30:1 were attained after a 40 min incubation.3. After incubations at 37 degrees C for 40 min, almost all (98%) the radioactivity in the tissue was present as unchanged [(14)C]glycine.4. The process responsible for [(14)C]glycine uptake showed many of the properties of an active transport system: it was temperature sensitive, required the presence of sodium ions in the external medium, was inhibited by dinitrophenol and ouabain and showed saturation kinetics.5. The estimated K(m) value of glycine was 3.1 x 10(-5)M, and V(max) was 0.48 mu-mole/min.g cord.6. The uptake of [(14)C]glycine was not affected by the presence of large molar excesses of L-histidine, L-proline, L-aspartate, L-glutamate, L-valine or GABA, but was inhibited in the presence of L-alanine and L-leucine.7. The uptake of [(14)C]glycine was not reduced by strychnine, but a significant reduction in uptake was produced by p-hydroxymercuribenzoate.8. The uptake of [(14)C]glycine by the grey matter of rabbit spinal cord was 2 to 6 times greater than the uptake by slices of white matter incubated under the same conditions.9. Rat cerebral cortex, cerebellar cortex and medulla also accumulated [(14)C]glycine, and the uptake by the tissue slices in vitro appeared to parallel the concentration of glycine in these areas in vivo.10. It is suggested that the glycine uptake system may represent a possible mechanism for the inactivation of glycine at inhibitory synapses in the spinal cord.

Alanine↗

PubMed1976

Ethanol-induced regional and dose-response differences in multiple-unit activity in rabbits.

Multiple-unit activity (MUA), recorded simultaneously from many brain areas, was used to detect the existence ahd location of "target sites" for ethanol action in rabbits with chronically implanted electrodes in 14 areas. Each of 12 rabbits received intraperitoneal injection of 300, 600, 900, and 1200 mg/kg of 20% ETOH and a saline control injection given in random order with at least a 4-day interval between injections. Large amounts of MUA data, recorded continuously for a 2-min pre-injection control period and a 15-min post-injection period, were quantified by a sensitive and unique technique. MUA changes did not correlate with alcohol-induced changes in the corresponding EEG for the same locus. Whereas visual inspection of the EEG did not disclose any regional differences in response to ethanol, both temporal and topographical differences in ethanol effect on MUA were observed. There were 14 histologically verified brain areas with adequate sample size for statistical evaluation of MUA response. At high doses, all brain areas were affected. Included among the brain areas which were least affected by low doseas were the caudate nucleus, septum, fornix, and medial forebrain bundle. Those areas that met the criteria for target sites of responding quickly (less than 5 min) to low doses (300 mg/kg) were: cerebellar cortex, cerebral cortex, hippocampus, lateral and medial geniculate nuclei, midbrain reticular formation, and pyriform cortex. In conjunction with the preliminary study [Brain Res. 70, 361 (1974], the data indicate that the most ethanolsensitive tissue is found in the various kinds of cortex, cerebellar and cerebral (both paleocortex and neocortex).

Animals↗

PubMed1981

Cerebellar cortical atrophy in a puppy.

A description is given of the history and neuropathology of a mongrel puppy which had suffered from cerebellar cortical atrophy. The condition was attended by intractable cerebellar ataxia and characterised by selective degeneration of the Purkinje cells of the cerebellar cortex. Cerebellar dysfunction is briefly reviewed. The lesion and possible aetiology are briefly discussed.

Animals↗

PubMed2004

fMRI signal changes in response to forced expiratory loading in congenital central hypoventilation syndrome.

Congenital central hypoventilation syndrome (CCHS) patients show impaired ventilatory responses to CO2 and hypoxia and reduced drive to breathe during sleep but retain appropriate breathing patterns in response to volition or increased exercise. Breath-by-breath influences on heart rate are also deficient. Using functional magnetic resonance imaging techniques, we examined responses over the brain to voluntary forced expiratory loading, a task that CCHS patients can perform but that results in impaired rapid heart rate variation patterns normally associated with the loading challenge. Increased signals emerged in control (n = 14) over CCHS (n = 13; ventilator dependent during sleep but not waking) subjects in the cingulate and right parietal cortex, cerebellar cortex and fastigial nucleus, and basal ganglia, whereas anterior cerebellar cortical sites and deep nuclei, dorsal midbrain, and dorsal pons showed increased signals in the patient group. The dorsal and ventral medulla showed delayed responses in CCHS patients. Primary motor and sensory areas bordering the central sulcus showed comparable responses in both groups. The delayed responses in medullary sensory and output regions and the aberrant reactions in cerebellar and pontine sensorimotor coordination areas suggest that rapid cardiorespiratory integration deficits in CCHS may stem from defects in these sites. Additional autonomic and perceptual motor deficits may derive from cingulate and parietal cortex aberrations.

Adolescent↗

PubMed2000

Regional and cellular distribution of the P2Y(1) purinergic receptor in the human brain: striking neuronal localisation.

The biological actions of extracellular nucleotides are exerted via two families of P2 receptors, P2X and P2Y. The metabotropic P2Y receptors comprise at least 7 distinct subtypes, which have been cloned from a number of species. However, none of the P2Y receptor proteins have been visualised yet in human brain. In the present study, the regional and cellular distribution of the P2Y(1) receptor was investigated in the human brain by using immunohistochemistry. Polyclonal antibodies were raised against a synthetic peptide from the C-terminus of the P2Y(1) protein. Immunoblot analysis demonstrated that P2Y(1) antiserum specifically recognised a 63-kDa band in human and rat brain membranes. Similarly, the antiserum specifically detected the human P2Y(1) receptor in transfected 1321N1 cells. Immunohistochemical analysis on perfusion-fixed human brain tissue showed a widespread distribution for this receptor throughout the brain. At the cellular level, the P2Y(1) receptor was strikingly localised to neuronal structures of the cerebral cortex, cerebellar cortex, hippocampus, caudate nucleus, putamen, globus pallidus, subthalamic nucleus, red nucleus, and midbrain. Expression of the P2Y(1) receptor was not detected in other non-neuronal cell types. These results provide the first characterisation of the cellular distribution of a P2Y receptor in the human brain. The widespread and abundant distribution of the P2Y(1) receptor suggests its involvement in a number of important functions within the human brain. The neuronal localisation of this receptor points towards a possible role in neurotransmission, and also highlights a major role for extracellular nucleotides as signaling molecules within the brain.

Animals↗

PubMed1980

Selected ion monitoring determination of acetylcholine during methoxypyridoxine seizures.

The neurotransmitter gamma-aminobutyric acid is known to decrease preictally after administration of the potent convulsant methyoxypyridoxine, a competitive inhibitor of glutamate decarboxylase. An attempt was made to determine the effect of this gamma-aminobutyric acid decrease on the cholinergic system. Rabbits were immobilized and artificially ventilated in order to avoid hypoxidosis. Seizures were induced by intravenous injection of 100 mg kg-1 methoxypyridoxine; 40 minutes later the animals were decapitated and discrete brain areas removed. Tissue contents of acetylcholine and choline were estimated by gas chromatographic mass spectrometric analysis of the beta-dimethylaminoethyl acetate and propionate derivatives using deuterated internal standards. Gas chromatographic column optimization resulted in a considerable sensitivity gain. Computerized selected ion monitoring was carried out on the dimethylmethyleneimmonium ions using voltage switching. The use of a computer controlled solvent dump valve was implemented to increase precision. No significant difference was observed in the concentration of acetylcholine in the frontal cortex, cerebellar cortex, septum, hippocampus, or caudate of seizure versus control animals; septal choline increased, however. This suggests that the acetylcholine turnover could be increased during seizure.

Acetylcholine↗

PubMed1987

A quantitative cerebral and whole body autoradiographic study of a intravenously administered benzodiazepine antagonist 3H-Ro 15-1788 in mice.

3H-Ro 15-1788, a benzodiazepine receptor antagonist, was injected IV into male and pregnant mice. Autoradiograms were prepared from sagittal sections of animals killed after 30 s to 48 h. In the adult animal there was a rapid and high initial accumulation of radioactivity in the brain as compared to other organs and tissues. The highest accumulation was found in cortical brain areas, such as the olfactory bulb and the frontal cortex. Cerebellar cortex, globus pallidus, amygdala, substantia nigra, colliculus, hippocampus and pons followed in rank order. The rate of decline of radioactivity was highest in the pons and lowest in the olfactory bulb. The initial disappearance of radioactivity from the cerebellum was higher than from the other brain regions. Ro 15-1788 was rapidly eliminated; 4 h after drug administration there was an almost complete clearance of radioactivity from all tissues. After 24 h no trace of activity remained in the animal. The distribution of radioactivity at later time points indicates that metabolites of Ro 15-1788 are eliminated by fecal, urinary and nasal secretion. In the fetus also there was an early accumulation of radioactivity in the central nervous system. The radioactivity in fetal organs was lower than in the mother at all time intervals.

Animals↗

PubMed1993

Reduced [3H]flunitrazepam binding in cingulate cortex and hippocampus of postmortem schizophrenic brains: is selective loss of glutamatergic neurons associated with major psychoses?

UNLABELLED: Findings. Specific [3H]flunitrazepam binding to "neuronal"-type sites was significantly lower in anterior cingulate cortex, hippocampus, somatomotor cortex, cerebellar cortex, and globus pallidus in small postmortem samples of schizophrenic brains than in non-schizophrenic controls. Four of these five brain regions were reported by others to exhibit atrophy and/or neuronal loss in schizophrenia. INTERPRETATION: Selective loss of hippocampal pyramidal neurons in postmortem schizophrenic brains has been reported (11). Pyramidal neurons are known to be glutamatergic (14,26) and to exhibit high densities of benzodiazepine binding sites (25,31). Glutamatergic neurons are known to be abundant in most layers of the cerebral cortex, and most of these are pyramidal neurons (26). All layers of the cerebral cortex display high densities of benzodiazepine binding sites (24,25,31). The number of larger pyramidal cells is little affected in most layers of the anterior cingulate cortex, but the number of small neurons is significantly lower, particularly in layer II (10). Pyramidal neurons range in size from very large to very small, and many very small pyramidal cells are often counted, together with small "stellate" neurons, as "granule" cells (28). Further, non-pyramidal glutamatergic neurons are reportedly also found in cerebral cortex (26). Thus, it seems possible that the large reduction in [3H]flunitrazepam binding we find in anterior cingulate cortex reflects the selective loss of glutamatergic neurons. The hypothesis that selective loss of glutamatergic neurons form various brain regions is associated with major psychoses can be easily tested by immunohistochemical studies of these regions using glutamate- and GABA-specific antibodies.

Adult↗

PubMed1999

Benzodiazepine receptor imaging with iomazenil SPECT in aphasic patients with cerebral infarction.

To investigate the relationship between prognosis of aphasia and neuronal damage in the cerebral cortex, we evaluated the distribution of central-type benzodiazepine receptor (BZR) binding in post-stroke aphasics with [123I]iomazenil and SPECT. We performed iomazenil SPECT in six aphasic patients (aged from 45 to 75 years; all right-handed) with unilateral left cerebral infarction. Three patients showed signs of Broca's aphasia and the other three Wernicke's aphasia. Cerebral blood flow (CBF) imaging was performed with [123I]iodoamphetamine (IMP). The regions of interest (ROIs) on both images were set in the cerebral cortex, cerebellar cortex and language-relevant area in both hemispheres. Three patients were classified in the mild prognosis group and the other three in the moderate prognosis group. The left language-relevant area was more closely concerned with the difference in aphasic symptoms than the right one in both BZR and CBF distribution, but the ipsilateral to the contralateral ratio (I/C ratio) in the language-relevant areas in the BZR distribution was significantly lower in the moderate prognosis group than in the mild prognosis group, although no difference was seen for these values between the two groups in the CBF distribution. These results suggest that BZR imaging, which makes possible an increase in neuronal cell viability in the cerebral cortex, is useful not only for clarifying the aphasic symptoms but also for evaluating the prognosis of aphasia in patients with cerebral infarction.

Aged↗

PubMed1985

Electrophysiological mapping of the auditory areas in the cerebellum of the cat.

We mapped the topographic distribution of auditory evoked potentials over the posterior cerebellum of the cat. Within the posterior vermis, positive-going evoked potentials were primarily recorded in lobule VI and negative ones in lobule VII. Peak latencies of these evoked potentials were between 8 and 18 ms. The amplitudes of evoked potentials from adjacent surface cortical sites often differed significantly. Thus, besides the segregation of positive and negative polarities in the evoked potentials from lobules VI and VII, the distribution of cerebellar auditory evoked potentials within a given lobule contained high- and low-amplitude sites arranged in a patchy pattern. Within the posterior vermis, the evoked potentials showed significant polarity and amplitude changes as a function of depth during microelectrode penetrations which were vertical to the surface of the cerebellar cortex. Cerebellar auditory evoked potentials were not detected over the paramedian lobules and most of the cerebellar hemispheres. There were no significant changes in the electrical activities as a function of depth in these areas. Auditory responses, however, were observed in the most lateral part of the cerebellar hemispheres.

Animals↗