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PubMed2000

Expression and distribution of CYP2C enzymes in rat basal ganglia.

The function and integrity of the basal ganglia is modulated by sex steroids whose activity may be controlled by P450 enzymes, such as members of the CYP2C subfamily. The expression of CYP2C enzymes in rat basal ganglia was examined by immunohistochemistry along with some of the factors that might control their expression. Whereas no CYP2C11 or CYP2C12 immunoreactivity was detected in the basal ganglia of either male or female rats, marked CYP2C13 immunoreactivity was evident in neurones of the subthalamic nucleus, substantia nigra, and interpeduncular nucleus. Strong CYP2C13 immunoreactivity was also expressed in the cortex, olfactory tubercle, hippocampus, dentate gyrus, hypothalamic nuclei, medial habenular nucleus, red nucleus, and medial forebrain bundle. Similar results were found in male and female rats. Following 6-hydroxydopamine lesioning of the nigro-striatal tract, tyrosine hydroxylase immunoreactivity was absent and CYP2C13 immunoreactivity was decreased markedly in the substantia nigra pars compacta, implying its presence in dopaminergic neurones. Modulation of sex steroids, using castrated rats, had no effect on the number of CYP2C13 positive neurones in the substantia nigra pars compacta. These results indicate that CYP2C13 protein is constitutively and widely expressed in rat brain. However, its expression is not sex-specific and is unaffected by castration. The role of CYP2C13 in brain is unknown but it may be involved in the generation of neurosteroids and catecholoestrogens.

Animals↗
PubMed1986

Preliminary brain autopsy findings in progredient Rett syndrome.

Postmortem human brain analyses have been performed to further evaluate pathogenetic aspects of the Rett syndrome. While there are no significant abnormalities with respect to amino acid concentrations in putamen, caudate nucleus, red nucleus and thalamus, the concentration of kynurenine is increased in putamen, caudate nucleus, gl. pallidus, raphe and amygdaloid n. In contrast, serotonin and its metabolite 5-hydroxyindole acetic acid are below normal levels. D2-receptor number is decreased and there is a significant drop in the concentration of the iron-binding protein ferritin. It can be concluded, that reduction of D2-receptors is due to loss of cholinergic and GABA-ergic cell bodies in the striatum or may be a response to iron deficiency. Low serotonergic and high kynurenergic activity may be of pathogenetic importance in the frequently observed cerebral seizures in Rett syndrome.

Amino Acids↗
PubMed1991

Brain sites projecting to the spinal nucleus of the bulbocavernosus.

Motoneurons of the spinal nucleus of the bulbocavernosus (SNB) occupy a distinct dorsomedial position in the ventral horn of lumbar segments 5 and 6 and innervate sexually dimorphic striated muscles of the rat perineum, including the bulbocavernosus and levator ani. To begin the study of brain influences upon SNB function, we used retrograde tracers to identify brain regions that project to the area of SNB motoneurons. Our findings provide strong evidence that lateral vestibular and several reticular nuclei innervate the SNB. Additional possible afferents include the superior and medial vestibular nuclei, raphe nucleus, red nucleus, interstitial nucleus of the medial longitudinal fasciculus, and paraventricular nucleus.

Animals↗
PubMed1992

Sporadic amyotrophic lateral sclerosis with extensive neurological involvement.

We report an autopsy case of respirator-assisted long-survival sporadic amyotrophic lateral sclerosis (ALS) with extensive involvement extending beyond the motor system. The involved areas included the globus pallidus, subthalamic nucleus, red nucleus, substantia nigra, Clarke's column, intermediolateral nucleus, Onuf's (Onufrowicz) nucleus, middle root zone of the posterior column, and the spinocerebellar tract. There was no impairment of ocular movements. Such sporadic ALS cases with extensive involvement extending beyond the motor system may constitute a distinct subgroup of this disease that differs from long-survival ALS (with or without respirator support) in which only the motor system is affected.

Aged↗
PubMed1989

Immunohistochemical localization of intracellular plasma proteins in the human central nervous system.

The regional distribution of plasma protein immunoreactivity was studied in the postmortem central nervous system (CNS) of normal subjects 18 to 78 years old. Samples taken from various areas of brain and spinal cord were processed for peroxidase-antiperoxidase immunocytochemistry using polyclonal antibodies against plasma albumin, prealbumin, alpha 1-acid glycoprotein, alpha 2-macroglobulin, IgG, transferrin, haptoglobin, hemopexin, fibrinogen, as well against the glial fibrillary acidic and S-100 proteins. Many neurons of the spinal cord, cranial nerve nuclei, pontine nuclei, cerebellar dentate nucleus, red nucleus, thalamus and hypothalamus showed strong immunostaining for albumin and moderate to strong staining for alpha 1-acid glycoprotein, IgG, transferrin, haptoglobin, as well as relatively weak immunoreactivity against other plasma proteins. Less intense staining was seen in the nucleus basalis, putamen and Purkinje cells. In contrast, most cerebral cortical neurons were negative except for a few positively stained pyramidal neurons in the hippocampus and in layers III and V of the association neocortex, although more positive pyramidal neurons were observed in the motor and sensory neocortices. Reaction products were also seen in axons of motor and sensory long tracts. These findings suggest that plasma proteins may be transported to spinal cord and brain stem neurons by peripherally projecting nerves and that a series of anterograde and retrograde transneuronal transfers are responsible for the accumulation of plasma proteins in relay nuclei and in other CNS neurons.

Adult↗
PubMed2004

Mutism after evacuation of acute subdural hematoma of the posterior fossa.

CASE REPORT: A 7-year-old boy was involved in a road traffic accident. A computed tomography scan revealed an acute subdural hematoma (ASDH) of the posterior fossa, traumatic subarachnoid hemorrhage, and distortion of the brain stem. Removal of the ASDH was completed 3.5 h after injury. After extubation, the patient rapidly recovered consciousness. He was able to follow commands, although he did not speak. He began to utter 14 days after the injury. His speech became normal 39 days after injury. A magnetic resonance imaging scan revealed a post-contusional change in the right cerebellum and an ischemic lesion in the pons. DISCUSSION: Immediate removal of the hematoma is the only therapy for patients with ASDH of the posterior fossa. Although any lesions of the dentate nucleus, red nucleus, thalamus, cerebral cortex, and pons, all of which are involved in this case, are able to cause mutism, his mutism was primarily caused by the severe ASDH of the posterior fossa. The transient nature of this syndrome suggests that the cause of the mutism is trauma-related edema and/or transient ischemia of these structures.

Accidents, Traffic↗
PubMed1985

Selective neuronal uptake of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and other related substituted stilbenes in vivo: a fluorescent whole cell staining technique.

The uptake of fluorescent stilbene derivatives including 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) was shown to occur from the blood or cerebrospinal fluid in the adult albino rat. SITS was found to be internalized in select populations of neurons, especially pyramidal neurons in layers V and VI of neocortex, granule, hilar and pyramidal neurons in the hippocampus, Purkinje neurons of the cerebellar cortex and predominantly large multipolar neurons in the oculomotor nuclei, lateral vestibular nucleus, red nucleus and the medial gigantocellular brainstem reticular formation neurons. The extent and quality of labeling of neuronal somata, dendrites and axons can be exploited with this technique to produce selective, 'Golgi' type labeling in the nervous system. The methods utilized are fast, economical, long lasting and compatible with fluorescence tracers and immunofluorescence techniques.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Rolling mouse Nagoya as a mutant animal model of basal ganglia dysfunction: determination of absolute rates of local cerebral glucose utilization.

In order to elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling), a neurological mutant mouse (genotype rol/rol) showing frequent lurching and falling over on walking, we determined absolute rates of local cerebral glucose utilization (LCGU) with the [14C]deoxyglucose method. The rates were compared with those of heterozygote (+/rol) with normal behavior, and of normal mice (+/+) of the same strain (C3Hf/Nga). Rolling showed marked and significant increases in LCGU in the structures of the basal ganglia such as the globus pallidus, entopeduncular nucleus, substantia nigra pars compacta and pars reticulata, and subthalamic nucleus, confirming our previous finding with semiquantitative LCGU determination. Additional significant but much less marked increases in LCGU of rolling were found in some structures of the brainstem and limbic system, such as the pedunculopontine nucleus, red nucleus, ventral tegmental area, lateral habenula, and CA1 and CA3 of the hippocampus. Although rolling has been regarded as an animal model of cerebellar ataxia, rolling showed no alterations of LCGU in the cerebellum. The heterozygote showed intermediate increases in LCGU between rolling and normal mice in the basal ganglia structures such as the globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. Our findings indicate that rolling has a definite, genetically determined dysfunction of the basal ganglia. The primary site of the basal ganglia dysfunction might probably be in the striatum, involving both the neostriatum and limbic striatum, and resulting in secondary dysfunction in their target structures.

Animals↗
PubMed1992

Transneuronal labeling of spinal interneurons and sympathetic preganglionic neurons after pseudorabies virus injections in the rat medial gastrocnemius muscle.

The distribution of retrogradely and transneuronally labeled neurons was studied in CNS of rats 4 days after injections of the Bartha strain of pseudorabies virus (PRV) into the medial gastrocnemius (MG) muscle. Tissue sections were processed for immunohistochemical detection of PRV. Retrogradely labeled cells were identified in the ipsilateral MG motor column in the caudal L4 and the L5 spinal segments. In order to evaluate the efficacy of PRV retrograde cell body labeling, the number of PRV retrogradely labeled neurons in the MG motor column was compared to the number labeled with two conventional retrograde cell body markers--Fluoro-Gold and cholera toxin-HRP. A ratio of 1:3 representing medium-sized (less than 30 microns) versus large neurons (greater than 30 microns) was found in the Fluoro-Gold dye experiments; a 1:2 ratio was seen in the PRV experiments. In contrast, when cholera toxin-HRP was used as a retrograde marker, mainly large neurons were labeled; the medium-to-large cell body ratio was 1:10 suggesting cholera toxin-HRP may have a greater affinity for the terminals of alpha-motoneurons as opposed to gamma-motoneurons. Transneuronally labeled cells were identified in the L1-L6 spinal gray matter, intermediolateral cell column (T11-L2), lateral spinal nucleus and medial part of lamina VII in C4 and C5 spinal segments, brainstem (caudal raphe nuclei, rostral ventrolateral medulla, A5 cell group, paralemniscal nucleus, locus coeruleus, subcoeruleus nucleus, red nucleus) and paraventricular hypothalamic nucleus. In the L5 spinal cord, transneuronally labeled neurons were seen in the ipsilateral spinal laminae I and II and bilaterally in spinal laminae IV-VIII, and X. Similar results were obtained in rats that had chronic unilateral L3-L6 dorsal rhizotomies indicating most of the labeling was due to retrograde transneuronal cell body labeling. In order to determine whether PRV was transported into the spinal cord by the dorsal root axons, the ipsilateral dorsal root ganglia (DRGs) were examined for PRV immunoreactivity; none was found. However, using the polymerase chain reaction, viral DNA was shown to be present in the ipsilateral DRGs indicating that some of spinal cord cell body labeling may have resulted from anterograde transneuronal labeling, as well.

Animals↗
PubMed1987

The relationship between uncoupling of oxidative phosphorylation and neuronal necrosis within the CNS in rats dosed with trihalogenated imidazoles.

The trihalogenated imidazoles, trichloroimidazole (TCI), tribromoimidazole (TBI), and triiodoimidazole (TII), are in vitro uncouplers of oxidative phosphorylation with similar activities. Although TCI and TBI are also uncouplers in vivo, some doubt exists for TII, which is much less toxic and produces atypical signs of poisoning. Dibromo- and monobromoimidazole do not uncouple oxidative phosphorylation either in vitro or in vivo. Dosing of TCI and TBI to rats resulted within 24-48 hr in neuronal necrosis within the CNS involving the vestibular nucleus, red nucleus, and outer parietal neocortex and ataxia of the hindlimbs. However, no neuronal necrosis or ataxia was observed after dosing of TII to rats, even when given at doses four times greater than for either TCI or TBI, resulting in much higher brain concentrations. Although TBI was equitoxic to rats, mice, hamsters, and gerbils, CNS damage and ataxia were observed only in the rat, even though comparable brain concentrations of TBI were found in the gerbil. Measurement of the concentration of TBI in the dissected rat brain gave no indication of localized concentrations of compound in the areas associated with neuronal damage. Doses of TBI and the classical uncoupler 3,5-dinitro-o-cresol (DNOC), matched for whole body O2 consumption, caused comparable changes in rat brain blood flow although DNOC does not cause brain damage. Changes in blood flow were not restricted to those brain areas susceptible to damage. Thus, although we were unable to completely dissociate CNS damage from uncoupling of oxidative phosphorylation produced by TBI and TCI in the rat, it is unlikely that such damage is primarily related to the uncoupling ability of these compounds.

Animals↗
PubMed1984

Distribution of premotor neurons for orbicularis oculi motoneurons in the cat, with particular reference to possible pathways for blink reflex.

After injecting horseradish peroxidase into the facial nucleus regions containing orbicularis oculi motoneurons, labeled neuronal cell bodies were found in the lateral medullary reticular formation, pretectal olivary nucleus, sensory trigeminal nuclei, lateral and medial parabrachial nuclei, ventromedial reticular formation medial to the facial nucleus, red nucleus and its surroundings, anterior horn of the upper cervical cord, medullary raphe nuclei, oculomotor nucleus and its surroundings, nuclei of Darkschewitsch, Cajal and Edinger-Westphal, ventral part of the midbrain central gray, pontine tegmentum, lateral vestibular nucleus and deep layers of the superior colliculus.

Animals↗
PubMed1985

Afferent and efferent connections of the medial preoptic area in the rat: a WGA-HRP study.

Afferent and efferent connections of the medial preoptic area including medial preoptic nucleus (MP) and periventricular area at the MP level were examined using WGA-HRP as a marker. Injections were performed by insertion of micropipette containing (1) small amount of HRP powder or (2) dryed HRP solution for 24 to 48 hr until the fixation or for 5 min respectively. Dorsal and ventral approaches of injection micropipettes were performed and the results were compared. Previously reported reciprocal connections with lateral septum, bed nucleus of the stria terminalis, medial amygdaloid nucleus, lateral hypothalamic nucleus, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, arcuate nucleus, supramammillary nucleus, central gray at the mesencephalon, raphe dorsalis, raphe medianus, and lateral parabrachial nucleus have been confirmed. In addition, we found reciprocal connections with septo-hypothalamic nucleus, amygdalo-hipocampal nucleus, subiculum, parafascicular thalamic nucleus, posterior thalamic nucleus at the caudo-ventral subdivision, median preoptic nucleus, lateral preoptic nucleus, anterior hypothalamic nucleus, periventricular area at the caudal hypothalamic level, dorsomedial hypothalamic nucleus, posterior hypothalamic nucleus, dorsal and ventral premammillary nucleus, lateral mammillary nucleus, peripeduncular nucleus, periventricular gray, ventral tegmental area, interpeduncular nucleus, nucleus raphe pontis, nucleus raphe magnus, pedunculo-pontine tegmental nucleus, gigantocellular reticular nucleus and solitary tract nucleus. The areas which had only efferent connections from MP were accumbens, caudate putamen, ventral pallidum, substantia innominata, lateral habenular nucleus, paratenial thalamic nucleus, paraventricular thalamic nucleus, mediodorsal thalamic nucleus, reuniens thalamic nucleus, median eminence, medial mammillary nucleus, subthalamic nucleus, pars compacta of substantia nigra, oculomotor nucleus, red nucleus, laterodorsal tegmental nucleus, reticular tegmental nucleus, cuneiform nucleus, nucleus locus coeruleus, and dorsal motor nucleus of vagus among which substantia innominata and median eminence were previously reported. Efferent connections to the nucleus of Darkschewitsch, interstitial nucleus of Cajal, dorsal tegmental nucleus, ventral tegmental nucleus, vestibular nuclei, nucleus raphe obsculus were very weak or abscent in the ventral approach while they were observed in dorsal approach. Previously reported afferent connections from dorsal tegmental nucleus, cuneiform nucleus, and nucleus locus ceruleus were not detected in this study.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Cannabinoid CB2 receptors: immunohistochemical localization in rat brain.

Brain expression of CB2 cannabinoid receptors has been much less well established and characterized in comparison to the expression of brain CB1 receptors. Since CB2 receptors are intensely expressed in peripheral and immune tissues, expression in brain microglia has been anticipated. Nevertheless, we now describe expression of CB2-receptor-like immunoreactivity in brain in neuronal patterns that support broader CNS roles for this receptor. Two anti-CB2 affinity purified polyclonal antibodies were raised in rabbits immunized with peptide conjugates that corresponded to amino acids 1-33 and 20-33. Western blot analyses revealed specific bands that were identified using these sera and were absent when the sera were preadsorbed with 8.3 mug/ml of the immunizing peptides. These studies, and initial RT-PCR analyses of brain CB1 and CB2 mRNAs, also support the expression of brain CB2 receptor transcripts at levels much lower than those of CB1 receptors. CB2 cannabinoid receptor mRNA was clearly expressed in the cerebellum of wild type but not in CB2 knockout mice. CB2 immunostaining was detected in the interpolar part of spinal 5th nucleus of wild type but not in CB2 knockout mice, using a mouse C-terminal CB2 receptor antibody. Immunohistochemical analyses revealed abundant immunostaining for CB2 receptors in apparent neuronal and glial processes in a number of rat brain areas. Cerebellar Purkinje cells and hippocampal pyramidal cells revealed substantial immunoreactivity that was absent when sections were stained with preadsorbed sera. CB2 immunoreactivity was also observed in olfactory tubercle, islands of Calleja, cerebral cortex, striatum, thalamic nuclei, hippocampus, amygdala, substantia nigra, periaqueductal gray, paratrochlear nucleus, paralemniscal nucleus, red nucleus, pontine nuclei, inferior colliculus and the parvocellular portion of the medial vestibular nucleus. In-vitro, CB2 immunoreactivity was also present in hippocampal cell cultures. The multifocal expression of CB2 immunoreactivity in glial and neuronal patterns in a number of brain regions suggests reevaluation of the possible roles that CB2 receptors may play in the brain.

Animals↗
PubMed2006

Immunohistochemical labeling of the mu opioid receptor carboxy terminal splice variant mMOR-1B4 in the mouse central nervous system.

The mu opioid receptor gene Oprm is alternatively spliced into many variants, providing for the multiplicity of mu opioid receptor subtypes. One of the mouse variants, mMOR-1B4, is unique in that it displays high affinity towards a wide range of mu opioid receptor antagonists, but poor affinity towards most classical mu opioid agonists. The present study examined the immunohistochemical distribution of the mMOR-1B4 variant in mouse brain and spinal cord. mMOR-1B4-like immunoreactivity (mMOR-1B4-LI) was enriched in many regions of the brain, spinal cord and in the dorsal root ganglia. Some of the structures showing prominent mMOR-1B4-LI include the olfactory bulb, cerebral cortex, bed nucleus of stria terminalis, hippocampus, habenular nucleus, amygdala, thalamus, hypothalamus, medium eminence, substantia nigra, ventral tegmental area, oculomotor nucleus, red nucleus, raphe nuclei, periaqueductal gray, locus coeruleus, trigeminal nucleus, reticular formation, area postrema and Purkinje cell layer and deep nuclei of cerebellum. mMOR-1B4-LI was present in afferent neurons of the dorsal root ganglia and their projecting fibers into the superficial laminae of the spinal dorsal horn. Some motor neurons in the anterior horn of the spinal cord also were immunopositive. The overall distribution of mMOR-1B4-LI in the central nervous system is distinguishable from previously characterized variants such as MOR-1-LI, MOR-1C-LI and exon-11-LI. These studies provide evidence for the region- and neuron-specific processing of the Oprm gene and support the possibility of functional differences among the variants.

Alternative Splicing↗
PubMed1989

Corticobasal degeneration.

Three patients with clinical and pathological features of corticobasal degeneration are described. They presented with a progressive disease bearing some clinical resemblance to Steele-Richardson-Olszewski syndrome and displaying some pathological features of Pick's disease. Their illness began at the age of 59 to 66 yrs with focal dystonia and myoclonus of an arm, the 'alien hand' sign, or an akinetic-rigid syndrome. They developed a supranuclear gaze palsy, parkinsonian features and mild cerebellar signs. Two patients showed constructional dyspraxia when using the arms. The duration of disease to death was 4 to 6 yrs. Pathological examination showed frontoparietal atrophy with cortical cell loss, gliosis and Pick cells, but there was no significant hippocampal disease or Pick bodies in this region. There was nerve cell loss and gliosis in the thalamus, lentiform nucleus, subthalamic nucleus, red nucleus, midbrain tegmentum, substantia nigra and locus coeruleus. Neuronal inclusions in the substantia nigra, termed corticobasal inclusions, were reminiscent of the globose neurofibrillary tangle of Steele-Richardson-Olszewski syndrome, and other pale inclusions resembled the pale body of Parkinson's disease, but Lewy bodies and neurofibrillary tangles were generally absent. Some nigral inclusions were similar to those in Pick's disease. Despite some pathological similarities to Pick's disease we suggest that the distribution of nerve cell loss and the corticobasal inclusion are unique to corticobasal degeneration.

Aged↗
PubMed2005

Neuronal intranuclear inclusion disease without polyglutamine inclusions in a child.

Neuronal intranuclear inclusion disease (NIID) is a rare and heterogeneous group of slowly progressive neurodegenerative disorders characterized by the widespread presence of eosinophilic neuronal intranuclear inclusions (NII) accompanied by a more restricted pattern of neuronal loss. We report here the pathologic findings in a 13-year-old boy who died after a 6-year clinical history of progressive ataxia, extrapyramidal manifestations, and lower motor neuron abnormalities. Histological evaluation of the brain revealed widespread NII in most neurons. Marked loss of cerebellar Purkinje cells and neurons in the dentate nucleus, red nucleus, and spinal cord anterior horns was accompanied by a modest astrocytosis. Because of the abundance of NII and the absence of a relationship between NII and neuronal loss or microglial activation, we conclude that loss of cerebellar, brainstem, and spinal cord neurons reflects selective neuronal vulnerability. NII were immunoreactive for ubiquitin, glucocorticoid receptor, and SUMO-1, a small, ubiquitin-like protein purportedly involved in protein transport and gene transcription. NII were non-reactive for polyglutamine (1C2), TATA binding protein, promyelocytic leukemia protein, heat shock protein 90, tau, alpha-synuclein, neurofilament, and beta amyloid. The moderate ubiquitin and strong SUMO-1 staining of NII in juvenile cases is the reverse of the pattern noted in adult diseases, suggesting the two age groups are pathogenically distinct. We suggest that juvenile NIID is a spinocerebellar brainstem ataxic disease possibly related to an abnormality in SUMOylation.

Adolescent↗
PubMed1980

Metabolic mapping of neural pathways involved in gastrosecretory response to insulin hypoglycaemia in the rat.

1. The central nervous structures involved in the gastrosecretory effect of insulin hypoglycaemia were investigated in twenty urethane-anaesthetized rats, previously provided with a chronic gastric fistula, by means of the 2-deoxy-D-[(14)C]glucose autoradiographic technique.2. Gastric secretion increased in animals in which plasma glucose concentration was reduced to a range of 84-133 mg/100 ml. (mean +/- S.E. of mean, 94 +/- 3) as compared to a range of 125-215 mg/100 ml. (mean +/- S.E. of mean, 162 +/- 8) in animals with normal gastric secretion.3. In fourteen of nineteen structures examined the rate of glucose utilization remained constant over the range of plasma glucose concentrations of 84-215 mg/100 ml. These structures included the ventromedial nucleus of the hypothalamus, the mamillary nuclei, the medial geniculate nuclei, globus pallidus, zona incerta, nucleus ambiguus, supraoptic nucleus, paraventricular nucleus, medial nucleus of the solitary tract, dorsal tegmental nucleus, red nucleus, inferior olivary nucleus, hippocampus and amygdaloid complex.4. A significant inverse correlation between plasma glucose concentration and the rate of glucose consumption was found in the lateral nucleus of the solitary tract, dorsal nucleus of the vagus, perifornical area where fibres of the medial forebrain bundle course, the superior olivary nucleus and the interstitial nucleus of the stria terminalis.5. Except for the superior olivary nucleus and the interstitial nucleus of the stria terminalis, all the structures affected by low plasma glucose concentration have previously been shown to participate in the gastrosecretory response to blockade of glucose utilization by pharmacological doses of 2-deoxy-D-glucose, indicating that these same nuclei are also activated by hypoglycaemia.

Animals↗
PubMed1982

The methylphenidate-induced stereotypy in the awake rat: local cerebral metabolism.

The local cerebral metabolic rate for glucose (1=CMRg) was computed in rats with methylphenidate-induced stereotypy using the quantitative 14C-2-deoxyglucose (2-DG) technique. Four rats received methylphenidate 15 mg per kilogram IP. Compared to five control animals, treated rats showed statistically significant (p less than or equal to 0.05) increases in 1-CMRg in globus pallidus, ventral lateral nucleus of the thalamus, subthalamic nucleus, red nucleus, substantia nigra, entopeduncular nucleus, inferior olivary nucleus, and the lateral cerebellar cortex. Significantly, 1-CMRg decreased in area 4 of the motor cortex. The auditory system showed no change in 1-CMRg, demonstrating the specific action of methylphenidate in the rat brain. This technique allows evaluation of the functional anatomy of the entire central nervous system and may be helpful in understanding the mechanisms of methylphenidate-induced stereotypy.

Animals↗