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PubMed1997

ACTH/CLIP immunoreactivity in the cat brain stem.

The distribution of adrenocorticotropin hormone/corticotropin-like intermediate lobe peptide was studied in the cat brain stem, using an indirect immunoperoxidase technique. No immunoreactive cell bodies were observed. However, a high density of immunoreactive fibers was found in the periaqueductal gray, the dorsal nucleus of the raphe, the locus coeruleus, and the marginal nucleus of the brachium conjunctivum. A moderate density was found in the central linear nucleus, the central tegmental field, the Kolliker-Fuse nucleus, the inferior central nucleus, and the postpyramidal nucleus of the raphe. A low density was found in the superior and inferior colliculi, the interpeduncular nucleus, the nucleus sagulum, the superior central nucleus, the cuneiform nucleus, the accessory dorsal tegmental nucleus, the nucleus of the solitary tract, the dorsal motor nucleus of the vagus, and the paralemniscal, magnocellular, gigantocellular, and lateral tegmental fields. Moreover, single immunoreactive fibers were observed in numerous nuclei of the cat brain stem. In comparison with previous studies carried out in the same region of the cat, as well as the rat and the human, our results point to a more widespread distribution of adrenocorticotropin hormone/corticotropin-like intermediate lobe peptide immunoreactive structures in the cat brain stem. This widespread distribution indicates that the peptide might be involved in several physiological functions of the cat brain stem.

Adrenocorticotropic Hormone↗

PubMed2003

Neuronal nitric oxide synthase (bNOS) messenger RNA and protein expression in developing rat brainstem nuclei.

Neuronal nitric oxide synthase (bNOS) messenger RNA expression and immunoreactivity were mapped in series of cryosections through the developing rat brainstem nuclei. Between embryonic day E16 and postnatal day P16, brainstem nuclei expressed both bNOS messenger RNA (mRNA) in situ hybridization signals and protein immunoreactivity. However, NOS mRNA signals were absent from the Edinger Westphal, facial or motory trigeminal nucleus. Strong patterns of mRNA signals and immunoreactivity occurred in neurons located in the substantia nigra pars compacta and the laterodorsal tegmental nuclei. Between E24 and P16, altered patterns of bNOS mRNA positive and immunoreactive neurons, e.g. superior and inferior colliculi, raphe nuclei, solitary tract or pontine nucleus were documented. Altered NOS expression patterns thus may reflect developmental processes within distinct neuronal populations such as cell phenotype discrimination or synaptogenesis within efferent or afferent brainstem pathways. The NOS/NO system therefore appears to be a modulator for intra-/intercellular adjustment processes in normal development.

Animals↗

PubMed2000

Expression of the neuronal calcium sensor protein family in the rat brain.

The neuronal calcium sensor proteins are members of the calcium-binding protein superfamily. They control localized calcium signalling on membranes and may make G-protein cascades sensitive to cytosolic calcium. The family members are recoverin (visinin, S-modulin), neuronal calcium sensor-1 (frequenin), hippocalcin, neuronal visinin-like protein-1 (visinin-like protein, neurocalcin-alpha), neuronal visinin-like protein-2 and neuronal visinin-like protein-3. Recoverin is expressed only in the retina and pineal gland. Using in situ hybridization, we mapped the expression of the other neuronal calcium sensor protein genes in the adult rat brain. Neuronal visinin-like protein-1 messenger RNA has a widespread distribution and is abundant in all brain areas except the caudate-putamen. Neuronal calcium sensor-1 gene expression is pan-neuronal. Neuronal calcium sensor-1 messenger RNA is present in the dendrites of hippocampal pyramidal and granule cells, suggesting a specific role in dendritic function. Hippocalcin and neuronal visinin-like protein-2 are mainly expressed in the forebrain and have similar expression patterns (neocortex, hippocampus and caudate-putamen). Neuronal visinin-like protein-3 has the most restricted expression; its highest expression level is in the cerebellum (Purkinje and granule cells). However, the neuronal visinin-like protein-3 gene is also expressed in many ventral nuclei throughout the fore- and midbrain, in the medial habenulae, and in the superior and inferior colliculi. The neuronal calcium sensor proteins are a relatively unexplored family of Ca(2+)-binding proteins. They are likely to be involved in many diverse areas of neuronal signalling. In this paper, we describe their expression in the rat brain as determined by in situ hybridization. As all five neuronal calcium sensor protein genes have distinctive expression patterns, they probably perform specific functions.

Animals↗

PubMed1999

Distribution of the nociceptin and nocistatin precursor transcript in the mouse central nervous system.

The distribution of prepronociceptin messenger RNA, the recently identified endogenous ligand of the ORL1 receptor (opioid receptor-like-1), has been studied in the adult mouse central nervous system using in situ hybridization. Prepronociceptin is a new peptide precursor that generates, upon maturation, at least three bioactive peptides: nociceptin, noc2 and the recently described nocistatin. Considering both the density of labeled neurons per region and their intensity of labeling, the distribution of prepronociceptin messenger RNA-containing neurons can be summarized as follows: the highest level of prepronociceptin messenger RNA expression was detected in the septohippocampal nucleus, bed nucleus of the stria terminalis, central amygdaloid nucleus, and in selective thalamic nuclei such as the parafascicular, reticular, ventral lateral geniculate and zona incerta. High to moderate levels of prepronociceptin messenger RNA expression were detected in the lateral, ventral and medial septum, and were evident in brainstem structures implicated in descending antinociceptive pathways (e.g., the gigantocellular nucleus, raphe magnus nucleus, periaqueductal gray matter), and also observed in association with auditory relay nuclei such as the inferior colliculi, lateral lemniscus nucleus, medioventral preolivary nucleus and lateral superior nucleus. A moderate level of prepronociceptin messenger RNA expression was observed in the medial preoptic nucleus, ventromedial preoptic nucleus, periventricular nucleus, pedonculopontine tegmental nucleus, solitary tract nucleus and spinal trigeminal nucleus. A weak level of prepronociceptin messenger RNA expression was present in some areas, such as the cerebral cortex, endopiriform cortex, hippocampal formation, medial amygdaloid nucleus, anterior hypothalamic area, medial mammillary hypothalamic nuclei, retrorubral field and substantia nigra pars compacta. No labeled cells could be found in the caudate-putamen, nucleus accumbens and ventral tegmental area. The present data confirm that nociceptin is expressed in a broad array of regions of the central nervous system. In good correlation with the presently known physiological actions of nociceptin, they include, amongst others, brain areas conveying/integrating pain and auditory sensory afferences.

Animals↗

PubMed2000

Fos expression and 2-deoxyglucose uptake following seizures in developing genetically epilepsy-prone rats.

Juvenile genetically epilepsy-prone rats (GEPR)-3s display one of three types of seizures in response to sound: a typical class 3 seizure consisting of an explosive running/bouncing episode followed by a clonic seizure (audiogenic response score, ARS-3); an ARS-3 seizure followed by a forebrain seizure that includes facial and forelimb (F&F) clonus with rearing (ARS-3f); or, a running/bouncing episode followed by a severe tonic seizure with complete hindlimb extension (ARS-9) not accompanied with subsequent F&F clonus. The adult seizure phenotype, manifest in all GEPR-3s by age 45 days of age, consists of an ARS-3 not followed by F&F clonus or tonic extension. The present studies sought to determine the neuronal networks activated during these various developmental convulsive patterns by examining anatomical patterns of [(14)C]2-deoxyglucose (2-DG) uptake or immediate-early-gene (Fos) expression subsequent to seizures. Many, but not all, brain areas of control rats showed age-related increases in Fos expression in response to the acoustic stimulation. An age effect was not observed in 2-DG uptake. In GEPRs, the profiles of Fos expression and 2-DG uptake following seizures were often parallel; however, there were notable exceptions. For example, increased 2-DG uptake in the cochlear nuclei, central region of the inferior colliculi, and the substantia nigra were not accompanied by increased Fos expression in these areas regardless of the seizure phenotypes. Reciprocally, other regions, particularly in the amygdala, ventromedial hypothalamus and parabrachial areas, displayed intense seizure related Fos labeling without detectable increases in 2-DG uptake. Fos and 2-DG uptake patterns in response to acoustic stimulation varied according to brain region, seizure phenotype and severity. In general, the degree of 2-DG uptake correlated with seizure severity. For example, the ARS-9 seizures, being the most intense, resulted in significant increases in 2-DG uptake in almost all brain regions examined. 2-DG uptake following the ARS-3f and ARS-3 seizures, although increased, did not reach statistical significance in most brain areas. In contrast to the 2-DG findings, a seizure-severity dependent effect was not seen with Fos. Rather, the induction of Fos associated with acoustic stimulation and seizure was more associated with age and seizure-phenotype. Thus, the developmental profiles of Fos expression and 2-DG uptake in response to seizures are distinctly different and concurrent examination of both markers is useful in the identification of brain circuitry involved in seizure development.

Acoustic Stimulation↗

PubMed2003

Infantile hypermethioninemia and hyperhomocysteinemia due to high methionine intake: a diagnostic trap.

Studies were carried out to identify the cause of combined severe hypermethioninemia and moderate hyperhomocysteinemia in a cluster of 10 infants ascertained between 1999 and early 2001. Although several were thought initially to have cystathionine beta-synthase (CBS) deficiency and treated accordingly, CBS deficiency and other known genetic causes of hypermethioninemia were ruled out by assay of CBS activity in fibroblasts of four patients and by assays of plasma cystathionine and S-adenosylmethionine. Retrospective data on dietary methionine intakes and plasma concentrations of methionine and related metabolites established that the hypermethioninemia in nine of the 10 babies was related to ingestion of an infant protein hydrolysate formula, the methionine content of which had been increased from May 1998 to February 2001. The formula in question has now been reformulated and is no longer available. The 10th infant manifested similar metabolic abnormalities while receiving TPN containing excessive methionine. Brain MRI abnormalities indicative of cerebral edema, most marked in the cerebral cortex and posterior brainstem, occurred in two patients near times of extreme hypermethioninemia. Metabolic and MRI abnormalities resolved when the methionine intake decreased. A third infant had a normal MRI 1 day after the formula was changed. The possible relationship between extreme hypermethioninemia and cerebral edema is discussed and a working hypothesis offered to explain the relative sensitivity of the inferior colliculi, based upon the facts that this is the region most active in glucose utilization and that Na(+),K(+)-ATPase is inhibited by methionine and related metabolites.

Brain Edema↗

PubMed2000

Time course of brain neuronal degeneration and heat shock protein (72) expression following neck tourniquet-induced cerebral ischemia in the rat.

1. The present study was designed to examine the regional expression of HSP72/73 protein after a 7.5-min period of cerebral ischemia and to compare the distribution of HSP neurons with the localization of irreversible neuronal degeneration as analyzed by silver impregnation technique. 2. During 6-24 hr after cerebral ischemia clear-cut neuronal argyrophilia developed in several brain regions including the hippocampal hilus, nucleus reticularis thalami, and colliculi inferiores. With the exception of the hippocampal hilus, the structures which showed silver impregnability were HSP72 negative at 6-24 hr. 3. Despite the clear HSP72 expression seen in hippocampal CA1 neurons, a significant loss of these neurons was seen at 7 days after ischemia. 4. These data show that in some structures the presence of HSP72 is indicative of higher resistance of these neurons to ischemia-induced degeneration, however, the process of delayed neuronal degeneration appears to be independent of the accelerated synthesis of HSP72 seen during the early period of reflow.

Animals↗

PubMed1995

Development of susceptibility to audiogenic seizures following cardiac arrest cerebral ischemia in rats.

Susceptibility to audiogenic seizures (AGS) was investigated in Sprague-Dawley rats subjected to cardiac arrest cerebral ischemia (CACI), produced by compression of the major cardiac vessels. The onset of AGS was regularly observed 1 day after CACI of > 5 min duration. The duration of postischemic susceptibility to AGS was directly related to the density of cerebral ischemia, with 50% of more severely ischemic animals still showing AGS susceptibility 8 weeks after CACI. Lesioning of the inferior colliculi (IC) abolished the onset of AGS; no such effect was observed after lesioning the medial geniculate (MG). Glutamic acid decarboxylase (GAD) immunochemistry revealed approximately 50% loss of GAD-positive neurons in the IC, which was similar in animals with various durations of AGS susceptibility. Otherwise, there was a conspicuous sprouting of gamma-aminobutyric acid (GABA)-ergic terminals in the ventral thalamic nuclei, which peaked approximately 1 month after the CACI. Evaluation of GABA-A inhibitory function in the hippocampus by the paired pulse stimulation revealed changes indicating loss of GABA-A inhibition coinciding with the onset of AGS, and its return in animals tested 2 months after CACI. Our observations suggest a potential role of GABA-ergic dysfunction in the postischemic development of AGS.

Acoustic Stimulation↗

PubMed1996

Characterization of a cerebellar granule cell-specific gene encoding the gamma-aminobutyric acid type A receptor alpha 6 subunit.

The alpha 6 subunit of gamma-aminobutyric type A receptors is a marker for cerebellar granule cells and is an attractive candidate to study cell-specific gene expression in the brain. The mouse alpha 6 subunit gene has nine exons and spans approximately 14 kb. The largest intron (intron 8) is approximately 7 kb. For a minority of mRNAs, a missplice of the first exon was identified that disrupts the signal peptide and most likely results in the production of nonfunctional protein. The gene is transcribed from a TATA-less promoter that uses multiple start sites. Using transgenic mice, it was found that the proximal 0.5 kb of the rat alpha 6 gene upstream region confers expression on a beta-galactosidase reporter gene. One founder gave rise to a line with cerebellar granule cell-specific expression, although expression varied with lobule region. Other founders had ectopic but neuron-specific expression, with beta-galactosidase found in cerebellar Purkinje cells, neocortex, thalamus, hippocampus, caudate-putamen, and inferior colliculi. Thus, we have defined a region containing the basal promoter of the alpha 6 subunit gene and that confers neuron-specific expression.

Alternative Splicing↗

PubMed1997

MRI assessment of myelination of motor and sensory pathways in the brain of preterm and term-born infants.

A study was performed in 48 neurologically normal preterm and term-born infants, with a postconceptional age at MRI varying between 30 2/7 and 46 weeks and a mean age of 34 2/7 weeks. The purpose of the study was to determine the normal progress of myelination on MRI in that age range. T1- and T2-weighted images of the brain were assessed for changes in signal intensity of white matter relative to gray matter. Multiple sites in the brainstem, cerebellum and cerebral hemispheres were assessed separately. The findings were correlated with the ages of the infants. As judged from relative signal intensities, myelin was present at the post-conceptional age of 30-34 weeks in the following structures: tegmentum pontis (in particular medial lemniscus), superior and inferior colliculi, decussation of the superior cerebellar peduncles, crura cerebri, ventrolateral thalamus, lateral globus pallidus, dorsolateral putamen, dentate nucleus, middle and superior cerebellar peduncles, vermis cerebelli, cortex bordering the central sulcus and hippocampus. Little progress in myelination was noticed up to the post-conceptional age of 46 weeks. Between 34 and 46 weeks, myelin appeared in the lateral part of the posterior limb of the internal capsule and in the central part of the corona radiata and became more prominently visible in the cortex bordering the central sulcus.

Age Factors↗

PubMed1988

Diazepam binding inhibitor gene expression: location in brain and peripheral tissues of rat.

Diazepam binding inhibitor (DBI), an endogenous 10-kDa polypeptide was isolated from rat and human brain by monitoring displacement of radioactive diazepam bound to specific recognition sites in brain synaptic and mitochondrial membranes. The cellular location of DBI mRNA was studied in rat brain and selected peripheral tissues by in situ hybridization histochemistry with a 35S-labeled single-stranded complementary RNA probe. DBI mRNA was heterogeneously distributed in rat brain, with particularly high levels in the area postrema, the cerebellar cortex, and ependyma of the third ventricle. Intermediate levels were found in the olfactory bulb, pontine nuclei, inferior colliculi, arcuate nucleus, and pineal gland. Relatively low but significant levels of silver grains were observed overlying many mesencephalic and telencephalic areas that have previously been shown to contain numerous DBI-immunoreactive neurons and a high density of central benzodiazepine receptors. In situ hybridizations also revealed high levels of DBI mRNA in the posterior lobe of the pituitary gland, liver, and germinal center of the white pulp of spleen, all tissues that are rich in peripheral benzodiazepine binding sites. The tissue-specific pattern of DBI gene expression described here could be exploited to further understand the physiological function of DBI in the brain and periphery.

Animals↗

PubMed1991

D1 and D2 dopamine receptor mRNA in rat brain.

Physiological and pharmacological criteria have divided dopamine receptors into D1 and D2 subtypes, and genes encoding these subtypes have recently been cloned. Based on the sequences of the cloned receptors, we prepared oligodeoxynucleotide probes to map the cellular expression of the corresponding mRNAs in rat brain by in situ hybridization histochemistry. These mRNAs showed largely overlapping yet distinct patterns of expression. The highest levels of expression for both mRNAs were observed in the caudate-putamen, nucleus accumbens, and olfactory tubercle. Within the caudate-putamen, 47 +/- 6% and 46 +/- 5% of the medium-sized neurons (10-15 microns) expressed the D1 and D2 mRNAs, respectively, and only the D2 mRNA was observed in the larger neurons (greater than 20 microns). The D1 and D2 mRNAs were expressed in most cortical regions, with the highest levels in the prefrontal and entorhinal cortices. Within neocortex, D1 mRNA was observed primarily in layer 6 and D2 mRNA in layers 4-5. Within the amygdala, D1 mRNA was observed in the intercalated nuclei, and D2 mRNA in the central nucleus. Within the hypothalamus, D1 mRNA was observed in the suprachiasmatic nucleus and D2 mRNA in many of the dopaminergic cell groups. Within the septum, globus pallidus, superior and inferior colliculi, mammillary bodies, and substantia nigra only D2 mRNA was detected. These data provide insight into the neuroanatomical basis of the differential effects of drugs that act on D1 or D2 receptors.

Animals↗

PubMed1997

Cooperation of Pax2 and Pax5 in midbrain and cerebellum development.

Midbrain and cerebellum development depends on an organizing center that is located at the midbrain-hindbrain junction of the vertebrate embryo. Expression of the two closely related transcription factors Pax2 and Pax5 overlaps spatially and temporally in this region of the developing central nervous system. To study a possible interaction of these transcription factors in midbrain and cerebellum patterning, we have generated Pax5, Krd double mutant mice. The transgene-induced Krd mutation corresponds to an approximately 7-centimorgan chromosome 19 deletion that eliminates the entire Pax2 locus. The heterozygous Krd mutation deleting one Pax2 allele had no effect on midbrain and cerebellum development. Moreover, only minor developmental defects were previously observed at the midline of the inferior colliculus and anterior cerebellum in mice that were homozygous for a targeted Pax5 mutation. Similar morphological alterations were observed in 80% of all compound heterozygous Pax5 (+/-) Krd (+/-) mice. However, in the remaining 20% of compound heterozygotes, the inferior colliculi were missing, and the vermis of the cerebellum was severely disrupted due to the failure of the cerebellar primordia to fuse at the midline. Inactivation of the second Pax5 allele in Pax5 (-/-) Krd (+/-) mice resulted in complete loss of the posterior midbrain and cerebellum, as the tissue originating from the midbrain-hindbrain boundary region was deleted in the embryo as early as day 9.5. On the basis of these data, we propose that the cooperation of Pax2 and Pax5 is essential for normal functioning of the organizing center at the midbrain-hindbrain junction.

Animals↗

PubMed1998

Acute study on the efficacy and safety of an auditory brainstem prosthesis.

Patients with profound binaural sensorineural hearing loss can be treated with cochlear implantation. In recent years, patients who have lost the integrity of the auditory nerve between the spiral ganglion and the cochlear nucleus in the brainstem, and cannot benefit from a cochlear implant, have reported auditory sensations following direct stimulation of the cochlear nucleus with an auditory brainstem prosthesis. To examine the safety and efficacy of such a prosthesis, the cochlear nuclei of guinea-pigs were acutely implanted and stimulated unilaterally with bipolar surface electrodes using the parameters of human implants. The activation of the central auditory pathway by the prosthesis was demonstrated using the 2-deoxyglucose technique. There was broad 2-deoxyglucose labelling in the ipsilateral cochlear nucleus and bilaterally in the inferior colliculi, indicating unusual stimulation of the ipsilateral ascending pathway. Histological examination was performed on all cochlear nuclei. The volumes of cochlear nuclei and the neuron sizes and density in the cochlear nuclei were analysed with three-dimensional reconstruction techniques, and comparisons were made between the stimulated and unstimulated sides. No histological difference, either by direct visual observation or by statistical comparisons, was observed between the stimulated cochlear nuclei and the control sides. These results suggest that in the acute case the auditory brainstem prostheses can safely and effectively activate the auditory pathway in guinea-pigs.

Acoustic Stimulation↗

PubMed1981

Locomotor control in macaque monkeys.

We carried out experiments on young adult macaque monkeys (M.fascicularis) in an attempt to establish whether or not primates possess a locomotor control system consisting of spinal pattern generators modulated by brain-stem locomotor regions. We could not induce 'spinal stepping' in our subjects after spinal cord transection. Sparing of pathways contained in the central sector of the white matter of the cord was sufficient for stepping and walking. 'Controlled locomotion' was elicited in thalamic monkeys by electrical stimulation of the posterior subthalamic region or the midbrain tegmentum just ventral to the inferior colliculi. We conclude that there are significant homologies between this primate species and the cat regarding the probable existence of supraspinal locomotor control structures, but it seems that the presumed spinal step generators in monkeys depend more on supraspinal inputs than they do in cats.

Animals↗

PubMed2006

Hemispheric asymmetry for auditory processing in the human auditory brain stem, thalamus, and cortex.

We report evidence for a context- and not stimulus-dependent functional asymmetry in the left and right human auditory midbrain, thalamus, and cortex in response to monaural sounds. Neural activity elicited by left- and right-ear stimulation was measured simultaneously in the cochlear nuclei, inferior colliculi (ICs), medial geniculate bodies (MGBs), and auditory cortices (ACs) in 2 functional magnetic resonance imaging experiments. In experiment 1, pulsed noise was presented monaurally to either ear, or binaurally, simulating a moving sound source. In experiment 2, only monaural sounds were presented. The results show a modulation of the neural responses to monaural sounds by the presence of binaural sounds at a time scale of tens of seconds: In the absence of binaural stimulation, the left and right ICs, MGBs, and ACs responded stronger to stimulation of the contralateral ear. When blocks of binaural stimuli were interspersed in the sound sequence, the contralateral preference vanished in those structures in the right hemisphere. The resulting hemispheric asymmetry was similar to the asymmetry demonstrated for spatial sound processing. Taken together, the data demonstrate that functional asymmetries in auditory processing are modulated by context. The observed long time constant suggests that this effect results from a "top-down" mechanism.

Acoustic Stimulation↗

PubMed2003

FGFR1 is independently required in both developing mid- and hindbrain for sustained response to isthmic signals.

Fibroblast growth factors (FGFs) are signaling molecules of the isthmic organizer, which regulates development of the midbrain and cerebellum. Tissue-specific inactivation of one of the FGF receptor (FGFR) genes, Fgfr1, in the midbrain and rhombomere 1 of the hindbrain of mouse embryos results in deletion of the inferior colliculi in the posterior midbrain and vermis of the cerebellum. Analyses of both midbrain-hindbrain and midbrain-specific Fgfr1 mutants suggest that after establishment of the isthmic organizer, FGFR1 is needed for continued response to the isthmic signals, and that it has direct functions on both sides of the organizer. In addition, FGFR1 appears to modify cell adhesion properties critical for maintaining a coherent organizing center. This may be achieved by regulating expression of specific cell-adhesion molecules at the midbrain-hindbrain border.

Animals↗

PubMed1992

Biocytin injections produce selective neuronal labeling in the rat CNS.

Large injections of biocytin into the lateral ventricle or brain resulted in the labeling of particular neuronal subpopulations in the rat CNS. Localization was accomplished using the avidin-biotin-peroxidase technique. In many cases the staining of neurons was totally complete and resembled that obtained with the Golgi technique. Regions containing labeled cells included the olfactory bulb, cerebral cortex, hippocampus, amygdala, striatum, hypothalamus, superior and inferior colliculi, cerebellar cortex, and dorsal horn of the spinal cord. Only particular cell types were labeled in each of these regions. The results of this study suggest that there is selective uptake and/or retention of biocytin, or a biotinylated metabolite of biocytin, by subpopulations of CNS neurons.

Animals↗