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PubMed1996

The avian IGF type 1 receptor: cDNA analysis and in situ hybridization reveal conserved sequence elements and expression patterns relevant for the development of the nervous system.

Insulin-like growth factor type 1 receptor (IGF-1R) is a tyrosine kinase with a key role in development. The primary structure of IGF-1R is known for mammalian species, but not for birds. The avian embryo, however, provides an ideal system for the experimental study of neurogenesis. We therefore cloned the complete coding sequence of the chicken IGF-1R from a cDNA library and analyzed its embryonic expression by Northern blot and in situ hybridization. The deduced chicken IGF-1R precursor of 1363 amino acids was 85% identical to human IGF-1R and did not show deletions or insertions in critical positions, when compared to its mammalian homologues. Notably, all cysteine residues in the extracellular domains, and 15 of the 17 N-linked glycosylation sites found in human IGF-1R were also present in the chicken receptor. An 11 kb transcript was abundant in developing nervous tissues, kidney, pancreas and the gastrointestinal tract. The early in situ expression patterns in 20-somite embryos revealed high levels of IGF-1R mRNA in the neuroepithelia, notochord and somites. At embryonic day 4 (E4), high concentrations of IGF-1R transcripts were found again primarily in the neuroepithelia and, to a lesser degree, in the sensory ganglia and diverse mesenchymal derivatives. During the second half of embryonic development, IGF-1R expression in the CNS was particularly abundant in telencephalic regions, including the olfactory bulb, hippocampus, striatum and piriform cortex, and also in the optic tectum and cerebellum. By the use of cDNA cloning and in situ hybridization this study reveals conserved amino acid sequence elements between birds and mammals, and developmental expression patterns that are compatible with an important role of this receptor in growth, differentiation and maturation of the avian CNS.

Animals↗
PubMed1998

Alterations in GLUT1 and GLUT3 glucose transporter gene expression following unilateral hypoxia-ischemia in the immature rat brain.

The brain damage produced by unilateral cerebral hypoxia-ischemia in the immature rat results from major alterations in cerebral energy metabolism and glucose utilization which begin during the course of the insult and proceed into the recovery period. Consistent with a lack of pathology, the alterations in the hemisphere contralateral to the carotid artery ligation are transient and return to normal within 24 h of recovery, whereas the hemisphere ipsilateral to the ligation exhibits both early and late responses, and infarction. The facilitative glucose transporter proteins mediate glucose transport across the blood-brain barrier (55 kDa GLUT1), and into neurons and glia (GLUT3 and 45 kDa GLUT1), and demonstrate both early and late responses to perinatal hypoxia-ischemia. This study employed in situ hybridization histochemistry to investigate the temporal and regional patterns of GLUT1 and GLUT3 gene expression following a severe (2.5 h) hypoxic-ischemic insult in the 7-day old rat brain. Enhanced GLUT1 mRNA expression was apparent in cerebral microvessels of both hemispheres and remained elevated in the ipsilateral hemisphere through 24 h of recovery, consistent with our previous observation of increased microvascular 55 kDa GLUT1 protein. The expression of the neuronal isoform, GLUT3, was enhanced in penumbral regions, such as piriform cortex and amygdala, but was rapidly reduced in the affected areas of cortex, hippocampus and thalamus, reflecting necrosis. The late response, observed at 72 h of recovery, was characterized by extensive necrosis in the ipsilateral hemisphere, loss of GLUT3 expression, and a gliotic reaction including increased GLUT1 in GFAP-positive astrocytes. This study demonstrates that cerebral hypoxia-ischemia in the immature rat produces both immediate-early and long-term effects on the glucose transporter proteins at the level of gene expression.

Animals↗
PubMed1998

Metabolic activity is increased in discrete brain regions before the occurrence of spike-and-wave discharges in weanling rats with genetic absence epilepsy.

In the present study, we measured basal local cerebral metabolic rates for glucose (LCMRglcs) in immature genetic absence epilepsy rats from Strasbourg (GAERS) at postnatal day 21 (P21), at which age no spike-and-wave discharges can be recorded. LCMRglcs in GAERS were compared to those in control non-epileptic (NE) rats of the same age selected from our breeding colony. LCMRglcs were measured in 60 structures by the quantitative [14C]2-deoxyglucose (2DG) autoradiographic technique. In P21 GAERS, LCMRglcs were similar to those of P21 NE rats in 46 areas. They increased over NE control levels in two groups of structures. First, metabolic increases were recorded in limbic structures such as entorhinal and piriform cortex, lateral septum as well as all hippocampal subfields and basolateral amygdala, although no spike-and-wave discharges can be recorded from those areas in adult GAERS. On the other hand, increases in LCMRglcs were also recorded in substantia nigra pars reticulata, superior colliculus and globus pallidus which are structures involved in the control of seizure activity. Finally, significant metabolic decreases in P21 GAERS were recorded in two posterior auditory regions, the inferior colliculus and the superior olive. In conclusion, our data show that the genetic mutation(s) underlying the cellular and molecular events responsible for the expression of spike-and-wave discharges in adult GAERS is(are) able to increase metabolic activity in limbic structures and in the nigral inhibitory system before the occurrence of absence seizures. Conversely, the full electrocortical maturation seems necessary for the expression of spike-and-wave discharges with the concurrent increase in LCMRglcs in adult GAERS.

Animals↗
PubMed2003

The fundamental role of memory in olfactory perception.

Current emphasis on odorant physiochemical features as the basis for perception largely ignores the synthetic and experience-dependent nature of olfaction. Olfaction is synthetic, as mammals have only limited ability to identify elements within even simple odor mixtures. Furthermore, olfaction is experience-bound, as exposure alone can significantly affect the extent to which stimuli can be discriminated. We propose that early analytical processing of odors is inaccessible at the behavioral level and that all odors are initially encoded as 'objects' in the piriform cortex. Moreover, we suggest that odor perception is wholly dependent on the integrity of this memory system and that its loss severely impairs normal perception.

Animals↗
PubMed2001

Cloning the full-length IL-2/15 receptor-beta cDNA sequence from mouse brain: evidence of enrichment in hippocampal formation neurons.

Numerous studies have implicated interleukin-2 (IL-2) in various brain processes, and more recently, several studies have also attributed neurobiological actions to interleukin-15 (IL-15). On lymphocytes, receptors for IL-2 and IL-15 share a common subunit, the IL-2/15 receptor-beta (IL-2/15Rbeta) that is essential for intracellular signaling. Although a short segment of IL-2/15Rbeta has been cloned (0.35 kb) from normal brain cells, attempts to isolate the full-length cDNA have been unsuccessful, suggesting the possibility that the genes expressed by brain cells and lymphocytes may differ. Using conventional and anchored PCR cloning strategies, we isolated the full-length cDNA of IL-2/15Rbeta (2038 bp) from well-perfused, normal mouse forebrain. The coding sequence and the adjacent 5' and 3' UTR sequences from brain and lymphocyte were found to be fully homologous. Although evidence of expression of IL-2/15Rbeta can be found in many brain regions using PCR, clear evidence of gene expression by in situ hybridization was detectable only in the hippocampal formation, habenula and piriform cortex. This same pattern of mRNA expression in situ was also observed for the common gamma subunit shared by IL-2 and IL-15. In the hippocampus, IL-2/15Rbeta expression was localized to neurons by high resolution in situ hybridization and evidence of IL-2 receptor protein expression was also detected by radioligand receptor binding using hippocampal homogenates. Comparison of undifferentiated and differentiated, immortalized H19-7 hippocampal neurons showed that IL-2/15Rbeta was constitutively expressed across disparate stages of hippocampal neuronal differentiation. These data indicate that IL-2/15Rbeta may serve to modulate neuronal processes in the hippocampus and associated limbic brain regions.

Animals↗
PubMed2002

Plasminogen mRNA induction in the mouse brain after kainate excitation: codistribution with plasminogen activator inhibitor-2 (PAI-2) mRNA.

Plasminogen (Plg), which can be converted to the active protease plasmin by plasminogen activators, has been previously implicated in brain plasticity and in toxicity inflicted in hippocampal pyramidal neurons by kainate. Here we have localized Plg. mRNA through in situ hybridization in brain cryosections derived from normal adult mice or after kainate injection (i.p.). The results indicated that Plg mRNA was undetectable in the normal brain, but after kainate injection it was induced in neuronal cells in multiple, but specific areas, including layers II-III of the neocortex; the olfactory bulb, anterior olfactory nucleus, and the piriform cortex; the caudate/putamen and accumbens nucleus shell; throughout the amygdaloid complex; and in the CAI/CA3 subfields of the hippocampus. Interestingly, this distribution pattern coincided with what we have recently described for the plasminogen activator inhibitor-2 (PAI-2) mRNA, however differing from that of the plasminogen activator inhibitor-1 (PAI-1) mRNA, as also shown here. These results suggest that enhanced Plg gene expression could be involved in events associated with olfactory, striatal, and limbic structures. Furthermore, because PAI-2 is thought to intracellularly counteract cytotoxic events, our results raise the possibility that PAI-2 can act in the brain as an intracellular neuroprotector against potential plasmin-mediated toxicity.

Animals↗
PubMed2002

Role of MAP kinase in signaling indispensable amino acid deficiency in the brain.

Deficiencies of indispensable amino acids (IAAs) appear to be sensed in the anterior piriform cortex (APC) where neurons are activated and potentiated, however, the mediating intracellular signaling mechanisms are largely unexplored. It is postulated that signaling of amino acid deficiency may share many of the same pathways seen with long-term potentiation (LTP). Phosphorylation of mitogen-activated protein kinase (pMAP kinase) has been shown to be a necessary signaling event for the genesis and maintenance of LTP. Immunoperoxidase immunohistochemistry was used to determine the number of neurons showing activation of the MAP kinase signal transduction system. Relative to rats eating a corrected diet, rats consuming threonine-devoid diet showed significantly greater pMAP kinase labeling in the APC, dorsomedial hypothalamus, and the paraventricular hypothalamic nucleus. These are areas previously associated with control of food intake. However, since the dorsomedial hypothalamus and the paraventricular hypothalamic nucleus have not previously been implicated as chemosensory areas for IAAs, phosphorylated MAP kinase expression in these areas may reflect secondary activation.

Animals↗
PubMed2003

Mouse dexamethasone-induced RAS protein 1 gene is expressed in a circadian rhythmic manner in the suprachiasmatic nucleus.

We identified the Dexamethasone-induced RAS protein 1 (Dexras1) gene as a cycling gene in the suprachiasmatic nucleus (SCN). Investigation of the whole brain using in situ hybridization demonstrated the localization of the expression of the gene in the SCN, thalamus, piriform cortex and hippocampus. However, rhythmic expression of the gene was observed only in the SCN. The rhythmic change in gene expression during 1 day was approximately five-fold, and the maximum expression was observed during subjective night. Real-time PCR using the SCN, paraventricular nucleus and cortex confirmed these results. Next, we analyzed the expression of the Dexras1 gene in the SCN of cryptochrome (Cry) 1 and 2 double knockout mice. We found that the rhythmic expression disappeared. The results indicate that Dexras1 rhythmicity and levels are dependent upon CRYs. This is the first time that the G protein, which may be involved in the input pathway, has been isolated as a cycling gene in the SCN.

Animals↗
PubMed2003

Expression of FERM domain including guanine nucleotide exchange factor mRNA in adult rat brain.

FERM domain including Rho GEF (FIR) belongs to Dbl family of guanine nucleotide exchange factors and specifically activates biochemical pathways specific for Rac1. FIR was shown to regulate neurite remodeling of the embryonic neurons. Here we report a distribution of FIR mRNA in adult rat brain using in situ hybridization. The expression was found all throughout the brain with the most intensive signals in hippocampus, piriform cortex, red nucleus and nuclei of cranial nerves. The signal was predominantly localized in the neuronal cells.

Aging↗
PubMed1998

Cloning of glucocorticoid receptor and mineralocorticoid receptor cDNA and gene expression in the central nervous system of the tree shrew (Tupaia belangeri).

The glucocorticoid (GR) and the mineralocorticoid (MR) receptor mediate corticosteroid actions in the mammalian brain. Here, we report the sequence and distribution of both receptor subtype mRNAs in the central nervous system of the tree shrew Tupaia belangeri, a non-rodent mammal, phylogenetically located between insectivores and primates. The specific glucocorticoid and mineralocorticoid receptor cDNAs were cloned, employing polymerase chain reaction (PCR) based methods. The GR cDNA and MR cDNA encode the 776-amino acid (aa) and 977-aa receptor, respectively. Comparisons of both GR and MR with corresponding cDNA-sequences of other species revealed the highest homology to the human equivalents (GR: 90%, MR: 89% nucleotide sequence identity of the coding regions). The localization of GR and MR mRNA in tree shrew brain was investigated by in situ hybridization using 35S-labeled riboprobes. The GR mRNA is widely distributed throughout all observed brain areas, with high signal intensities in the dentate gyrus, piriform cortex, cerebellum, anterior pituitary, subfornical organ and pineal gland. Whereas, moderate expression of GR mRNA was noted in region CA1 of the hippocampus, region CA3 displayed only low signal intensity. MR mRNA hybridization is mainly restricted to the strongly labeled hippocampal formation, but in contrast to the localization pattern found in rat, higher signal intensities are detected in field CA1 than in CA3. These data indicate that both GR and MR mRNAs are highly expressed in tree shrew brain with a species-specific expression pattern.

Amino Acid Sequence↗
PubMed1998

Acute 17 beta-estradiol treatment down-regulates serotonin 5HT1A receptor mRNA expression in the limbic system of female rats.

In situ hybridization histochemistry was used to investigate acute estrogen effects on serotonin 5HT1A receptor mRNA levels in limbic-related brain areas in the female ovariectomized rat. Acute administration of 17 beta-estradiol (10 micrograms) decreased 5HT1A receptor mRNA expression levels within the medial amygdala (after 2 and 24 h), piriform cortex (after 2 and 24 h), and perirhinal cortex (after 24 h). No changes in 5HT1A mRNA levels were observed in hippocampus or retrosplenial cortex. The findings suggest specific regional effects of estrogen on 5HT functions mediated through regulation of the 5HT1A gene.

Affect↗
PubMed1998

A tachykinin NK1 receptor antagonist, CP-122,721-1, attenuates kainic acid-induced seizure activity.

Substance P (SP) can play an important role in neuronal survival. To analyze the role of SP in excitotoxicity, kainic acid (KA) was administered to rats and in situ hybridization was used to analyze the levels of the SP encoding preprotachykinin-A (PPT-A) mRNA in striatal and hippocampal subregions 1, 4, and 24 h and 7 days after KA. In striatum and piriform cortex, PPT-A mRNA peaked 4 h after KA while in hippocampus, levels peaked after 24 h. KA caused seizures and neuronal toxicity as indicated by a reduction of the number of neurons in the hippocampal CA1 subregion after 7 days. KA was later administered alone or following pretreatment with the tachykinin NK1 receptor antagonist CP-122,721-1 (0.3 mg/kg). The pretreatment decreased seizure activity and a negative correlation was found between seizure activity and survival of CA1 neurons. Conclusively, treatment with CP-122,721-1 has a seizure inhibiting property and may possibly counteract KA-induced nerve cell death in CA1.

Animals↗
PubMed1998

Identification of brain regions that are markedly activated by morphine in tolerant but not in naive rats.

The induction of c-fos mRNA in rat brain due to morphine treatment was analyzed by in situ hybridization. A single dose of up to 100 mg/kg given to naive rats elicited only a weak c-fos expression. However, rats that were repeatedly pretreated with morphine displayed a marked c-fos induction in a few brain areas in response to morphine application. These brain areas essentially comprised the dorsal striatum, the shell of the nucleus accumbens, and some cortical areas. The c-fos signal was transient and not due to a residual withdrawal. Naloxone-precipitated withdrawal led to a more intense c-fos expression which also encompassed a greater range of brain areas. A similar but weaker pattern was observed in case of spontaneous withdrawal. A low morphine dose suppressed the c-fos expression nearly completely and was not sufficient to elicit the morphine-like expression pattern of c-fos. The brain areas which responded strongly to withdrawal included the piriform cortex, septal and hypothalamic nuclei and parts of the thalamus. Taken together, our data indicate that in certain circumscribed brain areas including the dorsal striatum and the shell of the nucleus accumbens, a sensitization towards morphine takes place at the molecular level. These areas responded to morphine with an elevated c-fos expression only when morphine was repeatedly given previously. Sensitization processes are thought to be important for opiate dependence, in particular for the increased craving for the drug. Furthermore, our data indicate that in case of repeated application signs of withdrawal appear after each morphine dose at the molecular level. Repeated events of withdrawal were also implicated in the establishment of a drug dependence state.

Animals↗
PubMed1999

Phase-dependent induction by light of rat Clock gene expression in the suprachiasmatic nucleus.

To clarify the role of Clock in the photic signal transduction of rat circadian clock, we cloned and sequenced rat Clock and examined the effect of a single light pulse on the Clock mRNA expression in the suprachiasmatic nucleus (SCN) by in situ hybridization. Rats were exposed to a 30 min light pulse ( approximately 300 lx) at one of six circadian phases in constant darkness (DD), and sacrificed 60 min after the light on. In the rats without light exposure, the mRNA level in the SCN was high at ZT (Zeitgeber time) 6 and low at ZT 18 and 22. Light exposure increased Clock mRNA level in the SCN in phase dependent manner. The mRNA level was significantly increased during the subjective night (ZT10-22). The light had no effect on the mRNA level during the subjective day (ZT2 and 6). The Clock mRNA was also detected in the piriform cortex (PC), and increased by light at ZT14. These results suggest that Clock transcription in the SCN is involved in the photic signal transduction of circadian clock in rats.

ARNTL Transcription Factors↗
PubMed1999

Expression pattern and in situ localization of the mouse homologue of the human MYOC (GLC1A) gene in adult brain.

The MYOC (GLC1A) gene has recently been associated with both juvenile-onset primary open angle glaucoma (JOAG) and typical late-onset primary open angle glaucoma (POAG). As a result, much scrutiny has been focused on the pathology of these diseases. In order to better understand the pathophysiology of POAG, we have been developing a mouse model of the disease. As a step in this development, we have investigated the expression pattern of Myoc transcripts in embryonic and adult mouse tissue using Northern blot and in situ hybridization analyses. Myoc transcripts were found in high levels in adult eye, heart, brain, skeletal muscle and testis and to a lesser extent in lung and kidney. They were also present, albeit in very low amounts, during mouse embryogenesis. We present new evidence using in situ hybridization analysis that Myoc transcripts were present in widespread regions of the adult brain including the ependymal lining of the third and fourth ventricles, in the choroid plexus, the zonal layer of the junction of the inferior and superior colliculi, the neurons of the habenula, the piriform cortex, the median pre-optic nucleus of the hypothalamus, the olfactory tubercle, and in the inferior olive. In a functional sense, Myoc expression in the ependyma and choroid plexus, two regions of the brain involved in cerebrospinal fluid synthesis and resorption, parallels Myoc expression in the ciliary body and trabecular meshwork of the anterior segment of the eye where aqueous humor synthesis and outflow occur.

Animals↗
PubMed1999

Kainic acid-induced seizure upregulates Na(+)/myo-inositol cotransporter mRNA in rat brain.

A major organic osmolyte, myo-inositol protects cells from perturbing effects of high intracellular concentrations of electrolytes. Myo-inositol is accumulated into cells through Na(+)/myo-inositol cotransporter (SMIT). In order to investigate the regulation of SMIT in generalized seizure, we employed Northern blot analysis and in situ hybridization to study the changes in SMIT mRNA expression in kainic acid-injected rats. Northern blot analysis demonstrated that SMIT mRNA began to increase in the brain 2 h after onset of seizure, and peaked at 12 h. In situ hybridization revealed rapid increase of SMIT mRNA (2 h of seizure) in the CA3 hippocampal pyramidal cells and in the dentate granular cells. Then, at 4-6 h SMIT mRNA expression was observed in the other limbic structure such as amygdala and piriform cortex. Finally, in neocortex and in CA1 pyramidal cells, SMIT mRNA was slowly increased and peaked at 12 h. Microautoradiogram demonstrated that cells expressed SMIT mRNA were mainly neurons. These results suggest that SMIT mRNA is upregulated by kainic acid-induced seizure primarily in structures involved in seizure activity.

Animals↗
PubMed1999

An in situ hybridization study of the distribution of the GABA(B2) protein mRNA in the rat CNS.

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the mammalian central nervous system. GABA exerts its actions through two classes of receptors: GABA(A), multimeric ligand-gated Cl(-) ion channels (a class which has been proposed to include the homomeric variant previously called GABA(C), to be designated GABA(A0r)); and GABA(B), G-protein coupled receptors which regulate Ca(2+) and K(+) channels. Currently, within the GABA(B) receptor family two proteins have been identified through molecular cloning techniques and designated GABA(B1) and GABA(B2). Two N-terminal variants of GABA(B1) were isolated and designated GABA(B1a) and GABA(B1b). The distribution of neurons in the rat CNS expressing the mRNA for the GABA(B1) isoforms have been previously described by in situ hybridization histochemistry. The recent isolation and identification of the GABA(B2) protein by homology cloning has enabled the use of radiolabeled oligonucleotides to detect the distribution of the expression of GABA(B2) mRNA in the rat CNS. The expression of GABA(B2) mRNA was observed to be primarily related to neuronal profiles. The highest levels of GABA(B2) mRNA expression were detected in the piriform cortex, hippocampus, and medial habenula. GABA(B2) mRNA was abundant in all layers of the cerebral cortex, the thalamus and in cerebellar Purkinje cells. Moderate expression was observed in several hypothalamic and brainstem nuclei. In contrast to the distribution of GABA(B1) mRNA, only a weak hybridization signal for GABA(B2) was detected over cells of the basal ganglia, including the caudate-putamen, nucleus accumbens, olfactory tubercle and throughout most of the hypothalamus. Moderate-to-heavy GABA(B2) mRNA expression was also seen over dorsal root and trigeminal ganglion cells. In general, the pattern of GABA(B2) mRNA expression in the rat brain overlaps considerably with the distributions described for both GABA(B1) mRNAs, and is concordant with the distribution described for GABA(B) receptor binding sites. However, differences between GABA(B2) expression levels and GABA(B) binding sites were observed in the basal ganglia.

Animals↗
PubMed2000

Binding of a pure 125I-monoiodoleptin analog to mouse tissues: a developmental study.

The preparation of a pure 125I-labeled monoiododerivative of mouse leptin is described. This radiolabeled analog has been used to characterize and localize central and peripheral leptin binding sites (Ob-R) of the mouse at different stages of its development. The affinity values found in membrane homogenates of various mouse tissues are similar and range between 0.1 and 0.3 nM, indicating that all the Ob-R isoforms have a similar affinity. Leptin binding sites are highly expressed at the membrane level in lung, intestine, kidney, liver, and skin and to a lesser degree in stomach, heart, and spleen. Brain, thymus, and pancreas homogenates are devoid of any specific binding. The distribution of mouse Ob-R has also been explored by autoradiography and dipping techniques on whole mouse sections. In lung, leptin binding sites are located at the pulmonary parenchyma and at the bronchiolar epithelial level. Binding sites are expressed all along the digestive tract from the tongue to the rectum (esophagus, stomach, intestine, colon, and rectum). In muscular visceral structures (stomach, intestine, and bladder) the binding is mainly present in the lamina propria. During development, leptin receptors are early expressed in the liver, kidney, and bone. In the lung, the Ob-R level increased gradually from birth to adulthood where the expression is maximal. By contrast, leptin receptors located in the medulla of the kidney remain remarkably constant all along the development. A broad signal is present in cartilage and bone particularly in vertebrae, limb, and ribs. Interestingly, leptin receptors are barely detectable in the mouse brain except in the choroid plexus and leptomeninges, whereas in the rat brain leptin binding sites are located in the thalamus, the piriform cortex, the cerebellum (at the granular and molecular cell layer), and the pineal gland.

Animals↗