Biomedical subjects

F Stylianopoulou

Publications and source records attributed to F Stylianopoulou.

At least 19 recordsLinked to original sources

PubMed2006

Effects of neonatal handling on the basal forebrain cholinergic system of adult male and female rats.

Neonatal handling is an early experience which results in improved function of the hypothalamic-pituitary-adrenal axis, increased adaptability and coping as a response to stress, as well as better cognitive abilities. In the present study, we investigated the effect of neonatal handling on the basal forebrain cholinergic system, since this system is known to play an important role in cognitive processes. We report that neonatal handling results in increased number of choline-acetyl transferase immunopositive cells in the septum/diagonal band, in both sexes, while no such effect was observed in the other cholinergic nuclei, such as the magnocellular preoptic nucleus and the nucleus basalis of Meynert. In addition, neonatal handling resulted in increased M1 and M2 muscarinic receptor binding sites in the cingulate and piriform cortex of both male and female rats. A handling-induced increase in M1 muscarinic receptor binding sites was also observed in the CA3 and CA4 (fields 3 and 4 of Ammon's horn) areas of the hippocampus. Furthermore, a handling-induced increase in acetylcholinesterase staining was found only in the hippocampus of females. Our results thus show that neonatal handling acts in a sexually dimorphic manner on one of the cholinergic parameters, and has a beneficial effect on BFCS function, which could be related to the more efficient and adaptive stress response and the superior cognitive abilities of handled animals.

Analysis of Variance↗

PubMed2006

Effect of neonatal handling on serotonin 1A sub-type receptors in the rat hippocampus.

Serotonin 1A sub-type receptors play an important role in the etiopathogenesis of depression, which is known to occur more often in females than males. Early experiences can be a predisposing factor for depression; however, the underlying cellular processes remain unknown. In an effort to address such issues, we employed neonatal handling, an experimental model of early experience, which has been previously shown to render females more vulnerable to display enhanced depression-like behavior in response to chronic stress, while it increases the ability of males to cope. In rat pre-pubertal (30 days of age) and adult (90 days) hippocampus, of both males and females, the effect of neonatal handling on serotonin 1A sub-type receptor mRNA and protein levels was determined by in situ hybridization and immunohistochemistry, respectively, while the number of binding sites was determined by in vitro autoradiography using [(3)H]8-hydroxy-2(di-n-propylamino)tetralin as the ligand. Our results revealed a significant sex difference in serotonin 1A sub-type receptor mRNA, protein and binding sites, with females having higher levels than males. Handling resulted in statistically significant decreased numbers of cells positive for serotonin 1A sub-type receptor mRNA or protein, as well as [(3)H]8-hydroxy-2(di-n-propylamino)tetralin binding sites in the area 4 of Ammon's horn and dentate gyrus of both pre-pubertal males and females. In adult animals the number of serotonin 1A sub-type receptor mRNA positive cells was increased as a result of handling in the area 1 of Ammon's horn, area 4 of Ammon's horn and dentate gyrus of males, while it was decreased only in the area 4 of Ammon's horn of females. Furthermore, the number of serotonin sub-type 1A receptor immunopositive cells, as well as [(3)H]8-hydroxy-2(di-n-propylamino)tetralin binding sites was increased in the area 1 of Ammon's horn, area 4 of Ammon's horn and dentate gyrus of handled males, whereas it was decreased in these same brain areas in the handled females. We can thus infer that neonatal handling results in alterations in postsynaptic serotonergic neurotransmission, which may contribute to the sex dimorphic effects of handling as to the vulnerability toward depression-like behavior in response to chronic stressful stimuli.

Age Factors↗

PubMed2005

Sexually dimorphic effects of the Lhx7 null mutation on forebrain cholinergic function.

It has been reported recently that mice lacking both alleles of the LIM-homeobox gene Lhx7, display dramatically reduced number of forebrain cholinergic neurons. In the present study, we investigated whether the Lhx7 mutation affects male and female mice differently, given the fact that gender differences are consistently observed in forebrain cholinergic function. Our results show that in adult male as well as female Lhx7 homozygous mutants there is a dramatic loss of choline acetyltransferase immunoreactive forebrain neurons, both projection and interneurons. The reduction of forebrain choline acetyltransferase immunoreactive neurons in Lhx7 homozygous mutants is accompanied by a decrease of acetylcholinesterase histochemical staining in all forebrain cholinergic neuron target areas of both male and female homozygous mutants. Furthermore, there was an increase of M1-, but not M2-, muscarinic acetylcholine receptor binding site density in the somatosensory cortex and basal ganglia of only the female homozygous mutant mice. Such an increase can be regarded as a mechanism acting to compensate for the dramatically reduced cholinergic input, raising the possibility that the forebrain cholinergic system in female mice may be more plastic and responsive to situations of limited neurotransmitter availability. Finally, our study provides additional data for the sexual dimorphism of the forebrain cholinergic system, as female mice appear to have a lower density of M1-muscarinic acetylcholine receptors in the striatal areas of the basal ganglia and a higher density of M2-muscarinic acetylcholine receptors, in a number of cortical areas, as well as the striatal areas of the basal ganglia.

Animals↗

PubMed2003

Control of neuronal nitric oxide synthase and brain-derived neurotrophic factor levels by GABA-A receptors in the developing rat cortex.

Gamma-aminobutyric acid (GABA) plays an important morphogenetic role, acting through GABA-A receptors, which are depolarizing in the developing rat brain. Other molecules with major morphogenetic roles are the nitric oxide free radical (NO(.)) and brain-derived neurotrophic factor (BDNF), both of which are involved in the control of synaptic plasticity and apoptosis. In the present work, we investigated the effect of GABA-A receptor activation on neuronal NO(.) synthase (nNOS) and BDNF immunoreactivity in the developing cortex of 5-day-old rats. We also determined the effect of GABA-A receptor activation on phosphorylated cAMP-response element binding protein (pCREB) immunoreactivity in an effort to elucidate the molecular mechanisms involved. Our results show that activation of GABA-A receptors leads to increased numbers of nNOS, BDNF and pCREB, as well as nNOS-pCREB and BDNF-pCREB doubly immunopositive cells. This effect is abolished when L-type Ca(2+) channels are blocked. These results indicate that the following mechanism could be operating: depolarization following GABA-A receptor activation leads to opening of L-type voltage-gated calcium channels, resulting in an increased Ca(2+) influx, which in turn leads to phosphorylation and, thus, activation, of the transcription factor CREB; the phosphorylated CREB can then induce BDNF, as well as nNOS.

Animals↗

PubMed2002

Sex differences in the effects of neonatal handling on the animal's response to stress and the vulnerability for depressive behaviour.

Neonatal handling is known to affect the programming of the hypothalamic-pituitary-adrenal axis and, as a result, the ability of the organism to respond to stress. We determined the effect of neonatal handling on the animal's response in three animal models of depression, as well as to either (a) acute or (b) chronic forced swimming stress. Neonatal handling resulted in a significant increase in the immobility time in the Porsolt forced swimming test in both sexes, and in the 8-hydroxy-2-(di-n-propylamino) tetralin-induced hypothermia in the males. On the other hand, handling had sex-dependent effects when animals were exposed to a chronic stressor. After exposure to chronic restraint stress, statistically more handled than non-handled females failed to adapt, while no such difference was found in the males. In the chronic forced swimming stress, handled males had shorter immobility times, and higher plasma corticosterone levels, while the opposite held true in the females. Furthermore, neonatal handling significantly decreased basal plasma corticosterone levels in both pre- and post-pubertal animals. Thus, the early experience of handling provides males with a greater capacity to actively face chronic stressors, while in the females it increases their susceptibility to express 'depressive' behaviour since they are unable to cope and adopt a 'passive, despaired' behaviour.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2002

Effects of neonatal handling on basal and stress-induced monoamine levels in the male and female rat brain.

Neonatal handling has pervasive effects on the rat brain leading to increased ability to cope with and adapt to stressful stimuli. We determined the effects of neonatal handling on the dopaminergic and serotonergic system, in the male and female rat brain, under basal conditions before and after puberty and after short- and long-term forced swimming stress. Exposure of animals to neonatal handling resulted in sex-dependent changes in the concentration and turnover of monoamines in the different brain areas. In the prepubertal brain, the effect of neonatal handling was manifested as an increase in dopamine turnover in the females, particularly in the hypothalamus, an increase in serotonin levels and a decrease in its turnover in all three brain regions examined of both males and females. Certain of the handling-induced effects observed in the prepubertal brain were reversed in the postpubertal animals. Thus, in the postpubertal brain, the handling-induced changes in serotonin levels and its turnover observed in both sexes before puberty were abolished. On the other hand, the handling-induced increase in hypothalamic dopamine turnover was maintained. After exposure to short-term stress, the effect of handling was manifested on one hand as decreased striatal dopamine levels in the females, and decreased dopamine turnover in the hypothalamus of both males and females, and on the other, as increased serotonin levels in the hypothalamus. After exposure to long-term stress, handled females had decreased dopamine turnover in the hypothalamus and the striatum, but there was no effect of handling on the serotonergic system. Our results provide some neurobiological evidence supporting the determinant role of the mother-infant relationship in the development of psychopathology. Neonatal handling, which modifies normal mother-pup interactions, results in alterations in brain dopaminergic and serotonergic systems, both of which are involved in the etiopathogenesis of major psychoses. Exposure to either short- or long-term stress in adult life results in sex-dependent changes in brain monoamines, which are affected by handling thus making coping more efficient and rendering the stressful stimulus less noxious.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2001

In utero radiation-induced apoptosis and p53 gene expression in the developing rat brain.

PURPOSE: This study addressed the question of the role of the p53 gene in prenatal low-dose radiation-induced apoptosis in the neuroepithelium, in an effort to elucidate molecular mechanisms involved in the extreme radiosensitivity of the developing brain. MATERIALS AND METHODS: Pregnant Wistar rats were exposed to a single dose of 10, 20 or 40 cGy of X-rays on day 15 or 17 of gestation. Animals were sacrificed 4 or 24h after exposure. Apoptosis was studied by gel electrophoresis of isolated DNA and in situ by the TUNEL reaction. Expression of the p53 gene was studied by immunocytochemistry and Western analysis, as well as Northern analysis, for the detection of the protein and mRNA respectively. RESULTS: In utero low-dose irradiation led to apoptosis and an increase of p53 gene expression in the developing rat brain. Apoptotic as well as p53 immunopositive cells were detected among proliferating, migratory and post-mitotic neurones in the developing neuroepithelium following prenatal irradiation, even after only l0 cGy. In addition to the p53 protein, p53 mRNA brain levels were also increased following prenatal irradiation. CONCLUSIONS: Low-dose prenatal irradiation of the developing brain led to p53 induction and cell death by apoptosis.

Animals↗

PubMed2001

In utero radiation-induced changes in growth factor levels in the developing rat brain.

PURPOSE: To investigate the role of growth factors in the compensatory response to radiation injury during development of the brain. Levels of gene expression in the embryonic rat brain were assessed for IGF-I, IGF-II, BDNF and NT-3. MATERIALS AND METHODS: Pregnant Wistar rats were exposed to a single dose of 10, 20 or 40 cGy X-rays on day 15 or 17 of gestation. Animals were sacrificed 4 or 24 h after exposure. IGF-I, BDNF and NT-3 proteins were detected by immunocytochemistry, while IGF-I and IGF-II mRNA by in situ hybridization, and Northern analysis respectively. RESULTS: In utero low dose X-irradiation led to a decrease in IGF-I gene expression and a compensatory increase in the expression of IGF-II, BDNF and NT-3 in the developing rat brain. IGF-I, BDNF and NT-3 immunopositive cells were detected among proliferating, migratory and post-mitotic neurones in the developing neuroepithelium. CONCLUSIONS: Low dose prenatal irradiation of the developing brain results in down-regulation of IGF-I, which could lead to cell death by apoptosis. On the other hand, IGF-II, BDNF and NT-3 gene expression is increased following irradiation, possibly as a compensatory mechanism.

Animals↗

PubMed2001

Protooncogene c-fos Involvement in the Molecular Mechanism of Rat Brain Sexual Differentiation.

Brain sexual differentiation is mediated through testosterone, which acts during the perinatal period in the form of both 5alpha-dihydrotestosterone and estradiol. In order to gain insight into the molecular mechanisms involved, we studied induction of c-fos, an index of functional neuronal activation, in the 2-day-old female rat brain after injection of a masculinizing dose of testosterone. Administration of testosterone resulted in induction of c-fos gene expression in the hypothalamus, as determined by Northern analysis. Following immunocytochemistry, we demonstrated an increase in the number of Fos-positive nuclei in the median and medial preoptic nucleus, the medial preoptic area extending to the lateral preoptic area, and the peri- and paraventricular area. In an effort to see whether testosterone acted as 5alpha-dihydrotestosterone or as estradiol, we injected either steroid and looked at fos induction. Estradiol mimicked the effect of testosterone, while 5alpha-dihydrotestosterone was without effect. Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors. Electrophoretic mobility shift assays showed that nuclear extracts from 2-day-old female hypothalamus contain a protein, most probably the estrogen receptor, which binds specifically to oligodeoxynucleotides with the sequence of either vitERE, the consensus estrogen-responsive element (ERE) found in the vittelogenin gene, or fosERE, the ERE found in the 3'-untranslated region of the mouse c-fos gene. This suggests that the effect of testosterone-derived estradiol on c-fos expression is a direct one, mediated by binding of estrogen receptors to an ERE in the c-fos gene-regulatory regions.

Animals↗

PubMed2000

NMDA receptor mediated changes in IGF-II gene expression in the rat brain after injury and the possible role of nitric oxide.

This study was undertaken in order to investigate the role of insulin-like growth factor (IGF)-II, c-fos, N-methyl-D-aspartate (NMDA) receptors, and nNOS in the cellular processes following a penetrating brain injury. IGF-II mRNA levels, as determined by Northern analysis, were decreased at 4, 8, and 24 h after brain injury, in the lesioned, compared to the contralateral intact hemisphere. Forty-eight and 72 h after the injury, there was no difference between the lesioned and the contralateral intact hemisphere in IGF-II mRNA levels. c-fos mRNA levels followed a parallel, but opposite course: They were increased at 4, 8 and 24 h after the injury, while at 48 and 72 h c-fos mRNA levels in the lesioned hemisphere did not differ from those in the intact. Administration of MK-801 reversed the injury-induced decrease in IGF-II mRNA levels. Administration of MK-801 resulted in an increase in IGF-II mRNA in both the intact and the lesioned hemispheres. Brain injury resulted in an increase in nNOS immunopositive cells in the hippocampal formation, which was detectable at 4 and 12, but not 48 h after the injury. These results suggest that IGF-II, c-fos, NMDA receptors and nNOS are involved in the cellular responses to brain injury.

Animals↗

PubMed1999

p53 expression and regulation by NMDA receptors in the developing rat brain.

The p53 tumor suppressor gene, which is considered the guardian of the genome, encodes a phosphoprotein, which is a sequence-specific transcriptional activator or repressor of target genes. The role of p53 in developmental processes has not been studied extensively, although its expression appears to undergo temporal and spatial changes during prenatal and postnatal development. In the present study, we assessed the levels of p53 mRNA and protein in the developing rat brain and its relation to developmental cell death. Furthermore, we investigated the potential role of n-methyl-d-aspartate (NMDA) receptors in regulating p53 expression, since these receptors are involved in the control of cell death. We found that p53 mRNA and protein were detectable in the rat brain throughout perinatal development. In embryos, p53 immunoreactivity was mainly localized in the nuclei of neuroepithelial cells, with a maximum in staining at embryonic day (E)12. In the neuroepithelium, we also found significant numbers of TdT-mediated dUTP nick end labeling (TUNEL)-positive cells, both in dividing periventricular cells and in migrating neurons. In neonates, immediately after birth there was a reduction in the number of apoptotic cells, which then increased to reach a maximum at postnatal day (P)5. Postnatally, apoptotic as well as p53-positive cells were detected in most brain areas. P53 immunoreactivity was also highest on P5. In most cells, p53 immunoreactivity and the TUNEL signal colocalized. P53 immunoreactivity as well as the number of TUNEL- positive cells were dramatically decreased in the brains of newborns treated with MK-801, an NMDA receptor antagonist. Our results show that p53 is involved in the control of developmental cell death, and that NMDA receptors play a regulatory role in the expression of the p53 gene, and thus in apoptosis occurring in the developing rat brain.

Animals↗

PubMed1999

Neurotransmitter modulation of glucocorticoid receptor mRNA levels in the rat hippocampus.

Glucocorticoids in the hippocampus mediate adaptive responses elicited by stressful stimuli. In this study we investigated glucocorticoid receptor gene expression in the rat hippocampus following acute stress. A significant decrease in glucocorticoid receptor mRNA levels was observed in the hippocampus less than 1 h after the onset of stress. This decrease was inhibited by administering either MK-801, diazepam or propranolol prior to exposure to stress. The effect of diazepam on the stress-induced decrease in hippocampal glucocorticoid receptor mRNA was reversed by Ro-15-1788, suggesting that it is mediated by central benzodiazepine receptors, i.e. GABA-A. These results indicate that NMDA, GABA-A and beta-adrenergic receptors are involved in the mechanism of the stress-induced decrease in glucocorticoid receptor mRNA levels in the rat hippocampus.

Adrenergic beta-Antagonists↗

PubMed1998

Immunocytochemical localization of glycogen phosphorylase kinase in rat brain sections and in glial and neuronal primary cultures.

The physiological function of brain glycogen and the role of phosphorylase kinase as a regulatory enzyme in the cascade of reactions associated with glycogenolysis in the brain have not been fully elucidated. As a first step toward elucidating such a function, we studied the localization of phosphorylase kinase in glial and neuronal primary cell cultures, and in adult rat brain slices, using a rabbit polyclonal antibody against skeletal muscle glycogen phosphorylase kinase. Immunocytochemical examination of rat astroglia-rich primary cultures revealed that a large number of cells were positive for glycogen phosphorylase kinase immunoreactivity. These cells were also positive for vimentin, a marker for immature glia, while they were negative for glial fibrillary acidic protein, a marker for mature astroglia, and for galactocerebroside, an oligodendroglial marker. Neurons in rat neuron-rich primary cultures did not show any kinase-positive staining. In paraformaldehyde-fixed adult rat brain sections, phosphorylase kinase immunoreactivity was detected in glial-like cells throughout the brain, with relatively high staining found in the cerebral cortex, the cerebellum, and the medulla oblongata. Phosphorylase kinase immunoreactivity could not be detected in neurons, with the exception of a group of large neurons in the brain stem, most likely belonging to the mesencephalic trigeminal nucleus. Phosphorylase kinase was also localized in the choroid plexus and to a lesser degree in the ependymal cells lining the ventricles. Phosphorylase kinase thus appears to have the same cellular distribution in nervous tissue as its substrates, i.e. glycogen phosphorylase and glycogen, which suggests that the physiological role of brain phosphorylase kinase is the mobilization of glycogen stores to fuel the increased metabolic demands of neurons and astrocytes.

Animals↗

PubMed1998

Beta-adrenergic receptors mediate a stress-induced decrease in IGF-II mRNA in the rat cerebellum.

1. Exposure to a combined forced swimming-confinement stress resulted in a decrease in insulin-like growth factor II (IGF-II) mRNA levels in the whole brain (without the cerebellum) and in the isolated brain areas of the cerebral cortex, the hippocampus, and the cerebellum. 2. In an effort to elucidate the neurotransmitter systems involved in this stress-induced decrease, animals were injected prior to exposure to the stress, with either propranolol, diazepam, or MK-801. 3. Administration of diazepam or MK-801 did not affect the stress-induced decrease in IGF-II mRNA in any of the three brain areas examined. 4. Administration of propranolol prior to the exposure to the stress inhibited the stress-induced decrease in IGF-II mRNA in the cerebellum. Propranolol had no such effect in the cerebral cortex or the hippocampus. 5. Our results suggest that in the cerebellum, the stress-induced decrease in IGF-II mRNA is mediated by beta 2-adrenergic receptors.

Adrenal Cortex Hormones↗

PubMed1997

At least three neurotransmitter systems mediate a stress-induced increase in c-fos mRNA in different rat brain areas.

1. Protooncogene c-fos mRNA levels were determined in the rat cerebral cortex, hippocampus, and cerebellum after exposure to a combined forced swimming and confinement stress. The stress resulted in an increase in c-fos mRNA levels in all three brain areas. 2. In an effort to elucidate the neurotransmitter systems involved in this stress-induced increase, animals were injected, prior to exposure to the stress, with either diazepam, MK-801, or propranolol. 3. In both the cerebral cortex and the hippocampus the stress-induced increase in c-fos mRNA was inhibited by MK-801, suggesting that it is mediated via NMDA receptors. In the hippocampus, propranolol had a similar effect, indicating that beta-adrenergic receptors are also involved in the stress-induced increase in c-fos mRNA. 4. On the other hand, the increase in c-fos mRNA produced by the stress of the injection was inhibited in the cerebral cortex by diazepam or propranolol and in the hippocampus only by diazepam. Furthermore, administration of MK-801 resulted in an increase in c-fos mRNA in the hippocampus of the nonstressed animals. In the cerebellum no one of the three drugs employed affected c-fos mRNA levels in either stressed or nonstressed animals. 5. Our results thus show that various forms of stress activate, in different brain areas, neurons with either NMDA, beta-adrenergic, and/or GABA-A receptors.

Animals↗

PubMed1997

Glucocorticoid receptor gene expression during rat embryogenesis. An in situ hybridization study.

Glucocorticoids play an important role in embryonic development. The existence of sufficient amounts of their receptors during rodent embryogenesis has proved to be an absolute necessity for the physiological growth of the animal. We have analyzed the pattern of glucocorticoid receptor gene expression in the rat embryo through embryonic days 12 to 17, by using in situ hybridization histochemistry. Glucocorticoid receptor mRNA is present in the rat liver on embryonic day (E) 12, and by E13 the signal can also be detected in several other tissues, such as the lung, the heart, the mesonephros, the sclerotomes, the thymus and Rathke's pouch. Glucocorticoid receptor gene expression was quite ubiquitous in tissue derivatives of all three germ layers and appeared to vary in intensity within the same tissue during embryogenesis. These variations in the level of receptor gene expression paralleled the developmental stage of each tissue: Intense labelling was detected just prior to the final differentiation step of a structure. Upon differentiation, cell populations highly expressing glucocorticoid receptor gene in the previous stage were found to have reduced amounts of the receptor mRNA. Our results support a morphogenetic role for glucocorticoids during embryogenesis.

Animals↗

PubMed1996

Glucocorticoid receptor gene expression in the embryonic rat brain.

The early ontogenetic pattern of glucocorticoid receptor (GR) gene expression was studied in the rat brain through embryonic days (E) 12 to 17. Using a [35S]-labelled GR antisense RNA probe for in situ hybridization, we first detected GR mRNA in E13 embryos. The strongest signal was in Rathke's pouch, but the hypothalamic, and to a lesser degree the pontine and rhinencephalic neuroepithelium were also moderately labelled. Significant levels of GR mRNA were also detected in the choroid plexus and the epithelia lining the ventricles on E13. Receptor gene expression was further extended by E15 to the neuroepithelium and the differentiating field of several neuronal structure primordia, including the basal ganglia, rhinencephalon, hippocampus, pons and cerebellum. On E17, GR gene expression was in addition detected in the amygdala, subiculum and olfactory bulb and cortex. The integrity of the mRNA transcripts revealed by in situ hybridization was assessed by Northern blot analysis of total RNA from embryonic brain and pituitary. A major approximately 7-kb transcript was detected throughout embryonic development. An adult-like GR protein was shown by immunoblotting analysis to be expressed in brain and pituitary extracts already by E13. Based on our results, we postulate a receptor-mediated regulatory role for glucocorticoids in the embryonic development of the rat brain.

Animals↗

PubMed1995

Glucocorticoid regulation of glycerolphosphate dehydrogenase expression in the developing rat brain.

Glucocorticoid regulation of glycerolphosphate dehydrogenase (GPDH) activity and gene expression in the developing rat brain appears complex throughout the postnatal developmental period and attains the adult pattern after the first month of life. GPDH enzyme activity is higher in the limbic system than in the cerebral cortex of intact young animals. Adrenalectomy of young rats, before the first month of life, does not affect GPDH enzyme activity in the brain areas mentioned above, while in the adult animals it results in a statistically significant decrease in activity. Furthermore, "adult type" glucocorticoid responsivity of GPDH enzyme activity is attained in the developing limbic system earlier--by day 40 of life--than in the cerebral cortex. During the first month of life, GPDH basal mRNA levels are increased in the absence of glucocorticoids, in both the limbic system and the cortex, in contrast to the effect of adrenalectomy in the adults, where GPDH mRNA levels are decreased in the absence of the adrenals. The observed pattern of glucocorticoid regulation of GPDH during development in the rat is discussed in relation to the possible existence of various levels of regulation of GPDH gene and enzyme activity.

Animals↗