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PubMed2002

Lack of cell loss following recurrent neonatal seizures.

In the neonatal rat recurrent seizures have been associated with long-term changes in cerebral excitability and cognition. Whether recurrent seizures in the neonatal rat lead to cell loss in the cerebral cortex is not known. We counted cells in the parietal cortex, piriform cortex, and CA3 and CA1 hippocampal subfields in young adult rats that had undergone a series of 55 seizures during the first 12 days of life. There were no differences in cell counts between the controls and rats subjected to neonatal seizures. Like the hippocampus, the neonatal pririform and parietal cortex is resistant to seizure-induced cell loss.

Animals↗
PubMed2003

The effects of dentate granule cell destruction on behavioral activity and Fos protein expression induced by systemic MDMA in rats.

In this study, we examined the effect of the s.c. administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA) or saline on locomotor activity and Fos expression following the bilateral destruction of hippocampal dentate granule cells by colchicine in rats. The lesioned animals, when administered s.c. saline, showed a significantly greater increase in locomotor activity compared to the intact animals, and revealed a marginally significant level of increased locomotor activity compared to the sham-lesioned animals. In addition, when the lesioned animals were given s.c. saline or MDMA, there was a significant increase in Fos expression in the nucleus accumbens core, but not in the medial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, piriform cortex, dorsal striatum, or nucleus accumbens shell, compared to the intact and sham-lesioned animals. Overall, these results suggest that the nucleus accumbens core may be involved in the enhancement of locomotor activity induced by the injection of saline alone (stress loading) or MDMA following bilateral destruction of hippocampal dentate granule cells by colchicine.

Animals↗
PubMed2000

Regional expression of a gene encoding a neuron-specific Na(+)-dependent inorganic phosphate cotransporter (DNPI) in the rat forebrain.

We have analyzed expression of a gene encoding a brain-specific Na(+)-dependent inorganic phosphate cotransporter (DNPI), which was recently cloned from human brain, in rat forebrain using in situ hybridization. The expression of DNPI mRNA showed a widespread but highly heterogeneous pattern of distribution in the forebrain, where hybridization signals were observed in neurons but not in any other types of cells. Neurons expressing the mRNA were far more numerous in the diencephalon than in the telencephalon. In the thalamus, a number of neurons with high levels of signals were localized to all nuclei of the dorsal thalamus, habenular nuclei and subthalamic nucleus, but not the reticular nucleus and zona incerta. Moderate signal levels were seen in many neurons throughout the hypothalamus, particularly the ventromedial, paraventricular, supraoptic and arcuate nuclei, lateral hypothalamic area and mammillary complex. In contrast, expression of DNPI mRNA in the telencephalon was generally at a low level and occurred locally in some restricted regions within the neocortex, retrosplenial cortex, piriform cortex, olfactory regions, hippocampal formation and medial amygdaloid nucleus. The present results suggest that DNPI functions in heterogeneous neuron populations as a neuron-specific Na(+)-dependent inorganic phosphate cotransport system predominantly expressed in the diencephalon of the rat.

Animals↗
PubMed1999

The flinders sensitive line rats, a genetic model of depression, show abnormal serotonin receptor mRNA expression in the brain that is reversed by 17beta-estradiol.

The possible link between estrogen and serotonin (5-HT) in depression was investigated using a genetic animal model of depression, the Flinders Sensitive Line (FSL) rats, in comparison to control Flinders Resistant Line rats. The mRNA levels of the estrogen receptor (ER) alpha and beta subtypes and the 5-HT(1A) and 5-HT(2A) receptors were analyzed in several limbic-related areas of ovariectomized FSL and FRL rats treated with 17beta-estradiol (0.15 microg/g) or vehicle. The FSL animals were shown to express significantly lower levels of the 5-HT(2A) receptor transcripts in the perirhinal cortex, piriform cortex, and medial anterodorsal amygdala and higher levels in the CA 2-3 region of the hippocampus. The only significant difference between the rat lines in ER mRNA expression was found in the medial posterodorsal amygdala, where the FSL rats showed lower ERalpha expression levels. Overall, estradiol treatment increased 5-HT(2A) and decreased 5-HT(1A) receptor mRNA levels in several of the examined regions of both lines. Thus, in many areas, estradiol was found to regulate the 5-HT receptor mRNA expression in the opposite direction to the alterations found in the FSL rats. These findings further support the implication of 5-HT receptors, in particular the 5-HT(2A) subtype, in the etiology of affective disorders. Moreover, the ability of estradiol to regulate the expression of the 5-HT(1A) and 5-HT(2A) receptor genes might account for the reported influence of gonadal hormones in mood and depression.

Animals↗
PubMed2003

Immunocytochemical evidence that amyloid beta (1-42) impairs endogenous antioxidant systems in vivo.

Amyloid beta, the major constituent of the senile plaques in the brains of patients with Alzheimer's disease, is cytotoxic to neurons and has a central role in the pathogenesis of the disease. We have previously demonstrated that potent antioxidants idebenone and alpha-tocopherol prevent learning and memory impairment in rats which received a continuous intracerebroventricular infusion of amyloid beta, suggesting a role for oxidative stress in amyloid beta-induced learning and memory impairment. To test the hypothesis, in the present study, we investigated alterations in the immunoreactivity of endogenous antioxidant systems such as mitochondrial Mn-superoxide dismutase, glutathione, glutathione peroxidase and glutathione-S-transferase following the continuous intracerebroventricular infusion of amyloid beta for 2 weeks. The infusion of amyloid beta (1-42) resulted in a significant reduction of the immunoreactivity of these antioxidant substances in such brain areas as the hippocampus, parietal cortex, piriform cortex, substantia nigra and thalamus although the same treatment with amyloid beta (40-1) had little effect. The alterations induced by amyloid beta (1-42) were not uniform, but rather specific for each immunoreactive substance in a brain region-dependent manner. These results demonstrate a cytological effect of oxidative stress induced by amyloid beta (1-42) infusion. Furthermore, our findings may indicate a heterogeneous susceptibility to the oxidative stress produced by amyloid beta.

Amyloid beta-Peptides↗
PubMed2003

Distribution of the rhythm-related genes rPERIOD1, rPERIOD2, and rCLOCK, in the rat brain.

High densities of mRNAs for three rhythm-related genes, rPeriod1 (rPer1), rPer2, and rClock, which share high homology in Drosophila and mice, were found in the hypothalamic suprachiasmatic nucleus (SCN). The SCN, however, is not the only brain region that expresses these genes. To understand the distributions and possible physiological roles of these rhythm-related genes, we examined the gene expressions of rPer1, rPer2, and rClock in different brain regions by serial coronal, sagittal, and horizontal brain sections in Sprague-Dawley male rats. Animals were housed in a light-controlled room (lights on from 0600 to 1800 h) and killed at 1000 or 1200 h, which corresponds to Zeitgeber time 4 or 6. Semi-quantitative in situ hybridization with (35)S-riboprobes was used to evaluate mRNA levels. The mRNAs of rPer1, rPer2, and rClock were widely distributed in the rat CNS, including the olfactory bulb, cortex, piriform cortex, SCN, ventromedial hypothalamus, arcuate nucleus, hippocampus, mammillary nucleus, pontine nucleus, superior and inferior colliculus, cerebellum, median eminence/pars tuberalis, pineal gland, and pituitary. The expression patterns of mRNAs for rPer1 and rPer2 were almost identical. In contrast, different expression patterns were observed between rClock and rPer1 or rPer2 in several brain regions, including the hypothalamic supraoptic and suprachiasmatic nuclei, the paraventricular zone of the caudate putamen, the superior olivary nucleus, and anterior and intermediate lobes of the pituitary. These findings suggest that the different expression patterns observed for rPer1, rPer2, and rClock might be due to their different physiological role(s) in those brain regions.

Animals↗
PubMed1999

Distinct regional distribution in the brain of messenger RNAs for the two isoforms of synaphin associated with the docking/fusion complex.

Synaphin is a 19,000 mol. wt cytosolic protein we first found to co-purify with the docking/fusion complex crucial to neurotransmitter release from presynaptic terminals. Two isoforms of synaphin (synaphins 1 and 2) (also called complexins II and I, respectively) exist in the rat brain. On density gradient centrifugation of a Triton X-100 extract of brain membranes, synaphin was found to be associated with the 7S complex that contains synaptotagmin, syntaxin, synaptosomal-associated protein of 25,000 mol. wt and vesicle-associated membrane protein. A smaller complex devoid of synaphins was also identified by immunoprecipitation with a monoclonal antibody against synaptosomal-associated protein of 25,000 mol. wt. Messenger RNAs for synaphins 1 and 2 were expressed predominantly in the brain. In situ hybridization using probes specific to synaphins 1 and 2 indicated that the distribution of their mRNAs was significantly different in brain regions such as olfactory bulb, hippocampus, cerebral cortex, piriform cortex, cerebellum, thalamus and facial nuclei. These results show synaphin as a component of the 7S complex and suggest different physiological implications for the two isoforms.

Adaptor Proteins, Vesicular Transport↗
PubMed1997

Distribution and time course of appearance of "dark" neurons and EEG activity after amygdaloid kainate lesion.

To determine the extent and time course of local and distant neuronal damage produced by microiontophoretic administration of kainic acid (KA) into the central amygdaloid nucleus, distribution of neuronal damage was compared in various brain areas after different survival times. For demonstration of damaged, so-called "dark" neurons, a newly developed silver stain was employed. In addition, silver staining method was used to visualize microglia cells. In a separate experiment, electroencephalographic (EEG) activity was recorded from the amygdaloid body, hippocampus, and the frontal cortex before and after microiontophoretic KA lesion of the central amygdaloid nucleus. It was observed that (1) even a minute amount of KA into this nucleus caused transient neuronal damage in distant brain areas; (2) the hippocampal formation, subiculum, entorhinal cortex, piriform cortex, and lateral septum were consistently affected; (3) the extent and time course of neuronal damage and appearance of microglia cells varied from area to area; (4) the KA neurotoxicity in distant brain areas appeared to depend on specific excitatory circuits, especially in the hippocampal formation; (5) the appearance and time course of pathologic EEG activity paralleled the appearance of dark neurons; and (6) the absence of pathologic EEG activity and the lack of massive neuronal loss or microglia proliferation in distant brain areas of rats surviving longer than 48 h suggested that these areas may have recovered both morphologically and functionally. Although details of cellular mechanism responsible for development of "dark" degeneration of neurons are not known, the silver method employed in the present study proved to be sensitive, useful tool for fine histological analyses of early and distant consequences of excitotoxic lesions.

Amygdala↗
PubMed1998

Central 5-HT3 receptors in P and in AA alcohol-preferring rats: An autoradiographic study.

Considerable evidence exists for an involvement of serotonergic mechanisms in the control of alcohol consumption. In the present study, an extensive 5-hydroxytryptamine (5-HT3) receptor autoradiographical investigation was performed using two genetically selected rat strains, alcohol preferring (P) and Alko alcohol (AA) alcohol-preferring rats, as well as the corresponding alcohol nonpreferring (NP) and Alko nonalcohol (ANA) alcohol-nonpreferring rats. The aim was to determine if there are any differences in 5-HT3 binding levels that may illuminate mechanisms of alcohol preference in these animals. For quantitating 5-HT3 binding sites, [3H]S(-)zacopride (0.5 nM) was used. Non-specific binding was measured in the presence of granisetron 10(-6) M. The [3H]S(-)zacopride binding density was measured in two subregions of the amygdaloid nucleus, frontal cortex, piriform cortex, cingulate laminae, parietal anterior cortex, parietal medial cortex, hippocampus CA1, hippocampus CA3, and entorhinal cortex. In all the brain areas investigated, the results showed no differences between AA and ANA rats. In P rats, compared to NP controls, there was a 30% lower 5-HT3 binding level in the lateral nucleus and the posteromedial cortical nucleus of the amygdala. These findings suggest that the expression of high alcohol preference in genetically selected P and AA rats is not associated with a general alteration of central 5-HT3 receptors, although a lower 5-HT3 receptor level in the amygdala of P rats may contribute to the phenotype of this strain of animals.

Alcohol Drinking↗
PubMed2000

Expression and regulation of a gene encoding neural recognition molecule NB-3 of the contactin/F3 subgroup in mouse brain.

NB-3 is a neural recognition molecule which is a member of contactin/F3 subgroup in the immunoglobulin superfamily. We report here the developmental expression pattern and localization of NB-3 mRNA in mouse brain, determination of the NB-3 gene organization and identification of the promoter region. We also describe a splicing isoform of mouse NB-3. Mouse NB-3 exhibited 96% identity with rat NB-3 at the amino acid sequence level. The splicing isoform lacked the amino acid residues between 62 and 78 of the original NB-3, which constituted a part of the first immunoglobulin-like domain. The expression of NB-3 mRNA was evident after birth, reaching a maximum at the postnatal seventh day, and declined thereafter in the cerebrum, whereas the mRNA increased in the cerebellum to adulthood. In situ hybridization demonstrated that NB-3 mRNA was preferentially expressed in the accessory olfactory bulb, layers II/III and V of the cerebral cortex, piriform cortex, anterior thalamic nuclei, locus coeruleus of the pons and mesencephalic trigeminal nucleus, and in Purkinje cells of the cerebellum. The mouse NB-3 gene consisted of 23 exons spanning more than 130kb. The overall organization of the gene was similar to those of the F11, axonin-1 and TAX-1 genes of the subgroup. By reporter gene analysis with the 5'-flanking region of the gene, we found a basal promoter activity in the 1.2kb fragment upstream of the putative transcription initiation site. This study provides a basis for elucidating the biological significance of the contactin/F3 subgroup molecules.

Alternative Splicing↗
PubMed2002

Hydroethidine detection of superoxide production during the lithium-pilocarpine model of status epilepticus.

Hydroethidine is reported to be selectively oxidized to ethidium by superoxide. Using digital imaging and fluorescence microscopy it is possible to evaluate neuronal ethidium accumulation in specific brain regions of rats damaged in the lithium-pilocarpine model of status epilepticus. Intravenous or intraperitoneal administration of hydroethidine prior to 1 h of status epilepticus produced diffuse cytosolic distribution of ethidium fluorescence suggesting an increased neuronal production of superoxide that was not observed in control animals. A significantly increased number of neurons with the enhanced ethidium fluorescence was observed in parietal cortex, piriform cortex, perirhinal cortex, lateral amygdala, mediodorsal thalamus and laterodorsal thalamus, suggesting superoxide as a mechanism of neuronal injury in those regions. Other regions injured by lithium-pilocarpine seizures, such as the basolateral amygdala and hippocampus, did not demonstrate the enhanced neuronal ethidium fluorescence. In such regions it is possible that superoxide is not a mechanism of injury or that 1 h of status epilepticus is not sufficient to produce superoxide or other reactive oxygen species.

Animals↗
PubMed1998

Functional anatomy of limbic epilepsy: a proposal for central synchronization of a diffusely hyperexcitable network.

The limbic/mesial temporal lobe epilepsy syndrome has been defined as a focal epilepsy, with the implication that there is a well defined focus of onset, traditionally centered around the hippocampus. The pathology of the hippocampus in this syndrome has been well described and a number of physiological abnormalities have been defined in this structure in animal models and humans with epilepsy. However, anatomical and physiological abnormalities have also been described in other limbic sites in this form of epilepsy. Previous studies have shown broadly synchronized or multifocal seizure onset within the limbic system of the animal models and human patients. We hypothesized that the epileptogenic circuit for the initiation of seizures was distributed throughout the limbic system with a possible central synchronizing process. In vitro studies showed that multiple limbic sites in epileptic animals (hippocampus, entorhinal cortex, piriform cortex and amygdala) have epileptiform changes with prolonged depolarizations and multiple superimposed action potentials. In vivo studies revealed that thalamic stimulation yields short latency excitatory responses in the entorhinal cortex and hippocampus. In addition, in epileptic animals, thalamic stimulation caused epileptiform responses in the hippocampus. Based on the findings of this study and on previous anatomy and physiology reports, we hypothesize that the process of seizure initiation involves broad circuit interactions involving multiple independent limbic structures, and that the midline thalamus may act as a physiological synchronizer. We offer a new proposal for the functional anatomy of limbic epilepsy that takes widespread hyperexcitability in the limbic system and the potential for thalamic synchronization into consideration.

Animals↗
PubMed2002

Comparative distribution of the mammalian mediator subunit thyroid hormone receptor-associated protein (TRAP220) mRNA in developing and adult rodent brain.

TRAP220 (thyroid hormone receptor-associated protein) is a recently cloned nuclear receptor coactivator, which interacts with several nuclear receptors in a ligand-dependent manner and stimulates transcription by recruiting the TRAP mediator complex to hormone responsive promoter regions. TRAP220 has been shown to interact with thyroid hormone receptors, vitamin D receptors, peroxisome proliferator-activated receptors, retinoic acid receptors and oestrogen receptors. Thyroid hormone and retinoic acid play very important roles in brain development and they also influence adult brain. Using in situ hybridization we have examined expression of TRAP220 mRNA in the central nervous system during development and in adult rat and mouse brain. Expression of TRAP220 was seen already during early embryonic development in the epithelium of neural tube at E9 in mouse and at E12 in rat. At later stages of development the strongest signal was seen in different layers of cerebral neocortex, external germinal layer of cerebellum, differentiating fields of hippocampus and neuroepithelium, and a moderate signal was detected in basal ganglia, different areas of diencephalon and midbrain. In adult rat brain the signal was more restricted than during development. TRAP220 expression occurred mostly in the granular layer of cerebellar cortex, piriform cortex and hippocampal formation. The signal was found predominantly in neurons. Our work supports the assumption that TRAP220 plays an important role in growth and differentiation of central nervous system and may have a function in certain areas of adult brain.

Animals↗
PubMed1996

MKP-3, a novel cytosolic protein-tyrosine phosphatase that exemplifies a new class of mitogen-activated protein kinase phosphatase.

MKP-1 (also known as CL100, 3CH134, Erp, and hVH-1) exemplifies a class of dual-specificity phosphatase able to reverse the activation of mitogen-activated protein (MAP) kinase family members by dephosphorylating critical tyrosine and threonine residues. We now report the cloning of MKP-3, a novel protein phosphatase that also suppresses MAP kinase activation state. The deduced amino acid sequence of MKP-3 is 36% identical to MKP-1 and contains the characteristic extended active-site sequence motif VXVHCXXGXSRSXTXXXAYLM (where X is any amino acid) as well as two N-terminal CH2 domains displaying homology to the cell cycle regulator Cdc25 phosphatase. When expressed in COS-7 cells, MKP-3 blocks both the phosphorylation and enzymatic activation of ERK2 by mitogens. Northern analysis reveals a single mRNA species of 2.7 kilobases with an expression pattern distinct from other dual-specificity phosphatases. MKP-3 is expressed in lung, heart, brain, and kidney, but not significantly in skeletal muscle or testis. In situ hybridization studies of MKP-3 in brain reveal enrichment within the CA1, CA3, and CA4 layers of the hippocampus. Metrazole-stimulated seizure activity triggers rapid (<1 h) but transient up-regulation of MKP-3 mRNA in the cortex, piriform cortex, and some amygdala nuclei. Metrazole stimulated similar regional up-regulation of MKP-1, although this was additionally induced within the thalamus. MKP-3 mRNA also undergoes powerful induction in PC12 cells after 3 h of nerve growth factor treatment. This response appears specific insofar as epidermal growth factor and dibutyryl cyclic AMP fail to induce significant MKP-3 expression. Subcellular localization of epitope-tagged MKP-3 in sympathetic neurons reveals expression in the cytosol with exclusion from the nucleus. Together, these observations indicate that MKP-3 is a novel dual-specificity phosphatase that displays a distinct tissue distribution, subcellular localization, and regulated expression, suggesting a unique function in controlling MAP kinase family members. Identification of a second partial cDNA clone (MKP-X) encoding the C-terminal 280 amino acids of an additional phosphatase that is 76% identical to MKP-3 suggests the existence of a distinct structurally homologous subfamily of MAP kinase phosphatases.

Aging↗
PubMed2002

Primary structure of a dynamin-related mouse mitochondrial GTPase and its distribution in brain, subcellular localization, and effect on mitochondrial morphology.

A new member of the dynamin GTPase family (OPA1) was recently identified in humans and shown to be mutated in patients with dominant optic atrophy. To understand better the function of mammalian OPA1, we isolated a mouse ortholog (mOPA1) from brain and raised a specific antibody against its C terminus. The subcellular distribution of mOPA1 overexpressed in COS-7 cells largely overlapped that of endogenous cytochrome c, a well known mitochondrial marker, and dramatically affected mitochondrial morphology, altering it from tubular to vesicular. Mitochondrial targeting was mediated by the N-terminal region of mOPA1 as follows: deletion of the 124 N-terminal amino acids eliminated mitochondrial targeting, although fusion of the N-terminal 60 or 90 amino acids of mOPA1 with green fluorescent protein resulted in its mitochondrial targeting. mOPA1 was expressed widely in the mouse brain, especially in neurons of olfactory bulb, cerebral cortex, piriform cortex, hypothalamus, hippocampus, red nucleus, cochlear nucleus, motor trigeminal nucleus, facial nucleus, cerebellar nucleus, and Purkinje cells. Within dissociated cerebellar cells, mOPA1 protein was clearly observed in the dendrites and somas of neuronal cells, as well as in astrocytes and meningeal cells. In each case, it was distributed in the vesicular pattern seen in other cell types.

Amino Acid Sequence↗
PubMed2005

Angiotensin AT2 receptor protects against cerebral ischemia-induced neuronal injury.

Several lines of clinical and experimental evidence suggest an important role of the renin-angiotensin system in ischemic brain injury although the cellular regulation of the angiotensin AT1 and AT2 receptors and their potential relevance in this condition have not yet been clearly defined. We first assessed the regulation of brain AT1 and AT2 receptors in response to transient unilateral medial cerebral artery occlusion in rats by real-time RT-PCR, Western blot, and immunofluorescence labeling. AT2 receptors in the peri-infarct zone were significantly upregulated 2 days after transient focal cerebral ischemia. Increased AT2 receptors, which were abundantly distributed in a large number of brain regions adjacent to the infarct area including cerebral frontal cortex, piriform cortex, striatum, and hippocampus, were exclusively expressed in neurons. By contrast, AT1 receptors, which remained unaltered, were mainly expressed in astrocytes. In neurons of ischemic striatum, increased AT2 receptors were associated with intense neurite outgrowth. Blockade of central AT2 receptors with PD123177 abolished the neuroprotective effects of central AT1 receptor blockade with irbesartan on infarct size and neurological outcome. In primary cortical neurons, stimulation of AT2 receptors supported neuronal survival and neurite outgrowth. Our data indicate that cerebral AT2 receptors exert neuroprotective actions in response to ischemia-induced neuronal injury, possibly by supporting neuronal survival and neurite outgrowth in peri-ischemic brain areas.

Angiotensin II↗
PubMed1995

Induction of Fos expression following anodal polarization in rat brain.

Expression of c-fos immunoreactivity was investigated in rat brain after unilateral application of a weak anodal direct current (anodal polarization) to the sensorimotor cortex of rats. Increases in Fosimmunopositive neurons were observed transiently in the neocortex, cingulate cortex, piriform cortex, and hippocampal formation, which were ipsilateral to the polarization, as a function of the duration and intensity of the current applied. It is likely that anodal polarization enhances the neuronal activities in the cortex dependent on polarization paradigms.

Animals↗
PubMed1991

Developmental changes in distribution of acidic fibroblast growth factor in rat brain evaluated by a sensitive two-site enzyme immunoassay.

We developed a sensitive two-site enzyme immunoassay (EIA) system for acidic fibroblast growth factor (aFGF), using a polyclonal antibody raised in rats. This assay is based on the sandwiching of the antigen between anti-aFGF antibody immunoglobulin G (IgG) coated on plates and biotinylated anti-aFGF antibody IgG; the detection of biotinylated IgG was performed by enzyme reaction of streptavidin-conjugated beta-D-galactosidase (beta-D-galactoside hydrolase; EC 3.2.1.23). Our system was specific for aFGF, because basic fibroblast growth factor, which shares a 55% homology of amino acid sequence with aFGF, hardly cross-reacted at all. The sensitivity of this system (0.2 ng/ml) enabled us to quantify endogenous immunoreactive aFGF in the CNS. Using this two-site EIA system, we examined the levels of aFGF in various regions of rat brain and their developmental changes. At the early stage of neonatal development, i.e., 2 days after birth, all brain regions registered low aFGF levels (less than 10 ng/g tissue). However, at the young adult stage (21- to 49-day-old animals), an extremely high level of aFGF (75-90 ng/g tissue) was found in the ponsmedulla; relatively high levels (30-40 ng/g tissue) were found in the diencephalon and mesencephalon; and comparatively low aFGF levels (5-15 ng/g tissue) were found in various other brain regions such as the frontal cortex, piriform cortex, hippocampus, olfactory bulb, cerebellum, and striatum. This marked change in the regional distribution of aFGF in the rat brain during postnatal development from 2 to 21 days after birth suggests that this factor plays a significant role in the brain during this period.

Aging↗