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PubMed1999

Expression and localization of the LGN protein in the mouse brain with reference to its relationship with Galphai2.

It has been suggested that the LGN protein is associated with Galphai2 by the yeast two-hybrid system and in vitro pull-down assay. To determine the functions of LGN in the central nervous system, we examined the expression and localization of LGN in mouse brain by immunoblotting and immunofluorescence microscopy. By immunoblotting, almost similar amounts of LGN were detected in the olfactory bulb, cerebral cortex, hippocampus, and cerebellum of the adult mouse brain, and the levels of the postnatal LGN expression in the whole brain were fairly constant. Immunofluorescence microscopy showed that LGN is localized in nuclei of the neurons in the olfactory bulb, cerebral cortex, and hippocampus, but in both nuclei and cytoplasm of Purkinje cells in the cerebellum. On the other hand, Galphai2 was distributed throughout the neuronal elements except for the nuclei. Thus, LGN and Galphai2 were colocalized in the cytoplasm of Purkinje cells, but not in other neurons examined. These results suggest that LGN may be involved not only in the Galphai2-mediated signaling but also in other signaling pathways.

Journal Article↗

PubMedDate not supplied

Long-term alterations in regional brain serotonin metabolism following maternal polychlorinated biphenyl exposure in the rat.

Pregnant Wistar WU rats were administered PCBs (0, 5 or 25 mg Aroclor 1254 per kg body weight) by gavage on day 10 to 16 of gestation. Levels of biogenic amines were measured in the lateral olfactory tract, prefrontal cortex, striatum, hippocampus and hypothalamus in male and female offspring 21 and 90 days after birth. 5-Hydroxyindole acetic acid (5-HIAA) concentrations and the ratio of 5-HIAA/5-hydroxytryptamine (5-HT, serotonin) were significantly increased in the lateral olfactory tract, prefrontal cortex and hippocampus on postnatal day 90 in male and female offspring following maternal PCB treatment. No effects were observed on regional brain levels of dopamine, 3,4-dihydroxyphenylacetic acid, norepinephrine and homovanillic acid. The results indicate that pre- and postnatal exposure to Aroclor 1254 results in regionally specific long-term alterations in the serotonergic system.

Animals↗

PubMed1997

Behavioral and neurochemical effects of a chronic choline-deficient diet in the rat.

Chronic administration of a choline-deficient diet for 20 days caused no modification in ACh levels in the cortex, hippocampus and olfactory system of the rat and an increase in the density (Bmax) of the muscarinic receptors in the hippocampus. The choline-deficient diet caused no modification in noradrenaline levels and a reduction in the density of alpha1-adrenoceptors in the cortex, hippocampus and olfactory system. This paper discusses the possibility that these neurochemical effects are correlated with the reduction in spontaneous memory decay which was observed in the staircase maze after 20 days of a choline-deficient diet.

Acetylcholine↗

PubMed1993

Cellular localization of messenger RNA for beta-1 and beta-2 adrenergic receptors in rat brain: an in situ hybridization study.

Selective, 35S-labeled, oligonucleotide probes were designed from sequences of the rat beta-1 and beta-2 adrenoceptor messenger RNAs for use in situ hybridization experiments on sections of unfixed rat brain and spinal cord. After hybridized sections were exposed to film or dipped in autoradiographic emulsion, specific and selective labeling patterns characteristic for each receptor messenger RNA and region of the central nervous system were observed. For example, labeling for beta-1 messenger RNA was found in the anterior olfactory nucleus, cerebral cortex, lateral intermediate septal nucleus, reticular thalamic nucleus, oculomotor complex, vestibular nuclei, deep cerebellar nuclei, trapezoid nucleus, abducens nucleus, ventrolateral pontine and medullary reticular formations, the intermediate gray matter of the spinal cord and in the pineal gland, while beta-2 messenger RNA labeling was strongest in the olfactory bulb, piriform cortex, hippocampal formation, thalamic intralaminar nuclei and cerebellar cortex. In some of these regions the beta-1 labeling seemed mainly confined to the cell nucleus. Whether or not this apparently nuclear labeling is specific, i.e. indicates synthesis of beta-1 receptor, remains to be established. However, all labeling patterns described disappeared when excess unlabeled probes were added to their respective radiolabeled probes or when sense probes were employed. Since the in situ method labels only cell bodies that produce the messenger RNA for these two beta receptor subtypes, a comparison between these maps and those of past autoradiographic studies mapping the location of central beta receptors using drugs as radioligands may produce further insights regarding the pre- and postsynaptic localization of these receptors in the various parts of the central nervous system circuitry.

Adrenergic Fibers↗

PubMed2001

The novel long PDE4A10 cyclic AMP phosphodiesterase shows a pattern of expression within brain that is distinct from the long PDE4A5 and short PDE4A1 isoforms.

In situ hybridisation methods were used to map the distribution of the novel long PDE4A10 isoform in the brain. PDE4A10 distribution was compared to that of the long PDE4A5 isoform and the short PDE4A1 isoform using probes specific for unique sequences within each of these isoforms. Coronal sections of the brain, taken at the level of the olfactory bulb, prefrontal cortex, striatum, thalamus, hippocampus and cerebellum, were analysed. Strongest expression of PDE4A isoforms was found in the olfactory bulb granular layer with high signals also in the piriform cortex, the dentate gyrus and the CA1 and CA2 pyramidal cells. For the two long forms, level general staining was noted throughout the striatum, thalamus and hippocampus but no signal was evident in the cerebellum. The long PDE4A10 and PDE4A5 isoforms localised to essentially the same regions throughout the brain, although PDE4A10 was uniquely expressed in the major island of Calleja. A signal for the short PDE4A1 isoform was found in regions in which the two long isoforms were both expressed, with the exception of the medial nucleus of the amygdala where weak signals for PDE4A5 and PDE4A10 were detected but PDE4A1 was absent. Uniquely, strong signals for PDE4A1 were detected in the glomerular layer of the olfactory bulb, the CA3 pyramidal cell region and the cerebellum; areas where signals for the two long forms were not evident. PDE4A transcripts for both PDE4A5 and PDE4A10 were not apparent in the brain stem and those for PDE4A1 were low. PDE4A isoforms are present in several key areas of the brain and therefore present valid targets for therapeutic interventions. Whilst the two long PDE4A isoforms show a remarkably similar distribution, in at least three regions there is clear segregation between their pattern of expression and that of the PDE4A1 short form. This identifies differential regulation of the expression of PDE4A long and short isoforms. We suggest that specific PDE4A isoforms may have distinct functional roles in the brain, indicating that PDE4A isoform-selective inhibitors may have specific therapeutic and pharmacologic properties.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1986

Antagonism of lateral olfactory tract synaptic potentials in rat prepyriform cortex slices.

Dose-response data were collected for the inhibition of the monosynaptic excitatory input onto prepyriform neurons from fibers of the rat lateral olfactory tract, using the potent antagonists of excitatory transmission, L(+)-2-amino-4-phosphonobutyrate (L(+)-AP4), kynurenate, N-(p-chlorobenzoyl)piperazine-2,3-dicarboxylate, and N-(p-bromobenzoyl)piperazine-2,3-dicarboxylate. Kynurenate and the piperazine derivatives blocked up to 80% of the synaptic response at doses of 1000 microM, with single-affinity dose-response curves. L(+)-AP4 blocked only 50% of the synaptic response at a dose of 1000 microM, with a multicomponent dose-response curve.

Aminobutyrates↗

PubMed2005

Efferent connections of the "olfactostriatum": a specialized vomeronasal structure within the basal ganglia of snakes.

The olfactostriatum is a portion of the basal ganglia of snakes that receives substantial vomeronasal afferents through projections from the nucleus sphericus. In a preceding article, the olfactostriatum of garter snakes (Thamnophis sirtalis) was characterized on the basis of chemoarchitecture (distribution of serotonin, neuropeptide Y and tyrosine hydroxylase) and pattern of afferent connections [Martinez-Marcos, A., Ubeda-Banon, I., Lanuza, E., Halpern, M., 2005. Chemoarchitecture and afferent connections of the "olfactostriatum": a specialized vomeronasal structure within the basal ganglia of snakes. J. Chem. Neuroanat. 29, 49-69]. In the present study, its efferent connections have been investigated. The olfactostriatum projects to the main and accessory olfactory bulbs, lateral cortex, septal complex, ventral pallidum, external, ventral anterior and dorsolateral amygdalae, bed nucleus of the stria terminalis, preoptic area, lateral posterior hypothalamic nucleus, ventral tegmental area, substantia nigra and raphe nuclei. Tracer injections in the nucleus accumbens proper, a structure closely associated with the olfactostriatum, result in a similar pattern of efferent connections with the exception of those reaching the main and accessory olfactory bulbs, lateral cortex, external, ventral anterior and dorsolateral amygdalae and bed nucleus of the stria terminalis. These data, therefore, help to characterize the olfactostriatum, an apparently specialized area of the nucleus accumbens. Double labeling experiments after tracer injections in the nucleus sphericus and the lateral posterior hypothalamic nucleus demonstrate a pathway between these two structures through the olfactostriatum. Injections in the olfactostriatum and in the medial amygdala show parallel projections to the lateral posterior hypothalamic nucleus. Since this hypothalamic nucleus has been previously described as projecting to the hypoglossal nucleus, both, the medial amygdala and the olfactostriatum may mediate vomeronasal influence on tongue-flick behavior.

Amygdala↗

PubMed1985

Intraventricular 6-hydroxydopamine increases thyrotropin-releasing hormone (TRH) content in regions of rat brain.

Rats were given intraventricular (ivt) injections of various doses (50-400 micrograms, hydrobromide salt) of 6-hydroxydopamine (6-OHDA) and killed 1, 3 or 6 days later. Brains were removed, dissected into 11 regions, and the thyrotropin-releasing hormone (TRH) content of each region was measured by radioimmunoassay. 6-OHDA (400 micrograms) caused significant elevations in the TRH content of 6 regions: olfactory bulb, anterior cortex, brainstem, posterior cortex, hippocampus, and amygdala-piriform cortex. The magnitude of these increases ranged from 59% in olfactory bulb to 497% in hippocampus and was, in all cases, greatest at 3 days. These results suggest that the TRH content of certain brain regions may be regulated by catecholamine neurotransmitters.

Animals↗

PubMed1984

The development of physiological responses of the piriform cortex in rats to stimulation of the lateral olfactory tract.

Extracellular recording techniques in rats were used to follow the postnatal development of the evoked response of the piriform cortex to electrical stimulation of the lateral olfactory tract (LOT) from birth to adulthood. As in other species, LOT shock in adult rats produces short-latency activation of units in piriform cortex and an extracellular field potential consisting of three components: a surface-negative component, the A1 wave (corresponding to the cortical monosynaptic EPSP evoked by the LOT fibers); a second surface-negative component, the B1 wave (corresponding to reactivation of layer I dendrites by intracortical fibers); and a late surface-positive component, the period 2 wave. A conditioning shock 20-150 msec before the test shock profoundly inhibits both evoked unit activity and the B1 wave, while it facilitates the A1. At birth, units can be orthodromically activated by LOT stimulation in association with the A1 wave. There is also a surface-positive spikelike wave, the S wave, which represents the summation of cortical unit activity. The B1 wave is apparent early in the first postnatal week. However, in contrast to the prominent inhibition in the adults, for the first few days after birth, single-unit responses, multiple-unit activity, and the S wave are all facilitated by a preceding conditioning shock with intervals of 200 msec or less, in association with the facilitation of the A1 wave. A shift to inhibition is apparent with longer intershock intervals of 300-700 msec, which exceed the period during which paired shocks facilitate the A1 wave. During the remainder of the first two postnatal weeks,, partial suppression of evoked activity with intervals of less than 200 msec appears and progressively increases in strength, but inhibition at very long intershock intervals remains greater in magnitude. During this time, the duration of the inhibitory period also decreases to near the adult value of 200-300 msec. In the third postnatal week the pattern was similar to that in the adult, but the inhibition was still clearly weaker than in adults. These results suggest a delayed maturation of the cortical inhibitory circuitry; this conclusion has also been suggested by previously published observations in the developing neocortex and hippocampus. In addition, the acceleration with age of the conduction velocity of axons in the LOT was analyzed. The adult value of 9.6 m/sec was not achieved until some time after postnatal day 15, which parallels the myelinization of the tract as observed with the light microscope.

Aging↗

PubMed1999

Odor-induced fast waves in the dentate gyrus depend on a pathway through posterior cerebral cortex: effects of limbic lesions and trimethyltin.

Previous research has shown that the odor of a variety of organic solvents and of components of the anal scent gland excretions of various predators will elicit a burst of fast waves of about 20 Hz in the olfactory bulb, pyriform cortex, and dentate gyrus of the rat. The present experiments show that large lesions of the caudal cerebral cortex, involving particularly the entorhinal and subicular cortices and the angular bundle, abolish the olfactory fast wave response of the dentate gyrus, but not the similar response of the olfactory bulb. In confirmation of previous work, such a lesion also abolishes an average evoked response elicited in the dentate gyrus by electrical stimulation of the olfactory bulb. Systemic treatment with the neurotoxin trimethyltin abolished the olfactory fast wave response in the olfactory bulb and both the olfactory fast wave and the olfactory evoked potential in the dentate gyrus. Large lesions of the amygdala or the septal nuclei did not eliminate either the dentate olfactory evoked potential or the odor-induced dentate fast wave response. However, the septal lesion reduced the amplitude of both spontaneous and odor-induced dentate fast wave activity. It is suggested that olfactory stimuli elicit 20 Hz dentate fast waves via a pathway from the olfactory bulb through the entorhinal cortex and, further, that cholinergic interneurons in the dentate gyrus may be essential to the dentate fast wave response.

Amygdala↗

PubMed1999

Chronic phencyclidine increases NMDA receptor NR1 subunit mRNA in rat forebrain.

The present study was designed to determine whether the sensitization of locomotor activity that results from chronic phencyclidine (PCP) administration is associated with altered NMDA receptor function or mRNA in rat brain. Female Sprague-Dawley rats were administered PCP (20 mg/kg, i.p.) once daily for 5 days. After withdrawal for 72 hr, challenge with 3.2 mg/kg PCP (i.p.) revealed a significant sensitization to the locomotor activating effect of PCP. In situ hybridization analysis with an oligonucleotide probe complementary to the mRNA encoding the NR1 subunit of the NMDA receptor demonstrated that chronic PCP treatment resulted in a marked increase in NR1 subunit mRNA in the forebrain. Quantitative image analysis revealed a significant increase in the labeling of NR1 mRNA in the olfactory tubercle, piriform cortex, frontal cortex, and anterior striatum. However, no significant difference between PCP and saline-treated rats was found in the hippocampus or cerebellum. In a parallel study, possible functional alterations in the NMDA receptor were assessed by measuring NMDA-stimulated release of [3H]DA from slices of the olfactory tubercle and piriform cortex. NMDA-stimulated release was not affected by chronic PCP treatment, but the inhibition of this release by PCP, 7-chlorokynurenic acid (7-CK), and DL-2-amino-5-phosphovaleric acid (AP-5) was significantly diminished by chronic PCP. This suggests that the behavioral plasticity associated with chronic PCP may be related to an altered subunit stoichiometry of NMDA receptors in selective forebrain regions.

Animals↗

PubMed1995

Identification of a putative estrogen response element in the gene encoding brain-derived neurotrophic factor.

We have been studying the role and mechanism of estrogen action in the survival and differentiation of neurons in the basal forebrain and its targets in the cerebral cortex, hippocampus, and olfactory bulb. Previous work has shown that estrogen-target neurons in these regions widely coexpress the mRNAs for the neurotrophin ligands and their receptors, suggesting a potential substrate for estrogen-neurotrophin interactions. Subsequent work indicated that estrogen regulates the expression of two neurotrophin receptor mRNAs in prototypic peripheral neural targets of nerve growth factor. We report herein that the gene encoding the neurotophin brain-derived neurotrophic factor (BDNF) contains a sequence similar to the canonical estrogen response element found in estrogen-target genes. Gel shift and DNA footprinting assays indicate that estrogen receptor-ligand complexes bind to this sequence in the BDNF gene. In vivo, BDNF mRNA was rapidly up-regulated in the cerebral cortex and the olfactory bulb of ovariectomized animals exposed to estrogen. These data suggest that estrogen may regulate BDNF transcription, supporting our hypothesis that estrogen may be in a position to influence neurotrophin-mediated cell functioning, by increasing the availability of specific neurotrophins in forebrain neurons.

Animals↗

PubMed1990

The distribution and cellular localization of the serotonin 1C receptor mRNA in the rodent brain examined by in situ hybridization histochemistry. Comparison with receptor binding distribution.

The regional distribution and cellular localization of mRNA coding for the serotonin 1C receptor were investigated in tissue sections of mouse and rat brain by in situ hybridization histochemistry. Several 32P-labelled riboprobes derived from mouse genomic clones were used. The serotonin 1C receptor binding sites were visualized autoradiographically and quantified using [3H]mesulergine as ligand, in the presence of spiperone to block serotonin 1C receptors. Strong hybridization signal was observed in the choroid plexus of all brain ventricles. High levels of hybridization were also seen in the anterior olfactory nucleus, pyriform cortex, amygdala, some thalamic nuclei, especially the lateral habenula, the CA3 area of the hippocampal formation, the cingulate cortex, some components of the basal ganglia and associated areas, particularly the nucleus subthalamicus and the substantia nigra. The midbrain and brainstem showed moderate levels of hybridization. The distribution of the serotonin 1C receptor mRNA corresponded well to that of the serotonin 1C receptors. The highest levels of serotonin 1C receptor binding were observed in the choroid plexus. In addition, significant levels of the serotonin 1C receptor binding were seen in the anterior olfactory nucleus, pyriform cortex, nucleus accumbens, ventral aspects of the striatum, paratenial and paracentral thalamic nuclei, amygdaloid body and substantia nigra pars reticulata. The cingulate and retrosplenial cortices as well as the caudal aspects of the hippocampus (CA3) were also labelled. Binding in brainstem and medulla was low and homogeneously distributed. No significant binding was seen in the habenular and subthalamic nuclei. Similar findings were obtained in rat brain. These results demonstrate that, in addition to their enrichment in the choroid plexus, the serotonin 1C receptor mRNA and binding sites are heterogeneously distributed in the rodent brain and thus could be involved in the regulation of many different brain functions. The combination of in situ hybridization histochemistry with receptor autoradiography opens the possibility of examining the regulation of the serotonin 1C receptor synthesis after pharmacological or physiological alterations.

Animals↗

PubMed1995

Quantitative distribution of the delta opioid receptor mRNA in the mouse and rat CNS.

We have used a sensitive solution hybridization assay that employs a riboprobe obtained from the mouse delta opioid receptor (DOR) coding sequence to quantitate the relative abundance of DOR mRNA in the central nervous system (CNS) of the adult mouse and rat. In brain Poly A+ RNA extracts this riboprobe hybridized to a single 10 kb transcript from mouse and two transcripts, one of 12 and the other of 4.5 kb in size from rat. In mouse CNS the highest levels of DOR mRNA were found in the caudate-putamen at 3.3 +/- 0.1 (SEM) pg/micrograms RNA. DOR mRNA levels in the range from 2.6 to 2.1 pg/micrograms RNA were measured in frontal cortex, nucleus accumbens, whole brain and olfactory tubercle. Spinal cord, periaqueductal gray and hippocampus had DOR mRNA levels in the range from 1.8 to 1.5 pg/micrograms RNA, while medial thalamus and cerebellum had the lowest levels (0.5 pg/micrograms RNA). These results correlate with the reported relative distribution of DOR mRNA in mouse using an in situ hybridization technique. In rat CNS, the highest levels of DOR mRNA were measured in caudate-putamen at 2.3 +/- 0.1 pg equivalents/micrograms RNA. Whole brain, cerebral cortex, olfactory bulb and brain stem had levels in the range from 1.5 to 0.9 pg equivalents/micrograms RNA while the lowest DOR mRNA levels were measured at 0.5 pg equivalents/micrograms RNA or less in thalamus, hippocampus, substantia nigra and cerebellum. This study demonstrates the ability of solution hybridization assays to quantitate homologous (mouse) as well as similar but heterologous (rat) DOR mRNA levels.

Animals↗

PubMed1999

Regional distribution and cell type-specific expression of the mouse F3 axonal glycoprotein: a developmental study.

The expression of the mouse axonal adhesive glycoprotein F3 and of its mRNA was studied on sections of mouse cerebellar cortex, cerebral cortex, hippocampus, and olfactory bulb from postnatal days 0 (P0) to 30 (P30). In cerebellar cortex, a differential expression of F3 in granule versus Purkinje neurons was observed. F3 was highly expressed during migration of and initial axonal growth from cerebellar granule cells. The molecule was then downregulated on cell bodies and remained expressed, although at low levels, on their axonal extensions. On Purkinje cells, F3 was strongly expressed on cell bodies and processes at the beginning of the second postnatal week; by P16 it was restricted to neurites of Purkinje cells subpopulations. In the cerebral cortex, the molecule was highly expressed on migrating neurons at P0; by P16, it was found essentially within the neuropil with a diffuse pattern. In the hippocampal formation, where F3 was expressed on both pyramidal and granule neurons, a clear shift from the cell bodies to neurite extensions was observed on P3. In the olfactory pathway, F3 was expressed mainly on olfactory nerve fibers, mitral cells, and the synaptic glomeruli from P0 to P3, with a sharp decline from P11 to P16. As a whole, the data show that F3 protein expression is regulated at the regional, cellular, and subcellular levels and suggest that, in different regions, it can be proposed as a reliable neuronal differentiation marker.

Aging↗

PubMed1983

Early recovery of function after olfactory tract section correlated with reinnervation of olfactory tubercle.

Behavioral recovery and cortical reinnervation after early olfactory tract section were assessed in the infant golden hamster (Mesocricetus auratus). Hamster pups show strong thermotaxis at birth which declines abruptly after postnatal day (P) 8 in normal pups. Unilateral olfactory bulbectomy on P5 causes persistent thermotaxis through the second postnatal week. In this study, the bulb's output pathway, the lateral olfactory tract, was unilaterally severed on P5 and pup thermotaxis was tested through P15. Complete tract section, like bulbectomy, prolonged thermal responding beyond P8. In contrast to bulbectomy, however, some tract-sectioned pups showed recovery before P15 while others continued to show persistent thermotaxis throughout testing. The olfactory bulb projection was examined 10 days after tract section in order to determine whether recovery and persistent thermotaxis were associated with different patterns of cortical innervation. Eleven pups with complete transections showed recovery during the second week. In 10 of these pups, olfactory bulb fibers had penetrated the damaged region after surgery to reinnervate the olfactory tubercle. Three of these pups also exhibited some reinnervation of piriform cortex. The lesions of pups showing persistent thermotaxis were more severe, extending bilaterally or into deep cortical layers, and olfactory fibers had failed to reinnervate caudal terminal fields. All pups with olfactory tract sections showed extensive sprouting rostral to the cut, regardless of their behavioral profile. In no case had postlesion growth innervated the entorhinal or amygdaloid areas. Inhibition of thermotaxis was associated with reinnervation of the olfactory tubercle rather than more rostral, lateral or caudal olfactory cortex. We conclude that regrowth of olfactory tract fibers caudal to early transection is rapid and has functional consequences for early behavioral development.

Animals↗

PubMed1995

Increases in hippocampal and frontal cortical acetylcholine release associated with presentation of sensory stimuli.

In vivo microdialysis was employed to monitor acetylcholine release in the hippocampus and frontal cortex of freely behaving rats. Four stimuli were presented on separate occasions in the course of a dialysis session to rats with microdialysis probes implanted in the hippocampus or frontal cortex. Visual, auditory, olfactory and tactile stimuli elicited a number of different responses such as exploratory and consummatory behaviours. Presentation of two of the stimuli (auditory and tactile) also produced periods of alert immobility (freezing). All of the stimuli increased acetylcholine release in both the hippocampus and cortex: in the hippocampus, this increase was statistically significant with all except the olfactory stimulus, whereas in the cortex all but the visual stimulus resulted in significant increases. In the hippocampus, there were no significant differences between the increases in acetylcholine release produced by the four stimuli. In contrast, in the cortex, there was significant variation between the magnitude of acetylcholine release produced by the different stimuli: acetylcholine release elicited by tactile stimulation was greater than that produced by the other stimuli. There was no significant variation in the duration of increases in acetylcholine release produced by the stimuli in either the hippocampus or cortex. These results provide evidence that acetylcholine release is associated with a variety of behavioural responses to stimuli designed to produce arousal, and point to a role for cortical and hippocampal cholinergic mechanisms in arousal or attention. Further, the results suggest that under some circumstances cortical and hippocampal acetylcholine release may be regulated differentially.

Acetylcholine↗

PubMed1991

Localization of insulin-like growth factor I (IGF-I)-like immunoreactivity in the developing and adult rat brain.

The cellular distribution of insulin-like growth factor I (IGF-I) immunoreactivity was examined in the rat brain from embryonic day 15 to maturity. IGF-I immunoreactivity was found in the perikarya of neurons distributed along the entire extension of the neuronal tube in all the embryonic ages studied (E15, E17, E19 and E21). In E21 animals, the majority of immunoreactive neurons was located in the olfactory bulb, cerebral cortex, hippocampus, striatum, diencephalon, mesencephalic colliculi, trigeminal nuclei, trigeminal ganglion and in motoneurons of the brainstem. In 10- and 20-day-old rats, in addition to the above areas, IGF-I immunoreactivity was also observed in capillary walls, ependymal cells, choroid plexus, glial cells and most fiber paths. In postnatal ages, immunoreactivity in neuronal somas was mainly restricted to the cell nuclei. However, IGF-I immunoreactivity in the neuronal cytoplasm was observed in 20-day-old rats treated with colchicine while fiber paths and neuronal cell nuclei were negative in these animals. In the telencephalon of 20-day-old rats injected with colchicine, the most intense immunoreactive neurons were observed in the olfactory bulb, cerebral cortex, tenia tecta, hippocampus, islands of Calleja, septal nuclei, striatum, endopyriform nucleus and amygdala. Most diencephalic nuclei, the substantia nigra, the mesencephalic colliculi, Purkinje cells in the cerebellar cortex and several nuclei in mesencephalon, pons and medulla oblongata were also immunoreactive. In adult rats injected with colchicine, IGF-I immunoreactivity was located in the same areas as in 20-day-old rats. The number of immunoreactive cells and the intensity of the staining was reduced in adult rats as compared to that found in young postnatal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗