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PubMed1994

Distribution of mRNA for CCK-B receptor in the brain of Mastomys natalensis: abundant expression in telencephalic neurons.

The distribution of cholecystokinin B (CCK-B) receptors in the Mastomys brain was studied using Northern blot analysis and in situ hybridization technique. By Northern blot analysis using 32P-labeled cDNA probe, the cortex had the highest hybridization signal of CCK-B receptor mRNA in the brain. The olfactory bulb and hippocampus showed a moderate level of signals. In situ hybridization using 35S-labeled cRNA probes revealed a wide and region-specific distribution of CCK-B receptor mRNA in the telencephalon. Throughout the cerebral cortex, labeled cells were found in all layers, with higher intensities in layers II, V and VI. Pyramidal cells of the layer II of the piriform cortex showed the highest level of signals in the brain. In the hippocampus, most of the pyramidal cells of the Ammon's horn were labeled, although labeled cells were not detected in other layers. Distinct signals were also detected in the various amygdaloid nuclei, caudate-putamen, reticular thalamic nucleus, hypothalamic ventromedial nucleus and inferior colliculus. This distribution pattern may further support the prominent existence of CCK-B receptors in the brain particularly in the telencephalon.

Animals↗
PubMed1999

Neurocircuitries of the basal ganglia studied in organotypic cultures: focus on tyrosine hydroxylase, nitric oxide synthase and neuropeptide immunocytochemistry.

The nigrostriatal and mesolimbic systems of the rat were reconstructed using an organotypic culture model, whereby neonatal brain tissue was grown in vitro for approximately one month. The nigrostriatal system comprised of tissue from the substantia nigra, the dorsal striatum and the frontoparietal cortex, while the mesolimbic system included the ventral tegmental area, ventral striatum (including the fundus striati, accumbens nucleus, olfactory tubercle, lateral septum, ventral pallidum and piriform cortex) and cingulate cortex. These regions were also cultured alone or in pairs. The cultures were monitored in vitro, and after one month fixed in a formalin-picric acid solution, and processed for immunohistochemistry using antibodies raised against tyrosine hydroxylase, nitric oxide synthase, preprocholecystokinin, glutamate decarboxylase, neuropeptide Y, dopamine- and cyclic AMP-regulated phosphoprotein-32 and glial fibrillary acidic protein. The tissue survived in single, double or triple cultures, although differences were found depending upon the source and combination of cultured region. Neurons had localization and shape as in vivo. Local networks were especially prominent in the mesencephalon, where both tyrosine hydroxylase-positive axons spread from the "substantia nigra" to the rest of the tissue, and where nitric oxide synthase-positive networks also surrounded tyrosine hydroxylase-positive neurons. Glutamate decarboxylase-positive nerve terminals formed dense networks around tyrosine hydroxylase-positive neurons. In the striatum, nitric oxide synthase and dopamine- and cyclic AMP-regulated phosphoprotein-32 neurons were surrounded by tyrosine hydroxylase-positive nerve terminals. The nigral and ventral tegmental area dopamine neurons projected to striatal and cortical structures, but the projection from the ventral tegmental area to the cingulate cortex was more prominent. With regard to co-existence, preprochole-cystokinin-like immunoreactivities was found in many tyrosine hydroxylase-positive neurons and neuropeptide Y- and nitric oxide synthase-like immunoreactivity co-existed in striatal and cortical tissues. In general terms, the chemical neuroanatomy in the cultures was similar to that described earlier in vivo. Nitric oxide synthase staining was particularly intense. Taken together, the organotypic model captures many of the morphological and neurochemical features seen in vivo, providing a valuable model for studying neurocircuitries of the brain in detail, where 'normal' and 'pathological' conditions can be simulated.

Animals↗
PubMed1999

Environmental control of collateral branching and target invasion of mitral cell axons during development.

During development, mitral cell axons, the major efferents of the olfactory bulb, exhibit a protracted waiting period in the lateral olfactory tract (LOT) before giving off collateral branches and innervating the target olfactory cortex. To investigate the target invasion mechanism, a series of heterochronic and heterotopic cocultures of olfactory bulbs with various olfactory cortical strips were conducted. These experiments indicated that development of collateral branches is triggered by environmental cues but not by intrinsic mechanisms in mitral cells. The collateral-inducing cues are apparently different from the cues directing outgrowth of primary mitral cell axons. Coculture experiments also indicated that the target olfactory cortex undergoes a developmental change to become accessible to mitral cell fibers. Primary mitral cell axons, however, still preferred the LOT position over such accessible piriform cortex when encountered both the locations. These results suggest that mitral cell projection comprises multiple steps which are controlled by various environmental cues.

Animals↗
PubMed1992

Systematisation of the olfactory bulb efferent projections in a lemurian primate: Microcebus murinus.

In order to investigate a sensorial pathway essential in animal behavior, the efferent projections of the olfactory bulbs in Microcebus murinus were identified after transection of one olfactory peduncle and revelation of degenerating fibers by various silver staining methods. Total and partial sections have enabled the demonstration of the involvement in the olfactory projection areas of each olfactory tract: the lateral olfactory tract (LOT) and the intermediate olfactory tract (IOT), either via the medial forebrain bundle (MFB) or not. The IOT fibers innervate the cortex, the anterior olfactory nucleus, the caudate-putamen, the septum and the hippocampus on both sides. The LOT fibers reach the olfactory tubercle, the piriform cortex, the entorhinal cortex and the amygdala on both sides. Olfactory fibers could also be observed in the MFB innervating on both sides firstly the hypothalamic areas (the lateral hypothalamus, the suprachiasmatic, posterior supraoptic, mammillary nuclei and the median eminence), and then the mesencephalic structures (the locus coeruleus and the raphe nuclei). It may be concluded that the olfactory bulbs are not only connected with above-mentioned telencephalic areas, but are also directly related to the vegetative and integrative brain areas located in the hypothalamus and the brainstem and especially with the major nuclei which play an essential role in neurovegetative, neuroendocrine and behavioral regulation.

Animals↗
PubMed1986

Cholinergic and non-cholinergic projections from the rat basal forebrain revealed by combined choline acetyltransferase and Phaseolus vulgaris leucoagglutinin immunohistochemistry.

A two-color fluorescence method is described for demonstrating immunohistochemically the anterogradely transported plant lectin Phaseolus vulgaris leucoagglutinin (PHAL, fluorescein isothiocyanate label) and choline acetyltransferase (ChAT, rhodamine label) on the same rat brain section. Application of this method to the study of projection neurons in the vertical and horizontal limbs of the diagonal band, the substantia innominata and nucleus basalis revealed that both cholinergic and non-cholinergic pathways followed similar trajectories to their targets. These included: projections from the vertical, and, to a lesser extent, horizontal limb of the diagonal band coursing through the dorsal fornix, alveus and fimbria to the hippocampus; fibers from the vertical and horizontal limbs of the diagonal band traveling anteriorly to the anterior olfactory nucleus, posterolaterally to the entorhinal cortex, and anterodorsally into the cingulum to the cingulate and retrosplenial, and, in some cases, the frontal and occipital cortices; projections, mostly non-cholinergic, from the substantia innominata traveling laterally to the piriform cortex and amygdala, and anteriorly to the anterior olfactory nucleus and olfactory bulb; and fibers from cells in the nucleus basalis coursing dorsally to the frontal and parietal cortices or laterally to the basolateral amygdala and piriform, insular and temporal cortices. Some axon terminations ended at right angles to the parent axon shaft in short protuberances resembling terminal boutons.

Animals↗
PubMed1993

Adrenalectomy attenuates kainic acid-elicited increases of messenger RNAs for neurotrophins and their receptors in the rat brain.

Treatment with excitotoxin kainic acid is known to increase the level of messenger RNAs for nerve growth factor and brain-derived neurotrophic factor in the brain. In this study we have used quantitative in situ hybridization to analyse the effect of glucocorticoids on kainic acid-induced increase of nerve growth factor and brain-derived neurotrophic factor messenger RNA in the rat brain. In adrenalectomized animals, the kainic acid-mediated increase of brain-derived neurotrophic factor messenger RNA in the hippocampus and the cerebral cortex was reduced by 50% compared to sham-operated animals. The increase of nerve growth factor messenger RNA elicited by kainic acid in the dentate gyrus was almost completely abolished in adrenalectomized animals. No significant change was seen in c-fos messenger RNA in the hippocampus of adrenalectomized rat after kainic acid injection compared to sham-operated kainic acid-treated rats, while a three-fold reduction was seen in the cerebral cortex. Dexamethasone injection prior to kainic acid administration potentiated the kainic acid-induced increase of nerve growth factor messenger RNA in the dentate gyrus and the piriform cortex. In contrast, dexamethasone pretreatment did not potentiate the kainic acid-mediated increase of brain-derived neurotrophic factor messenger RNA. We also examined the effect of adrenalectomy and kainic acid injection on tropomyosin receptor kinase B and C messenger RNA, encoding essential components of high-affinity receptor for brain-derived neurotrophic factor/neurotrophin-4 and neurotrophin-3, respectively. Following adrenalectomy no change of tropomyosin receptor kinase B or C messenger RNA was detected in any of the brain regions studied compared to sham-operated animals. The injection of kainic acid caused four-fold and two-fold increases of tropomyosin receptor kinase B messenger RNA in the dentate gyrus and cerebral cortex, respectively, but no change in tropomyosin receptor kinase C messenger RNA in any of these regions. In adrenalectomized animals receiving kainic acid, the level of tropomyosin receptor kinase B messenger RNA was decreased both in the dentate gyrus and cerebral cortex as compared to sham animals treated with kainic acid. Taken together, the data suggest that excitotoxins and glucocorticoids both influence expression of brain-derived neurotrophic factor and nerve growth factor messenger RNA in the brain, but by two different mechanisms, where the effect of excitotoxin-evoked seizures is modulated by glucocorticoids.

Adrenalectomy↗
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↗
PubMed2004

Innate immune reaction in response to seizures: implications for the neuropathology associated with epilepsy.

In the present study, the expression of pro-inflammatory transcripts was assessed across the brain of mice having undertaken pilocarpine-induced seizures. Pilocarpine-induced marked neurodegeneration and demyelination in multiple regions of the forebrain. The pattern of genes encoding toll-like receptor type 2 (TLR2) and I kappa B alpha (index of NF-kappa B activation) was associated with the neurodegenerating areas, but this was not the case for the mRNA encoding other inflammatory proteins. Scattered tumor necrosis factor-alpha (TNF-alpha)-expressing cells were found across brain, whereas the signals for monocyte-chemoattractant protein-1 and microsomal prostaglandin mPGES E synthase were robust in thalamus and cerebral cortex and weak in the hippocampus and amygdala. TLR2 and TNF-alpha transcripts were expressed mainly in microglia/macrophages. Cyclooxygenase-2 was induced specifically in the hippocampus and piriform cortex. A low increase in interleukin-12 mRNA was detected in the brain, but the signal for interferon gamma (IFN-gamma) remained undetectable. Although pro-inflammatory markers were induced in a different manner across the CNS, their patterns were not characteristic of those caused by other inflammatory challenges, such as endotoxin. These data suggest a different mechanism involved in regulating the innate immune reaction in response to seizures and could have direct implications for the neuropathology associated with epilepsy.

Animals↗
PubMed2000

Neural mechanisms involved in odor pleasantness and intensity judgments.

Olfactory processing in the human brain was examined using positron emission tomography. Twelve normal volunteers were scanned while smelling pairs of odors: they were asked to judge which odor was more pleasant in one condition, and which was more intense in a second condition; they also were scanned while sniffing an odorless stimulus. As in prior studies, greater cerebral blood flow was found in the right orbitofrontal cortex during both pleasantness and intensity judgments as compared to baseline. Cerebellar activity was also seen, but contrary to expectations no activity was detected in the primary olfactory (piriform) cortex. Only the pleasantness judgment elicited additional activity within the hypothalamus, suggesting that this structure may be involved in affective processing that requires access to information about internal state.

Adult↗
PubMed1995

Developmental and regional expression pattern of a novel NMDA receptor-like subunit (NMDAR-L) in the rodent brain.

A novel NMDA receptor-like (NMDAR-L) cDNA was isolated that contained an open reading frame coding for a predicted polypeptide of 1115 amino acids that shares approximately 27% identity with NMDA receptor subunits. In situ hybridization experiments indicated that NMDAR-L mRNA was expressed in the developing rodent CNS. On postnatal day 1 (P1), NMDAR-L mRNA expression was pronounced in the entorhinal cortex, the subiculum and the thalamus, in layer V of the developing neocortex, in the superior and inferior colliculi, and various regions of the hindbrain, excluding the cerebellum. On P5, NMDAR-L mRNA was expressed in layer V of the neocortex, in the entorhinal cortex, in the subiculum, and in the thalamus. On P14, NMDAR-L mRNA was expressed in layers II-VI of the neocortex, in the entorhinal and piriform cortex, in the subiculum and CA1 field, and in the nucleus of the lateral olfactory tract. In the adult brain, NMDAR-L mRNA was detected predominately in the nucleus of the lateral olfactory tract. Injection of NMDAR-L cRNA into Xenopus oocytes did not lead to the expression of homomeric glutamate-activated channels. However, coinjection of the triple combination of NMDAR-L with NMDAR1 and NMDAR2B cRNAs led to a striking decrease in the current magnitude compared to currents obtained after coexpression of the double combination of NMDAR1 with NMDAR2B. While the function of NMDAR-L remains to be established, its developmental and regional expression pattern suggests that NMDAR-L may influence axonal outgrowth and synaptogenesis during brain development.

Aging↗
PubMed1994

Expression of soluble guanylyl cyclase gene in adult rat brain.

The synthesis of the intracellular messenger, cyclic GMP, is catalysed by particular or soluble guanylyl cyclase (sGCY). sGCY is activated by nitric oxide, a compound with putative neurotransmitter functions, especially in long-term potentiation. Hybridization histochemistry with a probe complementary to the rat lung large (alpha 1) subunit was used to assess the exact localization of sGCY mRNA in the rat brain. Many cells in the olfactory bulb contained sGCY mRNA. In the whole cerebral cortex, sGCY mRNA was found in all layers, with a predominance in layers II-III. A similar pattern was found in the olfactory tuberculum, in continuation with the piriform cortex and the cortical amygdaloid nucleus. All parts of the striatum expressed sGCY mRNA. sGCY mRNA was also found in the habenula medialis, in the pinealis in some diencephalic nuclei, and in the granule cell layers of the cerebellum. This study provides a description of the normal anatomy of sGCY gene expression in the rat forebrain as a basis for the study of the modulation of expression after physiological and pharmacological manipulations.

Animals↗
PubMed2005

Oxytocin receptors in brain cortical regions are reduced in haploinsufficient (+/-) reeler mice.

OBJECTIVE: Both oxytocin (OT) and reelin are particularly significant during development and the absence of either may interfere with normal brain development. In addition, reelin is critical to the development of the GABAergic system and GABA modulates the release of OT. Availability of the reelin haploinsufficient (+/-) reeler mouse (HRM) provides a model for examining the role of reelin in the development of the OT system and especially in the expression of the OT receptor (OTR). METHODS: In this study we used immunocytochemistry and in situ hybridization in HRM versus wild-type (+/-) mice (WTM) to quantify OTR abundance in regions of the brain cortex. RESULTS: Our findings reveal that the oxytocin receptor (OTR), measured either by immunohistochemistry or in situ hybridization, is significantly lower in HRM. Areas showing significant deficits included the piriform cortex, neocortex, retrosplenial cortex and certain regions of the hippocampus. CONCLUSION: Both reelin and OT play a role in regulating affect and mood. Down-regulation of reelin has been strongly correlated with schizophrenia and it is proposed that HRM may serve as a model for neural deficits seen in both schizophrenia and autism. We report that HRM show regionally specific reductions in OTRs, especially in cortical areas, which previously have been implicated in social memory and cognitive functions. These findings offer support for the more general hypothesis that down-regulation of reelin, of either genetic or epigenetic origin, through associated reductions in the OTRs, contributes to the deficiencies in social behavior that are characteristic of both schizophrenia and autism.

Animals↗
PubMed1992

Functional correlates of selective long-term potentiation in the olfactory cortex and olfactory bulb.

High-frequency stimulation of the granule cell layer of the olfactory bulb (OB) has previously been shown to result in a selective long-term potentiation (LTP) of late components of potentials evoked in the OB and piriform cortex (PC). The functional impact of this potentiation was explored in male Long-Evans rats with chronically implanted electrodes by comparing the effects of paired-pulse stimulation of the OB in potentiated and control animals. Effects were examined on two components of the potential evoked in the PC: A1, which represents the population EPSP produced by OB mitral cells in PC pyramidal cells via the lateral olfactory tract (LOT), and B1, which represents the subsequent population EPSP produced by PC pyramidal cells in other pyramidal cells. Two separate functional correlates of selective LTP were found. First, there was enhanced paired-pulse depression of B1, indicating increased inhibition of PC pyramidal cells. Second, there was a shift from paired-pulse facilitation to depression of A1, which was accompanied by a decrease in amplitude of the LOT volley, indicating that fewer mitral cells were activated by the stimulation. This shift was most prominent in animals with stimulating electrodes closest to the mitral cell layer, suggesting that it is dependent upon direct stimulation of mitral cell somata. These observations, together with other results reported in the manuscript, support the conclusion that there is an enhanced inhibition of mitral cells following selective LTP. Thus a primary consequence of selective LTP appears to be enhanced inhibition of principal neurons in both the PC and OB. These findings are consistent with our previous proposal that selective LTP represents potentiation at excitatory synapses made by PC pyramidal cells on inhibitory interneurons in the PC and OB.

Animals↗
PubMed1994

Differential effects of competitive (CGS19755) and non-competitive (MK 801) NMDA receptor antagonists upon local cerebral blood flow and local cerebral glucose utilisation in the rat.

The effects of the selective non-competitive NMDA receptor antagonist dizocilpine (MK801) and the competitive NMDA receptor antagonist CGS19755 upon local blood flow (lCBF) and local glucose utilisation (lCGU) were examined in 81 neuroanatomically discrete regions of the conscious rat brain using the [14C]iodoantipyrine and [14C]2-deoxyglucose quantitative autoradiographic techniques, respectively. Animals received dizocilpine (0.3 mg/kg), CGS19755 (30 mg/kg) or saline vehicle (2 ml/kg) 10 min prior to the initiation of lCGU studies while blood flow determinations were performed in parallel groups of animals 20 min after drug administration. Dizocilpine significantly increased lCGU in 33 of the 81 regions measured (most notably in cortical and subcortical limbic structures and in the basal ganglia) while reducing glucose use in seven brain areas (frontoparietal and somatosensory cortex, and in areas subserving auditory function). In contrast, CGS19755 significantly reduced lCGU use in 39 of the 81 areas examined while increases were observed in only three areas (anterior piriform cortex, substantia nigra pars reticulata, and posterior thalamic nucleus). Following Dizocilpine administration, there was evidence of widespread (64 of the 81 areas studied) increases in lCBF, while blood flow was reduced in the inferior colliculus. Significant increases in lCBF were also noted in 26 brain areas of CGS19755-treated rats while in one area (flocculus) blood flow was reduced. In saline-treated rats there was a close correlation between lCBF and lCGU. Dizocilpine administration was associated with an increase in the overall lCBF:lCGU ratio from 1.56 ml/mumol (in saline-treated rats) to 2.34 ml/mumol. In some brain areas (CA1 subfield of the dorsal hippocampus, somatosensory cortex and nucleus accumbens) there was evidence of focal disturbances in flow-metabolism relationship. While a similar increase in the overall lCBF-lCGU use ratio was evident in CGS19755 treated animals, there was no evidence of focal uncoupling of the flow metabolism relationship in any of the 81 brain areas examined. These data show that whilst both competitive and non-competitive NMDA receptor antagonists increased cerebral tissue perfusion beyond that required to meet underlying metabolic demand, focal disturbances in the flow metabolism relationship were observed only in dizocilpine-treated rats.

Animals↗
PubMed2004

Response to kainic acid injections: changes in staining for zinc, FOS, cell death and glial response in the rat forebrain.

A pool of zinc is present in synaptic vesicles in a population of glutamatergic neurones. Zinc appears to modulate synaptic transmission and cause neuronal death. The status of vesicular zinc, neuronal death and glial reaction in the rat forebrain was analysed after a systemic injection of kainic acid in order to establish a model for future studies on zinc function. Rats received a systemic injection of kainic acid (10 mg/kg) and were killed 3, 6, 12, 24 and 48 h post-treatment. Timm's method and zinquin staining were used to detect zinc. Immunostaining for Fos-like proteins and staining with Fluoro-Jade B were used to detect cell reaction and degeneration, respectively. Glial fibrillary acidic protein and tomato lectin were used as glial markers. Zinquin staining for zinc rose transitorily in neuronal somata 6 h after injection (not observed at 24-48 h) in the piriform and entorhinal cortices, amygdala and hippocampus. In contrast sulphide/silver staining for zinc showed virtually no rise in cytoplasmic zinc (except in cornus ammonis field 1 of the hippocampus) 6 h after injection, and a decrease (bleaching) in some terminal fields starting 12 h after injection and increasing at 24-48 h. The areas most affected by the zinc bleaching were the olfactory bulb, piriform and entorhinal cortices, endopiriform and amygdaloid nuclei. Transitory Fos immunostaining (within neuronal nuclei) was observed between 3 and 12 h after kainate treatment in many telencephalic areas: olfactory bulb, cortex (piriform, hippocampal and neocortex) and amygdaloid nuclei. This was accompanied by changes in glial markers starting 3 h after injection. Fluoro-Jade B staining in neurones (degeneration) appeared 6 h after treatment and increased later. Degenerating areas generally coincided with those showing Fos immunoreactivity. Zinquin and sulphide/silver methods revealed various pools of zinc after kainate injection: a cytoplasmic pool and a terminal field (or vesicular) pool. Cytoplasmic zinc (zinquin) was coincident, in time and location, with cell degeneration, thus implicating zinc in cell death. This zinc may not have come from presynaptic stores, since no bleaching (sulphide/silver method) was observed 6 h after injection. Future experiments altering zinc pools (e.g. by chelating agents) may elucidate the function of zinc.

Animals↗
PubMed1998

The messenger RNAs for both glial cell line-derived neurotrophic factor receptors, c-ret and GDNFRalpha, are induced in the rat brain in response to kainate-induced excitation.

Glial cell line-derived neurotrophic factor (GDNF) has two receptors, receptor-tyrosine kinase c-ret and glycosylphosphatidylinositol-linked cell surface receptor GDNFRalpha. Kainate-induced seizures, a widely studied model of neuronal plasticity and human epilepsy, have been shown to increase gene expression of several trophic factors, including GDNF, in the rat hippocampus. Here we show that systemic kainate-induced excitation leads to a transient increase of both c-ret and GDNFRalpha messenger RNAs in the rat brain. Northern analysis demonstrated that, in the hippocampus, the maximal 2.5-fold increase of c-ret and four-fold increase of GDNFRalpha messenger RNAs was observed after 12 h of kainate injection, in contrast to GDNF messenger RNA, which reaches its maximum in 4-6 h. The blocking of de novo protein synthesis by cycloheximide inhibited the induction of GDNF receptors by kainate, whereas blocking of the N-methyl-D-aspartate-type glutamate receptors by the antagonist dizocilpine maleate did not significantly alter the response. Thus, GDNF receptor messenger RNA increase by kainate depends on protein synthesis, but is not mediated by the N-methyl-D-aspartate receptor. GDNFRalpha and c-ret show distinct, but partially overlapping, patterns of expression in the brain after kainate treatment. GDNFRalpha messenger RNA was prominently induced in the dentate gyrus of the rat hippocampus, less in the habenular and reticular thalamic nuclei and cerebral cortex as revealed by in situ hybridization. C-ret transcripts were induced in the hilus of the hippocampus, several thalamic and amygdala nuclei and in superficial layers of the piriform cortex. These data suggest that GDNF and its receptors may play a local role in neuronal plasticity and in neuronal protection following epileptic insults.

Animals↗
PubMed1996

Alpha 1B-adrenoceptor-mediated excitation of piriform cortical interneurons.

Pharmacological techniques have defined the existence of two different alpha 1-adrenoceptors, the alpha 1A- and alpha 1B-adrenoceptor subtypes and both of these receptors have been cloned in addition to a cloned alpha 1d-adrenoceptor. A subpopulation of interneurons in layer III of the rat piriform cortex that are excited by 5-hydroxytryptamine (5-HT) via 5-HT2A receptors are also excited by norepinephrine via alpha 1-adrenoceptors. In the present study we determined the pA2 values against the norepinephrine-mediated excitation of piriform cortical interneurons for a number of antagonists that are (1) not selective for alpha 1A- or alpha 1B-adrenoceptors (prazosin), (2) selective for alpha 1A-adrenoceptors (5-methyl urapidil, 2-(2,6-dimethoxy-phenoxyethyl)- aminomethyl-1,4-benzodioxane hydrochloride (WB 4101), benoxathian, phentolamine) and (3) selective for alpha 1B-adrenoceptors (spiperone and risperidone). The pA2 values for the antagonist blockade of norepinephrine-mediated interneuron excitation were significantly correlated to literature values for the pKi values of antagonist binding to the alpha 1B-adrenoceptor (r = 0.919) and the cloned alpha 1b-adrenoceptor (r = 0.849) but were not correlated to the pKi values of antagonist binding to the alpha 1A-adrenoceptor or the cloned alpha 1a- and alpha 1d-adrenoceptor. Thus, we conclude that this population of piriform cortical interneurons is excited by norepinephrine via alpha 1B-adrenoceptors.

Action Potentials↗
PubMed1988

Current generators and properties of late components evoked in rat olfactory cortex.

Following main olfactory bulb (MOB) stimulation at frequencies of 0.1-0.3 Hz, in addition to early field potentials, a frequency-sensitive, surface negative late N2 wave (latency range: 63-96 msec) followed occasionally by a late N3 transient, was evoked in the piriform cortex and endopiriform nucleus of the rat. The N2 wave inverted polarity at the Ib-II cortical layer interface (P2 wave) and was associated with late unit discharges 200 to 1200 microns deep to the turnover point. Response probability, peak latency, recovery curve and frequency-sensitivity of the P2 wave were not significantly different in animals under urethane or pentobarbital. Current-source-density (CSD) analysis revealed that the N2 wave generators were localized to the Ib-II layer interface. Since inhibitory activity does not contribute substantially to the second derivative curve, CSD analysis strengthens the assumption that late components (LCs) are excitatory events (compound EPSPs) presumably generated on the proximal apical dendritic segments of pyramidal cells by association axons. The early "b" wave in a test response was facilitated, rather than occluded, when a LC was present in the conditioning response, or when the priming volley was delivered to the mediodorsal thalamic nucleus. Clustering of unit and field activity in two distinct periods of the evoked response separated by a prolonged interval of cell silence suggests that cortical coding of olfactory cues might be more efficiently achieved by temporal modulation of the neuronal response rather than by spatial distribution of firing patterns.

Animals↗