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PubMed1996

The ontogeny of a neurotoxic lesion in rat brain revealed by combined MRI and histology.

We have used magnetic resonance imaging (MRI) of the living rat brain to longitudinally analyze the ontogenesis of an ibotenic acid lesion targeted at the piriform cortex. The MRI data were systematically compared with data obtained from a battery of histopathological techniques, including Nissl stain, hematoxylin stain, and a stain for cytochrome oxidase activity. Two days after the lesioning, widespread and heterogeneous damage was detected in, around and distant from the toxin-targeted area. Some damage apparently diminished within approximately 10 days, whereas other damage remained throughout the length of this study (60 days). We found that the small-animal MRI technology used by us is useful in determining the initial, transient impact of surgery and neurotoxic lesioning, and in delineating the gross effects of the lesion over time. This is particularly useful for early elimination of animals from the protocol of physiological and behavioral experiments in which the lesion exceeds the target area. Our data also indicate that, in order to avoid confounding effects of transient post-lesioning phenomena, behavioral and physiological tests should be carried out in neurotoxically lesioned animals > 2 weeks after infliction of the lesion.

Animals↗
PubMed1996

The anticonvulsant action of fluoxetine in substantia nigra is dependent upon endogenous serotonin.

Fluoxetine, a serotonin (5-HT) reuptake inhibitor, has been documented to exert a protective action against convulsive seizures in animal models, when administered either systemically, or focally into substantia nigra. It is likely that the mechanism of anticonvulsant action of fluoxetine is due to an enhancement of endogenous 5-HT transmission. To evaluate this possibility in the context of the anticonvulsant action of intranigral fluoxetine, we examined the influence of 5-HT-mediated transmission in substantia nigra on seizure susceptibility in a rat model of focally evoked complex partial seizures. In addition to fluoxetine (3.5 nmol), we found that the directly acting 5-HT receptor agonists, 1-[3-(trifluoromethyl)phenyl]piperazine (TFMPP) (10 nmol), 1-(3-chlorophenyl)piperazine (m-CPP) (7.4 nmol), gepirone (70 nmol) and 2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronaphthalene hydrobromide (8-OH-DPAT) (10 nmol), when microinjected bilaterally into substantia nigra, protected rats from limbic motor seizures evoked focally from area tempestas, an epileptogenic site in the deep rostral piriform cortex. This indicates that multiple 5-HT receptor subtypes in substantia nigra may contribute to seizure regulation. Consistent with this, the 5-HT antagonist, metergoline, partially reversed the anticonvulsant action of intranigral fluoxetine. Depletion of endogenous 5-HT, by pretreatment with parachlorophenylalanine (PCPA), completely prevented the anticonvulsant action of intranigral fluoxetine, without modifying the anticonvulsant effect of intranigral TFMPP. These findings support the proposal that the anticonvulsant action of fluoxetine in substantia nigra is due to an enhancement of the synaptic action of endogenous 5-HT in substantia nigra which in turn is mediated via multiple 5-HT receptors. Endogenous 5-HT transmission in substantia nigra is therefore capable of limiting the development and propagation of seizure activity generated in limbic circuits.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Kindling antagonism: interactions of the amygdala with the piriform, perirhinal, and insular cortices.

We employed the kindling antagonism paradigm to characterize the role of the amygdala (AM), piriform cortex (PIR), perirhinal cortex (PRH), and insular cortex (INS) in the propagation and expression of generalized seizures. Alternating kindling stimulation was delivered to the AM and either the PIR, PRH, or INS. We found that kindling from the AM was retarded by stimulation only of the deep layers of both the INS and anterior PRH. Kindling antagonism was specific to the anterior cortical regions, since neither the posterior PRH or PIR were capable of antagonizing AM kindling. The results strongly implicate the deep layers of anterior limbic cortex in establishment of antagonism of AM kindling.

Amygdala↗
PubMed1983

Pharmacology of dopamine neurons innervating the prefrontal, cingulate and piriform cortices.

The pharmacology of a number of distinct dopamine (DA) systems was studied. Those DA projections possessing autoreceptors (striatum, olfactory tubercle and piriform cortex) exhibited large changes in DA metabolism in response to systemic administration of DA agonists and antagonists. In contrast, in those DA systems which lack autoreceptors (the prefrontal and cingulate cortical innervations) little or no response to DA agonists and a diminished response to DA antagonists was seen. When DA metabolism was inhibited by administration of a MAO inhibitor, reductions in HVA were observed in all brain regions studied. DA turnover appeared faster in the prefrontal and cingulate cortices than in the DA systems possessing autoreceptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam.

Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself.

Animals↗
PubMed1990

Effect of selective bilateral destruction of the substantia nigra on antiepileptic drug actions in kindled rats.

The substantia nigra (SN) is thought to be involved in the regulation of seizure activity and there is evidence that the nigra might be a site of anticonvulsant drug action, especially in the case of drugs that act by potentiating gamma-aminobutyric acid (GABA)-mediated neurotransmission. The current studies monitored the anticonvulsant effect of four major antiepileptic drugs, i.e. valproic acid, carbamazepine, phenobarbital and diazepam, in fully kindled rats before and after bilateral destruction of the SN. Rats were kindled by stimulation of either the basolateral amygdala or the piriform cortex. The SN was lesioned bilaterally by microinjection of ibotenic acid, and only animals with near-complete, selective destruction of the SN were used for final evaluation of the anticonvulsant drug experiments. The behavioural characteristics and the duration of fully kindled seizures were not altered by bilateral destruction of the SN. Phenobarbital, diazepam and valproate significantly reduced kindled seizures severity and duration before and after the SN lesions. Carbamazepine was the only drug to show a marked decrease in its anticonvulsant effects after SN lesion. Since benzodiazepines, valproate and phenobarbital are though to enhance GABAergic transmission, the lack of effect of SN lesions on the anticonvulsant effects of these drugs argues against the suggestion that the SN is the anatomical site responsible for exerting anticonvulsant effects in response to drug-induced augmentation of GABA transmission.

Amygdala↗
PubMed1990

Effects of 5-HT1A receptor agonists on hypothalamo-pituitary-adrenal axis activity and corticotropin-releasing factor containing neurons in the rat brain.

Corticotropin-releasing factor (CRF) is the major physiological regulator of the hypothalamo-pituitary-adrenal axis. There is evidence that CRF release from the hypothalamus is under stimulatory serotonergic control. The specific 5-HT receptor subtypes that mediate this effect is unclear. Administration of the 5-HT1A agonists, 8-OH-DPAT (1 mg/kg) and ipsapirone (4 mg/kg), to rats resulted in activation of the HPA axis as evidenced by increased plasma ACTH and corticosterone concentrations in acutely treated rats and increased plasma corticosterone concentrations in both acutely and chronically treated rats. However, chronic administration of these compounds failed to alter CRF concentrations in the medium eminence or CRF receptor number of affinity in the anterior pituitary. Chronic administration of both compounds resulted in increased CRF concentrations in the piriform cortex and hippocampus, whereas 8-OH-DPAT alone increased CRF concentrations in the amygdala and entorhinal cortex. These results suggest that both hypothalamic and extrahypothalamic CRF neurons are influenced by activation of 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Peripheral injection of arginine8-vasopressin increases Fos in specific brain areas.

Learned behaviors and tolerance to ethanol can be maintained by peripheral injection of arginine8-vasopressin (vasopressin) under conditions in which they would otherwise be lost. However, the sites of this action in the brain have not been clearly identified. Using a polyclonal antibody raised against Fos and Fos-like proteins, we have demonstrated increases in immunoreactive Fos and Fos-like proteins in the suprachiasmatic, supraoptic and paraventricular nuclei of the hypothalamus, and lesser increases in piriform cortex and amygdala, of the rat 2 h after a s.c. injection of vasopressin. Our results suggest that the exogenous vasopressin may exert its central action by activating a cellular immediate early gene in specific brain regions.

Animals↗
PubMed1992

Changes in polyamine levels and spectrin degradation following kainate-induced seizure activity: effect of difluoromethylornithine.

The induction of ornithine decarboxylase (ODC) in adult CNS and the resulting changes in polyamine levels are often observed under conditions associated with activation of NMDA receptors, calpain stimulation and spectrin degradation. The present study was directed at evaluating the links between these two sets of events. We measured the effects of an acute treatment of adult rats with difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, on biochemical alterations following kainate-induced seizure activity. Beside ODC activity and polyamine levels, we assayed the in situ spectrin degradation and the in vitro binding of 3H-Ro5-4864, a ligand for the peripheral benzodiazepine binding sites which is a good marker of glial proliferation, at various time intervals following systemic kainic acid (KA) injection. Kainate-induced seizure activity was followed by a transient increase in ODC activity, a long-lasting increase in putrescine levels and spectrin degradation, and a delayed increase in 3H-Ro5-4864 binding, mainly in hippocampus and piriform cortex. Treatment of the animals with DFMO markedly reduced the increase in putrescine levels up to 7 days after KA injection. It also reduced the increase in spectrin breakdown observed at 16 h but not at 4 and 7 days after KA injection. Finally, it did not modify the increase in 3H-Ro5-4864 binding measured 4 and 7 days after KA injection. The levels of putrescine were positively correlated with the extent of spectrin proteolysis in KA-treated animals whether or not they were treated with DFMO, at 16 h but not at 7 days after KA injection. The results indicate that the extent of spectrin breakdown observed shortly after KA-induced seizure activity is causally related to the changes in ODC activity and putrescine levels. Although the data are consistent with the idea that putrescine could be a marker for acute pathology, they do not support a role for polyamines in delayed neurotoxicity.

Animals↗
PubMed1995

Short-term effects of perinatal asphyxia studied with Fos-immunocytochemistry and in vivo microdialysis in the rat.

In the present study, the short-term consequences of various perinatal asphyctic periods were studied at the peripheral and CNS levels in the rat. Perinatal asphyxia was induced in rat pups delivered by caesarean section within the last day of gestation, by placing the uterus horns including the fetuses in a water bath at 37 degrees C for various periods of time (0-23 min). Following asphyxia, the uterus horns were opened. The pups were then removed and stimulated to breathe. Subcutaneous levels of pyruvate (Pyr), lactate (Lact), glutamate (Glu), and aspartate (Asp) were monitored with microdialysis 40 min after delivery. In parallel experiments, the pups were sacrificed 80 min after delivery. The brains were removed, fixed, cut, and processed for Fos immunocytochemistry. The number of Fos-immunoreactive (IR) cells in different brain structures was counted under light microscopy. Subcutaneous levels of Pyr, Lact, Glu, and Asp increased following perinatal asphyxia, as compared to caesarean-delivered pups or to spontaneously delivered controls. A maximum increase in Pyr levels (approximately threefold) was observed with 2-3 min of asphyxia, while Lact levels increased along with the length of asphyxia. A maximum increase in Glu and Asp levels (approximately threefold) was observed with 10-11 min of asphyxia. Fos-IR nuclei were predominantly found in the piriform cortex, and in the cortical amygdaloid complex. In some cases, mainly in pups exposed to asphyxia, Fos-positive cells were also seen in other tele-diencephalic structures.

Amino Acids↗
PubMed1995

Expression of the mouse and rat mas proto-oncogene in the brain and peripheral tissues.

We isolated the mas proto-oncogene from a mouse genomic library. Sequence analysis showed that it contains an open reading frame without intervening sequences. The amino acid sequence deduced confirms the seven-transmembrane-domain structure and exhibits 97% and 91% amino acid homology with the rat and the human Mas, respectively. In mice and rats, mas mRNA was detected in the testis, kidney, heart, and in the brain regions: hippocampus, forebrain, piriform cortex, and olfactory bulb. Testicular mas mRNA from rats increases markedly during development, while cerebellar mRNA is high postnatally but completely disappears at later stages. We conclude that the product of the mouse mas gene may be involved in the development of the brain and testis.

Amino Acid Sequence↗
PubMed1995

Cloning, functional expression and mRNA distribution of an inwardly rectifying potassium channel protein.

In GH3/B6 cells at least two different inward K+ currents are observed that are regulated by thyrotropin-releasing hormone and somatostatin, respectively. Using a polymerase chain reaction based approach a cDNA was isolated and functionally expressed in human embryonic kidney cells that encodes an inward rectifier K+ channel, rIRK3, with a predicted molecular mass of 49.7 kDa. Corresponding transcripts of 2.6 kb have been detected in rat brain, pituitary and GH3/B6 cells. In situ hybridization revealed that rIRK3 mRNA is distributed throughout the brain and occurs predominantly in the piriform cortex, indusium griseum, supraoptic nucleus, facial nucleus and cerebellar Purkinje cells.

Amino Acid Sequence↗
PubMed1996

Differential distribution of classical inwardly rectifying potassium channel mRNAs in the brain: comparison of IRK2 with IRK1 and IRK3.

Distribution of IRK2 inwardly rectifying potassium channel mRNA in the mouse brain was studied using in situ hybridization histochemistry and compared with those of other classical inwardly rectifying potassium channel (IRK1 and IRK3) mRNAs. All these IRK channel mRNAs were detected in neurons, but not in glial cells. Their distribution patterns in the brain were, however, quite divergent: IRK2 mRNA was detected extremely high in granule cells of cerebellum, relatively high in motor trigeminal nucleus and moderate in olfactory bulb, piriform cortex, cerebral cortex, CA1 through CA3 regions of hippocampus, dentate gyrus and pontine nucleus. On the other hand, IRK1 mRNA was expressed throughout whole brain but in particular subsets of neurons, and IRK3 mRNA was in forebrain. Expression of these three IRK mRNAs overlapped in hippocampus, olfactory bulb, and cerebral cortex. This differential distribution of IRK mRNAs suggests that each of these channels has its specific function in regulation of the excitability of brain neurons.

Animals↗
PubMed1995

Elemental imbalances in the olfactory pathway in Alzheimer's disease.

Concentrations of 11 trace elements were determined in 56 control and 98 Alzheimer's disease (AD) olfactory bulb, olfactory tract, olfactory trigone, piriform cortex and amygdala specimens by instrumental neutron activation analysis. Iron and zinc were significantly elevated and bromine was significantly depleted in olfactory regions of AD patients, compared with normal age-matched control subjects. Elevated iron could possibly play a role in neuronal degeneration in AD by enhancing reactive free radical formation.

Aged↗
PubMed1993

Differential effects on GABAA receptor gamma 2-subunit messenger RNA by tolerance to and withdrawal from pentobarbital--an in situ hybridization study.

The heterogeneity of the GABAA receptors has been confirmed structurally and functionally. The present study demonstrates the pharmacological heterogeneity of the GABAA receptors. Rats were rendered tolerant to pentobarbital by continuous intracerebroventricular infusion via osmotic minipumps and abruptly withdrawn from pentobarbital. In situ hybridization of mRNA coding for the GABAA receptor gamma 2-subunit showed decreases of mRNA levels in superior and inferior colliculus in pentobarbital tolerant rats compared to rats in withdrawal. In rats 24-hr after withdrawal from pentobarbital, increases of mRNA levels in neocortex, piriform cortex and in granular and Purkinje cell layers of the cerebellum were observed. These results indicate the fast adaptation of GABA synapses in response to abrupt withdrawal from chronic pentobarbital treatment. The differential responsiveness seen in different areas further confirms the pharmacological heterogeneity of the GABAA receptors. The observed increases and decreases of mRNA may underlie, at least in part, the previously reported changes in Bmax of GABAA receptor ligand binding sites.

Animals↗
PubMed1984

Changes in immunoreactive somatostatin in brain following lidocaine-induced kindling in rat.

The kindling phenomenon has become a useful model for studying epileptogenesis. The present authors have previously reported increased levels of immunoreactive somatostatin (IR-SRIF) in various regions of the brain of electrically-amygdaloid kindled (EAK) rats. In this study, an examination was made of immunoreactive somatostatin in pharmacologically-kindled (PK) rats. Sixteen male Sprague-Dawley rats were injected intraperitoneally (i.p.) with a subthreshold dose of lidocaine (60 mg/kg), once daily. Once the kindling phenomenon was established, kindled rats (7), non-kindled rats (9) and controls (6) were sacrificed by microwave irradiation. Another group of 5 rats was injected with a single suprathreshold dose of lidocaine (110 mg/kg) and killed 10 min after the resultant seizure. Various brain areas were removed and assayed for immunoreactive somatostatin in kindled rats. Immunoreactive somatostatin was significantly greater than in controls in the amygdala (56%; P less than 0.02), entorhinal + piriform cortex (50%; P less than 0.05) and hypothalamus (29%; P less than 0.02). In non-kindled rats, immunoreactive somatostatin increased only in the amygdala (58%; P less than 0.02). No difference was found in the immunoreactive somatostatin content of rats injected with an suprathreshold dose of lidocaine compared to controls. The alteration of immunoreactive somatostatin, in both lidocaine-kindled and electrically-amygdaloid kindled rats suggests a possible role of this neuropeptide in kindling.

Amygdala↗
PubMed1979

Functional development of dopamine receptors in the rat forebrain.

Dopamine (DA) was injected unilaterally into the dorsal caudate-putamen (D-CPU), ventral caudate-putamen (V-CPU), piriform cortex (PIR), olfactory tubercle (OTU) and frontal cortex (FC) of two day old rats and rotational behavior observed. Injection of DA into D-CPU, PIR, and OTU produced a contralateral postural deviation which differed significantly from the ipsilateral deviation produced by control injections. Only DA injections into PIR and OTU produced contralateral turning differing significantly from the effects of control injections. These results suggest that the DA receptors in C-CPU, PIR, and OTU involved in rotational behavior are functionally mature at two days of age and that the two components of rotation, postural deviation (direction) and turning (locomotion), involve different neural systems at this age. The developing rat is suggested as a valuable tool for understanding the neural circuitry and pharmacology of rotational behavior.

Animals↗
PubMed1991

Autoradiographic analysis of the in vivo distribution of 3H-imipramine and 3H-desipramine in brain: comparison to in vitro binding patterns.

Using high resolution autoradiographic techniques, the distribution of radioactivity in forebrain and brainstem was assessed after IV injection of 3H-impramine or 3H-desipramine. Results were compared with regional binding of the drugs to brain sections in vitro. Similar topographic binding of 3H-imipramine and 3H-desipramine was observed in vitro among brain regions, except in the paraventricular nucleus of the hypothalamus and locus coeruleus, where binding was greater for 3H-desipramine. For both 3H-desipramine and 3H-imipramine, some brain regions that exhibited high binding in vitro also showed high accumulation after in vivo injection. However, certain regions that contained high densities of binding sites for the antidepressant drugs as measured by in vitro binding showed very low accumulation of radioactivity after in vivo treatment. Such regions included the dentate gyrus of the hippocampus, layer 1 of piriform cortex, caudate-putamen, pontine and midbrain central gray, and cerebellar granular layer. Compared to in vitro binding of the drugs, the distribution of imipramine and desipramine in vivo appears more anatomically selective. For imipramine, primary sites of action in vivo, as indicated by the topographic distribution in brain, appear to be the locus coeruleus, hippocampus, lateral septal nucleus, and amygdala. For desipramine, the greatest accumulation in vivo was found in the locus coeruleus, paraventricular nucleus of the hypothalamus, and anterior thalamic nuclei.

Animals↗