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PubMed1999

Interactions between limbic, thalamo-striatal-cortical, and central autonomic pathways during epileptic seizure progression.

We used immunocytochemistry to determine the regional and temporal distribution of Fos protein expression in awake and unrestrained rats after a unilateral stereotaxic microinjection of a cholinergic agonist, carbachol, in the thalamic ventroposterolateral and reticular nuclei, previously shown to cause limbic and generalized convulsive seizures. The microinjection of carbachol elicits behavioral alterations including immobilization, staring, facial and jaw clonus, rearing, and falling, followed by recurrent generalized convulsive seizures, and a pattern of c-fos expression throughout the brain. In addition to the hypothalamic paraventricular and supraoptic nuclei, the initial induction of c-fos expression was observed as early as 15 minutes after the carbachol microinjection, in the piriform and entorhinal cortices, the thalamic paraventricular, the supramammilary, the lateral parabrachial nuclei, and the central gray. From 30 minutes to 2 hours, corresponding to the occurrence of motor expression of limbic and recurrent generalized convulsive seizures, Fos immunoreactivity was seen in a number of functionally related brain regions including the hippocampus, the amygdala, and the anterior thalamic nucleus (limbic system); the thalamus, the basal ganglia, and the cortex (thalamo-striatal-cortical system); and the hypothalamus, the central nucleus of the amygdala, the pons, and the medulla (central autonomic system). On the basis of the present results showing regional and temporal c-fos expression and well known neuroanatomical connections, we have constructed a neural network relating the limbic, thalamo-striatal-cortical, and central autonomic systems. This analysis provides, for the first time, neuronal circuits and pathways relating epilepsy-elicited behavioral expression of convulsive seizures and adaptive homeostatic responses and could serve as a basis for studying central autonomic regulation during epileptic disorders.

Acetylcholine↗
PubMed1999

Localization and expression of Jun-like immunoreactivity in apoptotic neurons induced by colchicine administration in vivo and in vitro depends on the antisera used.

The expression of members of the Jun family of transcription factors was examined by immunohistochemistry, Western blotting, in situ hybridization and Northern blotting in the developing and adult rat brain following colchicine administration. Apoptotic cells, as revealed by their typical morphology and positive staining with the method of in situ end-labeling of nuclear DNA fragmentation, were restricted to granule cells of the dentate gyrus and olfactory bulb, and a few cells in the upper layers of the entorhinal cortex in adult rats, whereas widespread apoptosis occurred in developing rats after colchicine administration. No modifications in the expression of Jun D and Jun B, except for a generalized and moderate Jun B expression in glial cells, were observed in colchicine-treated rats. Generalized and strong c-jun mRNA induction and c-Jun/AP-1 (Ab-1) protein expression was observed in the cerebral neocortex, entorhinal and piriform cortices, CAI and CA3 areas of the hippocampus and granule cell layer of the dentate gyrus in adult treated rats, thus indicating a generalized c-Jun response to colchicine administration. In contrast, c-Jun/AP-1 (N) and c-Jun/AP-1 (Ab-2) immunoreactivity was restricted to apoptotic cells in colchicine-treated adult and developing brains. Western blots of hippocampal homogenates and total brain homogenates in adult and developing rats, respectively, demonstrated a band of 39 kDa for the c-Jun/AP-1 (Ab-1) antibody in control animals, the intensity of which increased in colchicine-treated rats. However, a band of 37 kDa, the intensity of which also increased following colchicine administration, was observed for the c-Jun/AP- (N) and c-Jun/AP- (Ab-2) antibodies. Selective c-Jun/AP-1 (N) and c-Jun/AP-1 (Ab-2) expression was also observed in apoptotic cells of the SH-SY5Y neuroblastoma line after the addition of colchicine to the culture medium. Taken together, the present in vivo and in vitro results indicate a generalized c-Jun response to colchicine in sensitive cells, whereas the antibodies c-Jun/AP- (N) and c-Jun/AP-1 (Ab-2) recognize vulnerable cells dying via apoptosis.

Aging↗
PubMed1996

Lack of Fos-like immunoreactivity after spontaneous seizures or reinduction of status epilepticus by pilocarpine in rats.

Acute seizures and status epilepticus induced by pilocarpine lead to the expression of Fos-like immunoreactivity in several specific brain areas in a manner similar to that of other models of limbic seizures. Upon development of status epilepticus after systemic pilocarpine injection, animals develop a state where chronic spontaneous seizures recur. Assessment of Fos-like immunoreactivity after such spontaneous seizures or after status epilepticus reinduction reveals either lack of staining or a weak reaction in a few brain areas including the ventral tip of the dentate gyrus, prepiriform, lateral piriform and perirhinal cortices, and scattered locations throughout temporal neocortex. Our results suggest that status epilepticus induction may lead to a long-lasting state of Fos down-regulation.

Animals↗
PubMed1988

Immunocytochemical localization of protein kinase C isozymes in rat brain.

Recently, we isolated 3 protein kinase C (PKC) isozymes from rat brain (Huang et al., 1986a). Using isozyme-specific antibodies for immunoblot, we have determined the relative levels of each isozyme in various regions of the rat brain (Huang et al., 1987b). The present paper describes the cellular distributions of PKC isozymes in rat brain as determined by light microscopic immunocytochemistry. Staining with PKC antibodies revealed strong immunoreactivities in neuronal somata and their dendrites and weak to no reaction in axon and the astroglial structures. In the cerebellum, the type I PKC antibodies stained the Purkinje cell bodies and dendrites; the type II PKC antibodies stained the granule cells; and the type III PKC antibody stained both Purkinje and granule cells. In the cerebral cortex, all antibodies stained neurons resembling pyramidal cells and their apical dendrites in layers II to VI, while layer I was nearly devoid of staining. However, the various isozyme-specific antibodies revealed distinct laminar distribution patterns of the positively stained neurons, and the type III PKC-positive neurons exhibited a higher density than those of type I or II PKC-positive ones, especially in layer II of cingulate (retrosplenial) and piriform cortices. In the hippocampal formation, both pyramidal cells of the hippocampus and granule cells of the dentate gyrus were stained by all PKC antibodies. Subcellularly, type III PKC appeared mostly in the cytoplasm of these neurons, whereas type I and II PKC seemed to associate with the nucleus as well. In the olfactory bulb, both type II and III PKC antibodies stained the periglomerular and granular cells, and the latter also stained the mitral cells. The distinct cellular and subcellular distribution of PKC isozymes suggests that each isozyme plays a unique role in the various neural functions.

Animals↗
PubMed2002

Artificial rearing causes changes in maternal behavior and c-fos expression in juvenile female rats.

This study investigated the effects of early-rearing experiences on responsiveness to pups and on the pattern of c-fos activation in the brain of juvenile female rats. From Days 4 to 20, littermate females were reared with their mothers (MR) or artificially (AR). AR rats received minimal licking-like tactile stimulation (AR-min) or maximal stimulation (AR-max). On Day 20, rats were exposed to pups for 4 or 8 days, exposed to a playmate for 4 or 8 days, or left in isolation for 4 or 8 days. Compared with MR rats, pup-exposed AR rats engaged in less pup licking, and all AR rats showed significant reductions in c-fos immunoreactivity in the medial preoptic area and the parietal and piriform cortices. The AR-min group showed the greatest difference in Fos-lir compared with the MR groups. Possible mechanisms that mediate the effects of rearing on the development of neural circuits underlying maternal behavior are discussed.

Animals↗
PubMed1997

Sex hormones enhance the impact of male sensory cues on both primary and association cortical components of visual and olfactory processing pathways as well as in limbic and hypothalamic regions in female sheep.

Differential activation of neural substrates was investigated in female sheep exposed to a male when they were in oestrus, and sexually receptive and attracted to males, as opposed to anoestrus when they were not. Changes in neuronal activation were visualized in ovariectomized, hormone-treated ewes by quantifying changes in cellular expression of c-fos messenger RNA by in situ hybridization histochemistry. Results showed that, while oestrus induction had no significant effects on c-fos expression per se, a 5-min exposure to a male significantly increased it in a number of primary and association cortical regions (the mitral and granule cell layers of the olfactory bulb, visual, somatosensory, orbitofrontal, piriform, cingulate and temporal cortices), the limbic system (CA1 region of the hippocampus, subiculum, lateral septum, lateral and basolateral amygdala, bed nucleus of the stria terminalis) and hypothalamus (mediobasal hypothalamus, medial preoptic area and paraventricular nucleus) as well as the nucleus accumbens and mediodorsal thalamus. Intromissions did not contribute significantly to these c-fos changes however. In anoestrus females, exposure to a male only produced a small significant increase in c-fos messenger RNA expression in the temporal cortex inspite of receiving similar amounts of visual and olfactory cues from him and a number of mating attempts. These results clearly demonstrate that changes in sexual motivation markedly alter the neural processing of sensory cues from males. They also show that the hormonal induction of sexual attraction to males cues and the resultant stimulation of sexual behaviour is due not only to altered responsiveness of oestrogen-sensitive brain regions involved in mediating behavioural responses towards the male, but also to changes in primary and secondary/tertiary somatosensory, olfactory and visual processing regions which relay sensory information to them.

Animals↗
PubMed2002

Magnetic resonance imaging in the study of the lithium-pilocarpine model of temporal lobe epilepsy in adult rats.

PURPOSE: In temporal lobe epilepsy, it remains to be clarified whether hippocampal sclerosis is the cause or the consequence of epilepsy. We studied the temporal evolution of the lesions in the lithium-pilocarpine model of epilepsy in the rat with magnetic resonance imaging (MRI) to determine the progressive morphologic changes occurring before the appearance of chronic epilepsy. METHODS: MRI was performed on an MR scanner operating at 4.7 T. We followed the evolution of lesions using T(2)- and T(1)-weighted sequences before and after the injection of gadolinium from 2 h to 9 weeks. RESULTS: At 2 h after status epilepticus (SE), a blood-brain barrier breakdown could be observed only in the thalamus; it had disappeared by 6 h. At 24 h after SE, edema was present in the amygdala and the piriform and entorhinal cortices together with extensive neuronal loss; it disappeared progressively over a 5-day period. During the chronic phase, a cortical signal reappeared in all animals; this signal corresponded to gliosis, which appeared on glial fibrillary acidic protein (GFAP) immunohistochemically stained sections as hypertrophic astrocytes with thickened processes. In the hippocampus, the correlation between histopathology and T(2)-weighted signal underscored the progressive constitution of atrophy and sclerosis, starting 2 days after SE. CONCLUSIONS: These data show the reactivity of the cortex that characterizes the initial step leading to the development of epilepsy and the late gliosis that could result from the spontaneous seizures. Moreover, it appears that hippocampal sclerosis progressively worsened and could be both the cause and the consequence of epileptic activity.

Animals↗
PubMed1989

Distribution of dopamine D1 and D2 receptors in rabbit cortical areas, hippocampus, and neostriatum in relation to dopamine contents.

The densities of dopamine D1 and D2 receptors were measured by using [3H]SCH23390 and [3H]raclopride, respectively, in the rabbit cingulate, visual, sensorimotor, and entorhinal-piriform cortical areas; the dorsal and ventral hippocampus; and the putamen as well as the medial and lateral caudate. Endogenous dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), 4-hydroxy-3-methoxyphenylacetic acid (HVA), and 3-methoxytyramine (3-MT) were assayed by HPLC with electrochemical detection. The distributions of [3H]SCH23390 and [3H]raclopride binding were heterogenous with the greatest densities in the neostriatum. The concentrations of DA and its metabolites were also highest in this structure. Regions with low DA content, i.e., cortex and hippocampus, had lower densities of [3H]SCH23390 and [3H]raclopride binding. Furthermore, these sites were differentially localized within the various regions and there were substantially more D1 than D2 receptors. The functional significance and heterogeneities in the distribution of D1 and D2 receptors are discussed in relation to the dopaminergic innervation and the turnover estimated by the ratios between endogenous DA and its metabolites.

Animals↗
PubMedDate not supplied

Necrosis of hippocampus and piriform lobe in 38 domestic cats with seizures: a retrospective study on clinical and pathologic findings.

The clinical records of 38 cats (1985-1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age 35 months) and had either generalized or complex-partial seizures of acute onset and rapid progression. The seizures had a tendency to become recurrent and to present as clusters or even status epilepticus later in the course of the disease. Fourteen cats died spontaneously, and 24 were euthanized. Histopathologic examination revealed bilateral lesions restricted to the hippocampus and occasionally the lobus piriformis. The lesions seemed to reflect different stages of the disease and consisted of acute neuronal degeneration to complete malacia, affecting mainly the layer of the large pyramidal cells but sometimes also the neurons of the dentate gyrus and the piriform lobe. The clinical, neuropathologic, and epidemiologic findings suggest that the seizures in these cats were triggered by primary structural brain damage, perhaps resulting from excitotoxicity. The cause remains unknown, but epidemiologic analysis suggests an environmental factor, probably a toxin.

Animals↗
PubMed1997

Regulation of central serotonin transporters by chronic lithium: an autoradiographic study.

The objectives of this study were to further characterize the effects of a chronic lithium (Li+) treatment on serotonin (5-HT) uptake sites, and to determine the eventual reversibility of the observed effects. Quantitative autoradiography experiments were carried out on sections from rat brain, using [3H]citalopram to label selectively the 5-HT transporters or uptake sites. In these experiments, we were able to saturate the 5-HT transporters using an isotopic dilution of the radioligand. The lowest densities of [3H]citalopram binding were measured in all cortical regions studied, with the highest cortical labelling in the anterior cingulate cortex. The rostral neostriatum presented a moderate density of labelling, with slightly higher levels in its ventral portion. Relatively high densities were measured in the globus pallidus, hippocampus, and hypothalamus. Finally, the highest densities were found in the brain stem. Indeed, the dorsal raphe nuclei as well as the substantia nigra were characterized by very high amounts of [3H]citalopram binding. The chronic administration of Li+ increased the density of 5-HT uptake sites in cortical regions, and significant differences were observed in the frontal, temporal, and entorhinal-piriform cortices, with an elevation, albeit not significant, in the anterior cingulate region. A significant increase was also observed in the lateral hypothalamus. Since the 5-HT uptake sites were studied with saturating concentrations of citalopram, we can propose that this increase in binding densities can be attributed to an increase in the number of 5-HT transporters. Interestingly, the only modifications observed were located in regions containing nerve terminals of 5-HT neurons, while regions with cell bodies remained unaffected. Moreover, these effects were completely reversed following a recovery of 48 h without Li . Also, there were no modifications in the density of 5-HT uptake sites after only 2 days of Li+. These results, suggesting an anatomically heterogenous increase in 5-HT uptake in chronically treated rats, are in accord with clinical observations and previous reports with homogenate binding assays. Finally, the conclusions from this study further support the importance of central 5-HT synaptic transmission in the pathophysiology and treatment of human affective disorders.

Animals↗
PubMed2006

Role of CNS alpha1-adrenoceptor activity in central fos responses to novelty.

The present study investigated, by use of fos immunohistochemistry, whether the functional activity of alpha(1)-adrenoceptors is elevated during heightened behavioral activity in brain regions shown earlier to contain motoric alpha(1)-receptors. In confirmation, marked c-fos responses that were blocked by an alpha(1)-antagonist (prazosin) were found in four of these brain regions (secondary motor, cingulate, piriform cortices, and nucleus accumbens) of animals exposed to a mildly novel environment (clean cage), which elicits a high degree of sustained exploratory activity. Experimental restriction of exploratory activity in the novel cage by a small enclosure did not reduce the fos responses in these areas, and in fact, enhanced gene expression when carried out in home-caged animals suggesting that the fos response may be more closely associated with the motivation to be active rather than activity itself. Experiments with locally administered alpha(1)-agonists and antagonists in the cortex by reverse dialysis showed that the above mentioned alpha(1)-dependent-fos responses were the result of activation of local alpha(1)-receptors in these brain regions. Unlike the aforementioned brain regions, the fos response of the locus coeruleus was not blocked by prazosin, and this nucleus also showed a marked fos increase to prazosin itself possibly as a compensatory response to the blockade of forebrain alpha(1)-receptors.

Adrenergic alpha-Antagonists↗
PubMed1996

Differential sensitivity of various temporal lobe structures in the rat to kindling and status epilepticus induction.

Using focal brain stimulation (kindling), discrete seizures can be triggered from many neuroanatomic sites with varying degrees of facility. From several of these sites, protracted seizures or status epilepticus (SE) also can be triggered. To date, no comparison has been made between different brain sites in their sensitivity both to kindling and to SE development. In this report, we have compared the kindling profiles of three amygdala nuclei, namely the basal (BL), central (CE), and medial (ME) nuclei, to the adjacent piriform (PIR) and perirhinal (PRH) cortices. In addition, three weeks following kindling, the susceptibility of each kindled site to status epilepticus (SE) was assessed by exposing the site to 60 min of electrical stimulation. We observed that (a) during the course of daily kindling, the afterdischarge threshold dropped progressively and significantly in all structures, (b) the rate of kindling in the PRH and PIR cortices and the CE amygdala was significantly faster than either the BL or ME amygdala, (c) when discrete convulsions were triggered, the latency to forelimb clonus in the PRH cortex and CE amygdala was significantly shorter than the other three structures, and (d) despite being slower to kindle than most other sites, stimulation of the BL nucleus most readily triggered SE. The kindling data suggest that discharges triggered from the PRH and CE more readily access motor systems supporting limbic convulsions than discharges triggered from the BL, ME nuclei or the PIR cortex. On the other hand, the SE data indicate that the mechanisms and circuits associated with the development of discrete kindled seizures are not identical to those associated with the induction of limbic SE.

Amygdala↗
PubMed1995

Kainic acid-induced heat shock protein-70, mRNA and protein expression is inhibited by MK-801 in certain rat brain regions.

The regional expression of inducible 72 kDa heat shock protein (HSP-70), HSP-70 mRNA and the neuropathological outcome of their expression were examined in the rat brain following systemic administration of kainic acid (9 mg/kg), and also after pretreatment with the non-competitive N-methyl-D-aspartate antagonist MK-801 (1 mg/kg). Five hours after administration of kainic acid alone, dense expression of HSP-70 mRNA was found within the limbic system, mainly in the hippocampus, piriform and entorhinal cortices, amygdaloid complex, thalamic nuclei, subiculum and in other cortical areas in rats that had shown convulsive behaviour. At 24 h, HSP-70 immunoreactivity was seen in most areas previously expressing HSP-70 mRNA, except the piriform and entorhinal cortices and several ventral nuclei of the amygdaloid complex. Histopathological examination at 24 h revealed marked cell loss in these latter regions and less severe histopathological changes in other areas of the limbic system in brains of convulsive rats. No alterations were apparent in non-convulsive rats. The percentage of rats showing convulsive behaviour with kainic acid was reduced from 74 to 4% following pretreatment with MK-801. In addition, MK-801 inhibited the kainic acid-induced expression of HSP-70 mRNA and protein in certain brain regions, notably the cortex, the pyramidal cell layer of CA1, and discrete thalamic nuclei. However, HSP-70 mRNA induction was sustained in the pyramidal cell layer of CA3, the amygdaloid complex and the subiculum, despite the fact that none of these rats convulsed. MK-801 prevented necrosis in all rats examined except the single rat that had shown convulsive behaviour. These results show that early regional expression of inducible HSP-70 mRNA allows the visualization of regions affected by kainic acid and maps regions inhibited by MK-801. In addition, the results identify brain regions putatively involved in the manifestation of limbic convulsions. Furthermore, these data illustrate that the induction of HSP-70 mRNA is not predictive of cell death or survival.

Animals↗
PubMed1996

Distribution of the mRNA for a pituitary adenylate cyclase-activating polypeptide receptor in the rat brain: an in situ hybridization study.

The distribution of the mRNA for a pituitary adenylate cyclase-activating polypeptide (PACAP) receptor (PACAP-R) was examined in the rat brain, and also in the hypophysis and pineal gland, by in situ hybridization with a specific 35S-labeled riboprobe which was generated from a rat PACAP-R cDNA clone. In the brain, expression of PACAP-R mRNA was most prominent in the periglomerular and granule cells of the olfactory bulb, granule cells of the dentate gyrus, supraoptic nucleus, and area postrema. The expression was also intense in the piriform, cingulate, and retrosplenial cortices, pyramidal cells in CA2, non-pyramidal cells in CA1-CA3, neuronal cells in the hilus of the dentate gyrus, lateral septal nucleus, intercalated amygdaloid nucleus, anterodorsal thalamic nucleus, most of the midline and intralaminar thalamic nuclei, many regions of the hypothalamus, dorsal motor nucleus of the vagus nerve, hypoglossal nucleus, and lateral reticular nucleus. No significant expression was detected in the mitral and tufted cells in the olfactory bulb, pyramidal cells in CA1 and CA3, posterior nuclear group of the thalamus, dorsal lateral geniculate nucleus, and Purkinje, Golgi, and granule cells in the cerebellar cortex. Moderate-to-weak expression was further observed in many other regions of the brain. In the cerebellar cortex, presumed Bergmann glia cells showed moderate expression. In the hypophysis, the expression was moderate in the anterior lobe, and weak to moderate in the posterior lobe; no significant expression was observed in the intermediate lobe. In the pineal gland, the expression was very weak, if any. Thus, the expression of PACAP-R was detected not only on neuronal cells but also on some particular glial cells. The present study has shown, for the first time, the exact site of PACAP-R expression in the brain and hypophysis. Although the functional significance of PACAP and PACAP-R in the brain still remains to be clarified, the present results are considered to provide some direction for future functional studies.

Animals↗
PubMed2000

Status epilepticus-induced neuronal loss in humans without systemic complications or epilepsy.

PURPOSE: To determine the regional distribution of neuronal damage caused strictly by status epilepticus (SE) without systemic complications, underlying brain pathology, or a history of preexisting epilepsy. METHODS: The medical records and electroencephalograms (EEGs) of three deceased patients who developed SE in the hospital were reviewed. Their brains were formalin-fixed, and 17 brain regions were selected, embedded in paraffin, and sectioned. Alternate sections were stained with either hematoxylin and eosin and cresyl violet to determine the extent of neuronal loss and gliosis or glial fibrillary astrocytic protein to confirm the extent of astrocytic proliferation. RESULTS: The three patients died 11 to 27 days after the onset of focal motor SE; none had hypotension, hypoxemia, hypoglycemia, or significant hyperthermia. Two patients had no prior seizures and no underlying brain pathology. The third patient, who had leptomeningeal carcinomatosis, had one seizure 2 months before the onset of SE. The duration of SE was 8.8 hours to 3 days. EEGs showed unilateral temporal lobe sharp-wave discharges in one patient and independent temporal lobe sharp-wave discharges bilaterally in the other two patients. In addition to widespread neuronal loss and reactive gliosis in the hippocampus, amygdala, dorsomedial thalamic nucleus, and Purkinje cell layer of the cerebellum, we report for the first time periamygdaloid (piriform) and entorhinal cortical damage occurring acutely after SE in humans. CONCLUSIONS: In the absence of systemic complications or preexisting epilepsy, SE produces neuronal loss in a distribution similar to that from domoic acid-induced SE in humans and from kainic acid- and pilocarpine-induced SE in rats.

Animals↗
PubMed1998

The significance of precisely replicating patterns in mammalian CNS spike trains.

Neuronal spike trains from both single and multi-unit recordings often contain patterns such as doublets and triplets of spikes that precisely replicate themselves at a later time. The presence of such precisely replicating patterns can still be detected when the tolerance on interval replication is shortened to a fraction of a millisecond. In this context we examine here data taken from various parts of the central nervous systems of anesthetized rats, cats and monkeys. The relative abundance of replicating triplets varies from centre to centre, and is nearly always significantly greater than obtained in Monte-Carlo simulations of either a Poisson-like process or a renewal process having the same interspike interval distribution as the neuronal data. However, a remarkable exception is found in the activity of retinal ganglion cells. Significant deviations were found in the primary visual cortex and, even more so, in the lateral geniculate body and the mitral cells of the olfactory bulb. Using a fixed tolerance for the replication of intervals (0.5 ms) it is usually observed that replicating patterns are produced in excess (with respect to renewal process models) mostly in low firing rate episodes (< or = 100 Hz). However, using a tolerance that varies in direct proportion to the mean interval (i.e. as the reciprocal of the firing rate), one generally observes that replicating triplets occur with higher than expected frequency in comparable proportions at all firing rates. This observation suggests the existence of a scale invariance principle in these phenomena with respect to certain neuronal codes. In order to decrease the influence of the estimated neuronal firing rate on the results of the comparisons, we computed also the ratio NT2/ND3, of the number of replicating triplets to the number of doublets replicating three times [Lestienne R. (1994) Proc. Soc. Neurosci. 20, 22; Lestienne R. (1996) Biol. Cybern. 74, 55-61], using both a fixed or a variable tolerance. In spike trains obeying a Poisson process, NT2/ND3 ratios should be nearly independent of the frequency, especially when using a variable tolerance. These studies supported previous results: significant deviations from the models are found in all the spike trains examined, except in the case of retinal ganglion cells, and the most significant deviations are found in recordings from the lateral geniculate nucleus and the mitral cells of the olfactory bulb. Removing spikes that belong to bursts having large "Poisson surprise" values [Legéndy C. R. and Salcman M. (1985) J. Neurophysiol. 53, 926-939] (except the very first spike of the burst) significantly decreases NT2/ND3 ratios in the record from the lateral geniculate nucleus, suggesting that in this case bursty episodes greatly contribute to the production of replicating patterns, but such a removal does not affect results from the piriform record. Finally, in both the lateral geniculate nucleus and in the mitral cells of the olfactory bulb records, perturbing the timing of spikes by applying to interspike intervals small jitters of uniform probability density with amplitude up to 3 ms, very significantly decrease NT2/ND3 ratios in these centres, but does not change much the NT2/ND3 ratios in other neuronal recordings. Implications of these findings for a possible role of precisely replicating patterns in temporal coding of neuronal information is discussed, as well as possible mechanisms for their production.

Animals↗
PubMed1981

Efferent connections of the olfactory bulb in the opossum (Didelphis marsupialis aurita): a Fink-Heimer study.

The efferent concentrations of the olfactory bulb (OB) in the opossum (Didelphis marsupialis aurita) were studied by the aid of the Fink-Heimer technique. Following lesions restricted to the OB, ipsilateral degenerating fibers entered the lateral olfactory tract and were treated to terminal fields essentially limited to the outer portion of the plexiform layer (sublamina IA) of the following structures: all the subdivisions of the anterior olfactory nucleus, the rostroventral tenia tecta, the full extent of the olfactory tubercle, the nucleus of the lateral olfactory tract, the anterior portion of the medial amygdaloid nucleus, the whole cortical amygdaloid nucleus (in the posteromedial subdivision of this structure the degeneration was very scanty), and the sulcal, piriform, and lateral entorhinal cortices. Some degree of topographical organization in the OB projections was noticed in the rostral portion of the lateral olfactory tract and within the external and lateral subdivisions of the anterior olfactory nucleus. In another series of experiments, when the lesion also involved the accessory olfactory bulb, heavy terminal degeneration occurred along the whole extent of the medial amygdaloid nucleus and in the posteromedial subdivision of the cortical amygdaloid nucleus. These findings indicate that, although very similar to those described in other mammals, the OB efferent connections in the opossum present some peculiarities; namely, the existence of dense terminal fields in the sulcal cortex and in the rostral district of the medial amygdaloid nucleus.

Amygdala↗
PubMed1992

Widespread increase of nerve growth factor protein in the rat forebrain after kindling-induced seizures.

Nerve growth factor (NGF) protein levels were determined in various forebrain regions using a two-site immunoassay following kindling-induced seizures. In the dentate gyrus the NGF content was significantly elevated 7 days after the last seizure (to 152% of control). In the piriform and parietal cortices, maximal increases were seen at 12 h (to 261% of control) and at 24 h (to 169% of control), respectively, and the NGF content was then normalized at 7 days. The increased production of NGF might be a protective response or could be involved in plastic changes underlying kindling epileptogenesis.

Animals↗