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PubMed2004

Necrosis of hippocampus and piriform lobe: clinical and neuropathological findings in two Italian cats.

The present paper reports the clinical and neuropathological findings in two cats with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and piriform lobe. The cats were presented because of acute onset of behavioural changes and complex partial seizures. The neurological examination suggested a forebrain lesion. The results of blood examination were within the normal range, and the cerebrospinal fluid (CSF) analysis and computed tomography (CT) scan in one cat did not show any abnormality. Despite therapy with diazepam (Valium; Roche) there was deterioration of the clinical signs and the cats were euthanased. The neuropathological examination revealed hippocampal necrosis that included the piriform lobe.

Amygdala↗
PubMed1989

Distribution of monoamines and metabolites in rabbit neostriatum, hippocampus and cortex.

The monoamines noradrenaline (NA), dopamine (DA), adrenaline (AD) and 5-hydroxytryptamine (5-HT) were assayed in the putamen (PUT), the lateral (lCAU) and medial (mCAU) portions of the caudate, the dorsal (dHIP) and ventral (vHIP) hippocampus, as well as in four cortical areas, i.e., anterior cingulate (CIN), entorhinal-piriform (EnPi), sensorimotor (SSC; somatosensory) and primary visual (VIS). The use of an HPLC procedure enabled us to perform these measurements in microdissected samples and to assay as well monoamine metabolites. The DA levels were highest in the neostriatum, moderate in the EnPi and CIN and very low in the SSC, VIS and hippocampus. The distribution of NA was more uniform, although higher concentrations were measured in the neostriatum, hippocampus and EnPi. The largest amounts of 5-HT were in the EnPi, while moderate concentrations were found in the other regions. The ratios between the neurotransmitters and their metabolites were used as an index of turnover and indicate that the terminal fields of the monoamine systems are heterogenous within the neostriatal, hippocampal and cortical subdivisions.

Animals↗
PubMed1993

Benzodiazepine receptor binding following chronic treatment with naloxone, morphine and met-enkephalin in normal rats.

The effects of chronic administration of naloxone, morphine and met-enkephalin on benzodiazepine (BDZ) receptor binding in rat brain were determined 2 and 50 days after treatments were accomplished. Two days after naloxone treatment (75 micrograms/h s.c. for 14 days), enhanced BDZ receptor binding was observed in cingulate, frontal, piriform, entorhinal and sensorimotor cortices; amygdala complex, hippocampus, substantia nigra and central gray. Two days after morphine treatment (20 mg/kg i.p. daily for 6 days), increased BDZ receptor binding was detected in cingulate, frontal, piriform, entorhinal and sensorimotor cortices; amygdala complex, hippocampus and substantia nigra. Two days after met-enkephalin treatment (10 micrograms/h i.c.v. for 6 days) enhanced BDZ receptor binding was shown only in sensorimotor cortex. No significant changes were observed 50 days after the treatments were completed. These data indicate an important interaction between GABAergic and opioid peptide systems.

Animals↗
PubMed1997

Phencyclidine (PCP) acts at sigma sites to induce c-fos gene expression.

Phencyclidine (PCP) is a compound that results in abnormal human behavior and has been proposed as a chemical model for schizophrenia. It was hypothesized that PCP induction of the immediate-early gene, c-fos, should be seen in areas associated with emotional behavior, such as the cortex and limbic system. It was also proposed that PCP may induce c-fos via the sigma receptor. PCP and two sigma ligands, 1,3-di(2-tolyl)guanidine (DTG) and pentazocine, were shown to induce c-fos in similar patterns. The three compounds abundantly induced c-fos in the cingulate, parietal, and piriform cortices and the midline structures of the thalamus and hypothalamus. Neither PCP nor the sigma ligands induced c-fos in the hippocampus. This suggests that PCP binding at NMDA receptors does not result in significant c-fos induction. Rimcazole, a putative sigma2 receptor antagonist, and other sigma ligands have been shown to ameliorate PCP stereotypic behavior. Rimcazole inhibited PCP c-fos induction in the cingulate and parietal cortices and DTG c-fos induction in the cingulate cortex. DTG shows both sigma1 and sigma2 binding affinity. Rimcazole failed to inhibit pentazocine c-fos induction. Pentazocine binds only to sigma1 receptors. This suggests that PCP may produce a significant fraction of its c-fos induction via sigma2 receptors.

Animals↗
PubMed1991

Localization and ontogeny of cells expressing preprodynorphin mRNA in the rat cerebral cortex.

The regional distribution of preprodynorphin (PPD) mRNA-containing cells (PPD cells) in the rat cerebral cortex was investigated by in situ hybridization histochemistry using a synthetic oligonucleotide probe. In the isocortex, PPD cells were small or medium-sized and were mainly located in layer V. While they were less numerous in the allocortex than in the isocortex. Only a few labeled cells were seen in the piriform and entorhinal cortices. In the hippocampal formation, labeled cells were observed in the granular layer of the dentate gyrus. An ontogenetic study revealed that PPD mRNA-containing cells appeared on postnatal day 7 in the isocortex and the allocortex and on day 14 in the dentate gyrus. Thereafter, they increased in number and signal intensity to reach a plateau on postnatal day 14 in both the isocortex and the allocortex and on day 35 in the dentate gyrus. The time-course of development of PPD mRNA-containing neurons in the cerebral cortex suggested that PPD-derived peptide has a neuromodulator and/or neurotransmitter role in these regions of the brain.

Animals↗
PubMed2003

Distribution and densitometry mapping of L1-CAM immunoreactivity in the adult mouse brain--light microscopic observation.

BACKGROUND: The importance of L1 expression in the matured brain is suggested by physiological and behavioral studies showing that L1 is related to hippocampal plasticity and fear conditioning. The distribution of L1 in mouse brain might provide a basis for understanding its role in the brain. RESULTS: We examined the overall distribution of L1 in the adult mouse brain by immunohistochemistry using two polyclonal antibodies against different epitopes for L1. Immunoreactive L1 was widely but unevenly distributed from the olfactory bulb to the upper cervical cord. The accumulation of immunoreactive L1 was greatest in a non-neuronal element of the major fibre bundles, i.e. the lateral olfactory tract, olfactory and temporal limb of the anterior commissure, corpus callosum, stria terminalis, globus pallidus, fornix, mammillothalamic tract, solitary tract, and spinal tract of the trigeminal nerve. High to highest levels of non-neuronal and neuronal L1 were found in the grey matter; i.e. the piriform and entorhinal cortices, hypothalamus, reticular part of the substantia nigra, periaqueductal grey, trigeminal spinal nucleus etc. High to moderate density of neuronal L1 was found in the olfactory bulb, layer V of the cerebral cortex, amygdala, pontine grey, superior colliculi, cerebellar cortex, solitary tract nucleus etc. Only low to lowest levels of neuronal L1 were found in the hippocampus, grey matter in the caudate-putamen, thalamus, cerebellar nuclei etc. CONCLUSION: L1 is widely and unevenly distributed in the matured mouse brain, where immunoreactivity was present not only in neuronal elements; axons, synapses and cell soma, but also in non-neuronal elements.

Animals↗
PubMed1996

Delayed, selective neuronal death following experimental cortical impact injury in rats: possible role in memory deficits.

Clinical and experimental studies show that loss of neurons in the hippocampus and/or the entorhinal cortex can impede formation and storage of spatial memory. Using a controlled cortical impact model of traumatic brain injury (TBI) in rats, we have examined the temporal and spatial pattern of neuronal death using silver impregnation and cresyl violet staining. Dystrophic neurons can be detected in the dentate gyrus, and the CA1 and CA3 subfields of the hippocampus for up to 2 weeks following injury. These dystrophic cells appeared shrunken and possessed features of apoptosis. Areas containing the dystrophic cells suffer substantial cell loss as demonstrated by thinning of the neuronal layers. Dystrophic cells are also found in the amygdala, entorhinal and piriform cortices, thalamic and hypothalamic regions, and surrounding the contusion site. The loss of these cells may contribute to the memory deficits observed following TBI.

Animals↗
PubMed2001

Clock gene expressions in the suprachiasmatic nucleus and other areas of the brain during rhythm splitting in CS mice.

The CS mouse is a mutant strain which displays spontaneous splitting in the circadian locomotor rhythm under continuous darkness. To clarify whether the rhythm splitting occurs in the suprachiasmatic nucleus (SCN) where the mammalian circadian clock is located, the circadian rhythmicities of mammalian clock genes, mPer1, mBMAL1 and mClock, were examined in the SCN and cerebral cortex during rhythm splitting. The circadian profiles of the clock genes during rhythm splitting were essentially the same as those observed under unsplit conditions. However, the mPer1 gene expression throughout the day was bimodal in the piriform and cingulate cortices, peaking in correspondence with two split components of behavioral rhythm. These results indicate that the circadian profiles of three clock gene expressions in the SCN are not consistent with the overt circadian locomotor rhythm, suggesting that the site of rhythm splitting is somewhere outside the SCN, or alternatively different subregions or other clock genes in the SCN are involved in rhythm splitting.

ARNTL Transcription Factors↗
PubMed2001

Blood-brain barrier preservation in the in vitro isolated guinea pig brain preparation.

The morphofunctional preservation of the blood-brain barrier (BBB) was evaluated in the isolated guinea pig brain maintained in vitro by arterial perfusion. Electron microscopy evaluation after 5 hr in vitro demonstrated that cerebral capillaries and BBB specializations in this preparation retain features compatible with structural integrity. BBB-impermeable and -permeable atropine derivatives arterially perfused to antagonize carbachol-induced fast oscillatory activity confirmed the functional preservation of the BBB in vitro. To study BBB function further, changes in extracellular K+ concentration during arterial perfusion of a high-K+ solution were measured with K+-sensitive electrodes positioned in the cortex and, as control, at the brain venous outlet, where the solution perfused through the brain arterial system was collected. After 5 hr in vitro, the [K+](o) values measured during high-K+ perfusion in the piriform and entorhinal cortices were 5.02 +/- 0.17 mM (mean +/- SE) and 5.2 +/- 0.21 mM, respectively (n = 6). Coperfusion of the high-K+ solution with the Na+/K+ pump blocker ouabain (10 microM; n = 4) induced consistently spreading depression preceded by a rise in [K+](o). Finally, sporadic, isolated spots of extravasation of the fluorescent marker fluorescein isothiocyanate (FITC)-dextran preferentially circumscribed to deep cortical layers was observed in brains perfused with FITC-dextran after 5 hr in vitro. The study demonstrates that the in vitro isolated guinea pig brain is viable for studying cerebrovascular interactions and BBB permeability of compounds active in the central nervous system.

Animals↗
PubMed1981

An autoradiographic study of the efferent connections of the entorhinal cortex in the rat.

The longer connections of the entorhinal cortex have been studied autoradiographically in a series of rats, each of which received a small injection of 3H-amino acids in one of the various cytoarchitectonic subfields of the entorhinal cortex. The major findings can be summarized as follows. Whereas the projection of the lateral entorhinal area (LEA) to the dentate gyrus is broad in its longitudinal extent, the medial entorhinal area (MEA), and especially the ventral portion of this zone, projects in a more lamellar fashion. In the transverse plane the LEA preferentially projects to the inner (dorsal) blade of the dentate gyrus, while the MEA innervates both blades equally. Within the radial dimension, the entorhinal cortex projects to the dentate gyrus according to a medial to lateral gradient, with lateral portions of the LEA projecting along the pial surface and successively more medial portions of the entorhinal projecting closer to the granule cells. The commissural entorhinal to dentate projections are similar to the ipsilateral projections in location; however, they are considerably reduced in septotemporal extent and do not arise from cells in the ventral half of either LEA or the intermediate entorhinal area (IEA). The projection of the entorhinal cortex to Ammon's horn reflects the same longitudinal characteristics as the dentate projections. An alvear input which extends only to the pyramidal cells at the CA1-subicular junction was most noticeable at ventral hippocampal levels. Finally the extrahippocampal projections have been analyzed. These arise predominantly from cells in the LEA and project forward along the angular bundle to the piriform and periamygdaloid cortices, as well as the endopiriform nucleus, the lateral, basolateral, and cortical amygdaloid nuclei, the nucleus of the lateral olfactory tract, the olfactory tubercle, the anterior olfactory nucleus, the taenia tecta, and the indusium griseum. These extrinsic projections are to a large extent reciprocal to the major extrinsic inputs to the LEA.

Amino Acids↗
PubMed1987

The entorhinal cortex of the monkey: II. Cortical afferents.

The entorhinal cortex of the monkey is commonly viewed as the major link between the cerebral cortex and the other fields of the hippocampal formation. Until recently, however, little was known about the origins of the cortical projections to the entorhinal cortex, and most of the available information is still based on degeneration studies. We have carried out a systematic analysis of these connections by placing small injections of the retrograde tracer wheat germ agglutinin conjugated to horseradish peroxidase into each of the fields of the entorhinal cortex of the Macaca fascicularis monkey. Retrogradely labeled cells were observed in several areas of the frontal and temporal lobes, the insula, and the cingulate cortex. In the frontal lobe, the greatest number of labeled cells were observed in the orbital region and specifically in areas 13 and 13a: labeled cells were also seen in areas 14, 11, and 12. In the dorsolateral frontal cortex, labeled cells were observed mainly in the rostral half of area 46; occasionally cells were also seen in areas 9, 8, and 6. In the cingulate cortex, labeled cells were observed in area 25, area 32, and rostral levels of area 24; fewer cells were observed at caudal levels of area 24 or in area 23. The retrosplenial region (areas 30 and 29), including its caudal extension along the rostral calcarine sulcus and its ventral extension into the temporal lobe, contained numerous labeled cells. In the temporal lobe, retrogradely labeled cells were arranged in two rostrocaudally oriented bands. Rostral to the hippocampal formation, the first band encompassed the piriform and periamygdaloid cortices and areas 35 and 36; the labeling in area 36 was continuous to the temporal pole. At more caudal levels this band was located immediately lateral to the hippocampal formation and included areas 35 and 36 rostrally and areas TH and TF caudally. The second band was situated in the superior temporal gyrus where labeled cells were observed in several distinct cytoarchitectonic fields, including the parainsular cortex in the fundus of the inferior limiting sulcus. In the insula proper, retrogradely labeled cells were seen mainly in the rostral or agranular division; far fewer were observed in the dysgranular and granular insula. Whereas there is little available physiological information concerning many of the cortical regions that project to the entorhinal cortex, on anatomical grounds they may be generally characterized as polysensory associational regions.

Afferent Pathways↗
PubMed2000

Kindling modulates the IL-1beta system, TNF-alpha, TGF-beta1, and neuropeptide mRNAs in specific brain regions.

Cytokines and neuropeptides may be involved in seizure-associated processes. Following amygdala kindling in rats, we determined alterations of IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-1 receptor type I (IL-1RI), IL-1 receptor accessory proteins (IL-1R AcPs) I and II, TNF-alpha, TGF-beta1, neuropeptide Y (NPY), glycoprotein 130 (gp 130) and pro-opiomelanocortin (POMC) mRNA levels in the parietal, prefrontal and piriform cortices, amygdala, hippocampus and hypothalamus. Messenger RNAs expression in all brain regions was determined 2 h or 3 weeks following the last generalized convulsive seizure triggered from the ipsilateral kindled amygdala. The same brain region sample was used to assay for changes of all mRNA components. The results show that the 2 h-kindled group exhibited a significant up-regulation of IL-1beta, IL-1RI, TNF-alpha and TGF-beta1 mRNAs in all three cortical brain regions, amygdala and hippocampus. The largest up-regulation occurred in the prefrontal cortex (about 30-fold induction for IL-1beta and TNF-alpha mRNAs). IL-1R AcP I and II mRNA levels were also up-regulated in the cortical regions. No changes in IL-1beta, IL-1RI or TNF-alpha mRNA levels occurred in the 3 week-kindled group. NPY mRNA levels increased in the hippocampus, prefrontal and piriform cortices in the 2 h-kindled group, while IL-1Ra, gp 130, or POMC mRNA levels did not change in any group. The overall profile of mRNA changes shows specificity of transcriptional modulation induced by amygdala kindling. The data support a role of cytokines and NPY in the adaptive mechanisms associated with generalized seizure activity, with implications for neuroprotection, neuronal dysfunction and vulnerability associated with epileptic activity.

Amygdala↗
PubMed2000

Binge ethanol consumption causes differential brain damage in young adolescent rats compared with adult rats.

BACKGROUND: Adolescents respond differently to alcohol than adults. Furthermore, binge drinking in young adolescents is becoming increasingly common. METHODS: To determine if the effects of binge drinking on brain damage are different in juveniles compared with adults, the effects of a 4 day binge ethanol treatment (e.g., 4 days of 4 times per day 15% ethanol intragastrically, approximately 9-10 g/kg/day ethanol) were investigated in adolescent-juvenile rats (JVN) 35 days old and compared with adult (ADT) rats 80 to 90 days old. Brain damage was measured by using the amino cupric silver stain of de Olmos et al. (1994). RESULTS: Significant brain damage was found in both groups. The olfactory bulbs were equally damaged in both groups; however, the associated frontal cortical olfactory regions were damaged only in JVN. The anterior portions of the piriform and perirhinal cortices also were damaged only in JVN rats. Quantitation of silver-stained frontal areas in binge ethanol-treated JVN rats ranged from 400% to 1,260% of control values. For example, in anterior perirhinal cortex, silver stain increased from 48 +/- 14 to 444 +/- 114 (mm2 x 10(3) argyrophilic area; p < 0.01) in JVN control and binge ethanol-treated animals, respectively. In contrast, posterior perirhinal cortex showed greater damage in adults, being 236 +/- 76 vs. 875 +/- 135 (mm2 x 10(3) argyrophilic area; p < 0.005) in JVN and ADT, respectively. CONCLUSIONS: The young-adolescent brain shows differential sensitivity to alcohol-induced brain damage compared with adults.

Age Factors↗
PubMed1976

[Pathological anatomy of Edwards' syndrome (trisomy 18)].

Data of the literature (200 section observations) and those of 10 authors' own observations on the syndrome of trisomy with relation to chromosome 18 are presented. The pathologoanatomic diagnosis of Edwards' syndrome can be established without an investigation of chromosomes on the basis of a complex of congenital defects present in the newborn. The main of them are: prenatal hypoplasia, dolichocephaly, microgenia, concha auriculae drawn in the horizontal plane, flexor position of bones, shortness and thickness of the great toe and protruding heel, thickness and distortion of convolution of the dorsal lip of the olivary nucleus, hypoplasia of the cerebellum, heterotopia of the piriform Purkinje cells into the white matter of the cerebellum and foci of nondifferentiated cells in the white matter of the great hemispheres; complex cardiac defects--Meckel's diverticulum, fused kidneys (horseshoe- or L-shaped) with small cysts in the renal cortex; and the presence of 10 or more arches on fingers and toes in combination with proximal or intermediate localization of axial triradius.

Abnormalities, Multiple↗
PubMed1988

Localization and induction of c-fos protein-like immunoreactive material in the nuclei of adult mammalian neurons.

The distribution of the proto-oncogene product, c-fos protein, has been studied in tissue from adult rat brain using immunocytochemical techniques. Sections of rat brain were incubated with a polyclonal antibody to a synthetic fragment of the c-fos protein (M-peptide) and visualized for immunoreactivity using the avidin-biotin technique. Low levels of c-fos protein-like immunoreactivity were concentrated in the nucleus. Dark nuclear staining of cells was observed in the cerebral cortex, in hippocampal pyramidal neurons, in granule cells of the dentate gyrus and other regions. Neurons in the cat visual cortex also showed low levels of c-fos protein-like immunoreactivity. Pre-absorbing the antibody with the M-peptide abolished the immunostaining. Generalized seizures evoked by injection of pentylenetetrazol produced a massive induction of fos protein(s) in the piriform and cingulate cortices as well as the dentate gyrus of rats. These results demonstrate that c-fos protein-like immunoreactive material is found within the nuclei of fully differentiated adult mammalian neurons at low basal levels and that activation of nerve cells leads to an induction of c-fos proteins.

Animals↗
PubMed2006

Efferent projections of reuniens and rhomboid nuclei of the thalamus in the rat.

The nucleus reuniens (RE) is the largest of the midline nuclei of the thalamus and exerts strong excitatory actions on the hippocampus and medial prefrontal cortex. Although RE projections to the hippocampus have been well documented, no study using modern tracers has examined the totality of RE projections. With the anterograde anatomical tracer Phaseolus vulgaris leuccoagglutinin, we examined the efferent projections of RE as well as those of the rhomboid nucleus (RH) located dorsal to RE. Control injections were made in the central medial nucleus (CEM) of the thalamus. We showed that the output of RE is almost entirely directed to the hippocampus and "limbic" cortical structures. Specifically, RE projects strongly to the medial frontal polar, anterior piriform, medial and ventral orbital, anterior cingulate, prelimbic, infralimbic, insular, perirhinal, and entorhinal cortices as well as to CA1, dorsal and ventral subiculum, and parasubiculum of the hippocampus. RH distributes more widely than RE, that is, to several RE targets but also significantly to regions of motor, somatosensory, posterior parietal, retrosplenial, temporal, and occipital cortices; to nucleus accumbens; and to the basolateral nucleus of amygdala. The ventral midline thalamus is positioned to exert significant control over fairly widespread regions of the cortex (limbic, sensory, motor), hippocampus, dorsal and ventral striatum, and basal nuclei of the amygdala, possibly to coordinate limbic and sensorimotor functions. We suggest that RE/RH may represent an important conduit in the exchange of information between subcortical-cortical and cortical-cortical limbic structures potentially involved in the selection of appropriate responses to specific and changing sets of environmental conditions.

Animals↗
PubMed2002

Age-related changes in expression of metallothionein-III in rat brain.

Metallothionein (MT)-III is a metal binding protein, called growth inhibitory factor, and is mainly expressed in the central nervous system. Since MT-III decreases in the brain of Alzheimer's disease (AD), a growing interest has been focused on its relationship to neurodegenerative diseases. To clarify age-related changes in the MT-III expression and its inducibility against oxidative stress, we analyzed the expression of MT-III and its mRNA in the brain of lipopolysaccharide (LPS)-treated aged rats. In the frontal cortex, basal expression of MT-III mRNA was significantly increased with aging, while it was observed no induction of MT-III mRNA against LPS administration in the aged rat brain. MT-III immunopositive cells were increased in the frontal, parietal and piriform cortices, hypothalamus and amygdaloid nucleus with aging. The LPS treatment induced MT-III expression in the brain of young-adult rats, but not in the aged rat brain. Furthermore, the MT-III induction with LPS treatment was mainly observed in oligodendrocyte and microglia. In the present study, we showed that inducibility of brain MT-III against oxidative stress may be reduced with aging. Since it has been reported that MT-III has neuroprotective roles as an antioxidant, present results suggest that MT-III is closely related to the neurodegeneration in the aged animals.

Aging↗