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PubMed1983

The islands of Calleja complex of rat basal forebrain II: connections of medium and large sized cells.

The connections of the medium (10-20 microns) and large (20-35 microns) cells of the islands of Calleja Complex (ICC) were studied in the albino rat with anterograde and retrograde transport of horseradish peroxidase (HRP) and fluorescent tracers. The medium and large size cells were found to project to the ipsilateral olfactory tubercle, ventral pallidum, septum, piriform cortex, periamygdaloid cortex, cortical nuclei of the amygdala, ventral endopiriform nucleus, lateral hypothalamic area, Forel's field H, ventral tegmental area, supramammillary complex, and nuclei gemini of the hypothalamus, midline, intralaminar and medial thalamic nuclei, and lateral habenula. Afferents of the ICC appear to include the same nuclei with the exception of the lateral habenula. In addition, the dorsal raphe projects to the ICC. These connections are consistent with the concept that the ICC is a striato-pallidal structure.

Animals↗
PubMed1996

Seizure activity causes elevation of endogenous extracellular kynurenic acid in the rat brain.

This study was designed to examine the effects of several classic convulsants on the extracellular concentration of the anticonvulsant and neuroprotective brain metabolite kynurenic acid (KYNA) in the rat brain. Drug effects were investigated in vivo, mostly by unilateral microdialysis in the dorsal hippocampus. Systemic administration of pentylenetetrazole (60 mg/kg, SC), pilocarpine (325 mg/kg, SC), bicuculline (6 mg/kg, SC), or kainic acid (10 mg/kg, SC) caused characteristic clonic and/or tonic convulsions. In all seizure paradigms, KYNA levels in the dialysate began to rise within 1 h and gradually reached a plateau approximately 4 h after administration of the convulsants. Peak increases were 1.5-3-fold over basal levels. The duration of the elevation in KYNA levels was significantly prolonged following kainic acid application. In the kainic acid model, extracellular KYNA was also measured and found to be increased in the ventral hippocampus, piriform cortex, and striatum. Moreover, temporary intrahippocampal infusion of the KYN synthesis inhibitor aminooxyacetic acid (1 mM) in the kainic acid- and pentylenetetrazole models attenuated the increase in extracellular KYNA levels, demonstrating that de novo production of KYNA in the brain accounts for the seizure-induced KYNA overflow. A separate group of animals received a unilateral intrahippocampal injection of the endogenous convulsant excitotoxin quinolinic acid (120 nmol) and showed long-lasting (> 24 h) bilateral increases in extracellular KYNA levels. Taken together, these data indicate that an increase in extracellular KYNA may constitute a common occurrence in response to seizures and that KYNA elevations may signify the brain's attempt to counteract seizure activity.

Animals↗
PubMed1994

Brain parenchyma apparent diffusion coefficient alterations associated with experimental complex partial status epilepticus.

The objective of this study was to evaluate whether water apparent diffusion coefficient (ADC) measurements provide more specific information than T2-weighted MRI about the evolution of brain parenchyma lesions secondary to prolonged complex partial seizures. We measured the ADC in the brain of rats exhibiting prolonged complex partial seizures induced by intraperitoneal injection of kainic acid (KA). The animals were imaged with diffusion and T2-weighted MRI at 2 T from 3 h up to 9 days after KA injection. In the piriform cortex and amygdala, the T2-weighted MRI signal intensity appeared to be uniformly increased from 24 to 72 h after KA injection, and returned to normal by 9 days. In the same regions between 24 and 72 h, the ADC first decreased and then increased. The ADC changes were consistent with the known histopathologic alterations. In this complex partial seizure model, the ADC measurement provides more specific information than T2-weighted MRI about the histopathologic evolution of the lesions. This supports the proposal that diffusion MRI may be valuable for the evaluation of the neuropathologic sequelae in patients with multiple or prolonged seizures.

Animals↗
PubMedDate not supplied

The distribution of dopamine D2 receptor heteronuclear RNA (hnRNA) in the rat brain.

Conventional in situ hybridization methods have been useful in characterizing the anatomical distribution of cells in the central nervous system that express dopamine D2 receptor mRNA. However, due to the large size of the D2 mRNA pool, this method may be insensitive to changes in D2 gene transcription. We have developed a method of hybridizing a 35S-labelled cRNA probe to an intron in the D2 receptor gene in order to measure the amount of primary transcript or heteronuclear RNA (hnRNA) in D2-expressing cells. Introns are found uniquely in hnRNA and are thought to be short-lived intermediates. Thus, monitoring introns could represent a more direct measure of D2 gene transcription. The anatomical distribution of the D2 hnRNA is similar to the distribution of D2 mRNA in the rat brain. D2 heteronuclear RNA was found in the nuclei of cells in the caudate putamen, nucleus accumbens, hippocampus, olfactory tubercle, substantia nigra, ventral tegmental area, and zona incerta. Other regions that contain D2 mRNA, but do not demonstrate intronic signal, include the globus pallidus, prefrontal, cingulate, entorhinal, and piriform cortex, septum, and amygdala. However, these areas have low amounts of D2 mRNA and may contain levels of D2 hnRNA that are below detection. Heteronuclear RNA quantitation by solution hybridization followed by RNase protection was performed on striatum, substantia nigra, cerebral cortex, hippocampus, hypothalamus, and pituitary using a D2 intron 7/exon 8 border probe. These results corroborate the distribution of hnRNA revealed with intronic in situ hybridization. In addition, protection assays were able to detect hnRNA in areas that express low levels of D2 like the cortex, hippocampus and hypothalamus. hnRNA/mRNA ratios calculated from intron/exon border probe protection assays were not equivalent for all the tissue areas studied, indicating that transcription and/or hnRNA half lives may differ between tissues that express D2 receptors. The combined use of intronic in situ hybridization and intron/exon border protection assay as an index of D2 gene transcription and RNA processing provides more information than measuring the mRNA pool alone. It may also prove to be a more useful measure of gene regulation, allowing for evaluation of gene responses to acute treatments.

Animals↗
PubMed1991

Changes in rat brain extracellular glutamate concentration during seizures induced by systemic picrotoxin or focal bicuculline injection: an in vivo dialysis study with on-line enzymatic detection.

An on-line enzymatic assay of dialysis fluid has been used to monitor the extracellular glutamate concentration in the rat hippocampus. Perfusion with artificial cerebrospinal fluid containing a glutamate uptake inhibitor (either dihydrokainate or 4,4'-diisothiocyanatostilbene-2,2' disulfonic acid) produced a marked stable increase in glutamate concentration; 10 min perfusion with 100 mM K+ produced a transient increase. Sustained epileptiform EEG discharges were induced in the hippocampus by focal injection of bicuculline into the piriform cortex or by systemic injection of picrotoxin. Extracellular glutamate did not change significantly during seizure activity, either in the absence or in the presence of glutamate uptake inhibitors. It is concluded that seizure activity is not necessarily accompanied by an overall increase in extracellular glutamate concentration.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Lack of changes in seizure susceptibility during the estrous cycle in kindled rats.

The threshold and pattern of focal and generalized seizures in fully kindled rats during the estrous cycle were investigated. Two groups of rats were studied; one was kindled from stimulation of the basolateral amygdala, the other from stimulation of the anterior portion of the posterior piriform cortex. Determinations of the threshold for focal afterdischarges were either carried out in the morning (between 8 and 9 a.m.) or in the afternoon (between 2 and 3 p.m.). In all experiments, stable and reproducible afterdischarge thresholds were obtained during the different stages of the estrous cycle. The only significant alteration was a reduced seizure duration during metestrus and/or the first day of diestrus in amygdala kindled rats. The data indicate that the natural changes in sex hormone levels during the estrous cycle in rats do not affect seizure susceptibility, at least in the kindling model of epilepsy.

Animals↗
PubMed1992

Mapping rat brain structures activated during ethanol withdrawal: role of glutamate and NMDA receptors.

Brain structures activated during ethanol withdrawal have been mapped by visualizing c-fos mRNA expression. The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801. The findings reveal that the dentate gyrus and piriform cortex are selectively activated during ethanol withdrawal and suggest that this may be mediated by glutamate activation of NMDA receptors.

Animals↗
PubMed1996

Induction of c-fos gene expression by the selective sigma receptor ligand EMD 57445 in rat brain.

Based on animal studies it has been reasoned that ligands to sigma binding sites might be effective in the treatment of schizophrenic disorders and may also be used to investigate this largely elusive disorder on a molecular level. Expression patterns of c-fos in rat brain were studied following treatment with single doses of the sigma ligand EMD 57445 (0.3, 1, 3, 30 mg/kg s.c.). Specific c-fos gene expression was detected at all concentrations tested in various cortical areas. The signals observed were dose-dependent with the highest intensities in the piriform cortex. Strong signals were also detected in hippocampal areas CA 1,2,3 and the gyrus dentatus, as well as in the medial habenula nuclei. In the caudate putamen, nucleus accumbens and lateral septal nucleus signals were detectable after administration of doses > or = 1 mg/kg. Furthermore, c-fos hybridization was visible in the amygdala, in the mammillary bodies, the islands of Calleja and in the olfactory tubercle. In the hypothalamus, c-fos expression was seen in the median eminence area after 30 mg/kg EMD 57445. No hybridization signals were obtained in brainstem or cerebellum. Since c-fos expression induced by EMD 57445 resembled the pattern obtained with atypical neuroleptics and studies on animal behavior point to antipsychotic activity, it is concluded that the drug might be suitable in the treatment of schizophrenia.

Animals↗
PubMed1994

Estrogen-receptor occurrence in the female mouse brain: effects of maternal experience, ovariectomy, estrogen and anosmia.

Maternal behavior (ultrasound-induced pup-searching and retrieving) was studied in eight groups of female house mice with various hormonal backgrounds, experience with pups and function of the olfactory system. In their brains, estrogen receptor immunoreactive (ER-IR) cells were localized and quantified. All animals of all groups had ER-IR cells in a 'reliable subset' of brain areas, the medial preoptic area (MPOA) and ventromedial (VMH) and arcuate nucleus (ARH) of the hypothalamus. In another subset of brain areas, the anterior hypothalamic area (AHA) and cortical (CA) and medial (MA) amygdaloid nucleus, ER-IR cells can be expected in at least some animals of all experimental groups ('expected subset'). In a variable subset of additional brain areas (bed nucleus of the stria terminalis, BNST; suprachiasmatic nucleus, SC; lateral septal nuclei, LS; paraventricular nucleus of the hypothalamus, PVH; entorhinal and piriform cortex, ENT, PIR; subiculum, SUB; hippocampus, HPC; periventricular gray of the midbrain, PVG), ER-IR cells occurred only in some animals of some groups. Numbers of ER-IR cells in a given brain area, volumes occupied by these cells, and cell densities varied considerably among the groups. A covariation of cell counts and volumes was significant for most brain areas indicating that increases of numbers of ER-IR cells relate mainly to volume increases within a given brain area. Experience with pups correlated with an increase of ER presence in the AHA, VMH, ENT, PIR, SUB, HPC and PVG, however, only in the presence of estrogen. Estrogen and pup-experience together led to an increased ER presence in mainly the VMH, ENT and PIR, however, only in females with intact olfaction. Full maternal behavior (retrieving, ultrasound recognition) occurred after the high pregnancy- or experience-induced ER content was reduced to lower levels. The ER occurrence in lactating and experienced virgin females differed, however, in the AHA, BNST, SC, PVH, ENT, PIR, SUB, HPC and PVG showing that the maintenance of maternal behavior can run under different profiles of ER content in the brain. Ovariectomy and/or prolonged high blood-estrogen levels correlated significantly with decreased levels of ER-IR cells in most brain areas which could not be increased by pup-experience.

Animals↗
PubMed2005

Learning-stage dependent Fos expression in the rat brain during acquisition of an olfactory discrimination task.

By using Fos immunocytochemistry, we investigated the activation in olfactory-related areas at three stages (the first and fourth days of conditioning and complete acquisition) of an olfactory discrimination learning task. The trained rats (T) had to associate one odour of a pair with water-reward within a four-arm maze whereas pseudo-trained (P) rats were only submitted to the olfactory cues without any reinforcement. In the piriform cortex, both T and P rats exhibited a higher immunoreactivity on the first day, which seemed to indicate a novelty-related Fos expression in this area, but whatever the learning-stage, no significant difference in Fos expression between T and P rats was observed. In hippocampus, Fos expression was significantly different between T and P rats in CA1 and CA3 on the first and fourth days respectively. Thus we showed a differential activation of CA1 and CA3 subfields which might support a possible functional heterogeneity. In the orbitofrontal cortex, Fos immunoreactivity was significantly higher in T rats compared to P rats when mastery of the discrimination task was complete. In contrast, no learning-related Fos expression was found in infralimbic and prelimbic cortices. The present data suggest an early implication of the hippocampal formation and a later involvement of neocortical areas throughout different stages of a progressively acquired olfactory learning task.

Analysis of Variance↗
PubMed2005

Identification of novel electroconvulsive shock-induced and activity-dependent genes in the rat brain.

Electroconvulsive shock (ECS) has been used as an effective treatment for patients suffering from major depression disorders and schizophrenia. However, the exact mechanisms underlying the action of ECS are poorly understood. Using high-density oligonucleotide microarrays, we identified 60 ECS-induced genes whose gene products are involved in the neuronal signaling, neuritogenesis and tissue remodeling. In situ hybridization and depolarization-dependent expression assay were performed to characterize 4 genes (lysyl oxidase, Ab1-046, SOX11, and T-type calcium channel 1G subunit) which have not yet been reported to be induced by ECS. Interestingly, the induction of these genes was observed mainly in the dentate gyrus of hippocampal formation and piriform cortex, where ECS-induced neural activation is highlighted, and depolarization of cultured cortical neurons also induced the expression of these genes. Taken together, our results suggest that therapeutic actions of ECS may be manifested by the activity-dependent induction of genes related to the plastic changes of the brain such as neuronal signaling neuritogenesis, and tissue remodeling.

Animals↗
PubMed2005

Memory of early maltreatment: neonatal behavioral and neural correlates of maternal maltreatment within the context of classical conditioning.

BACKGROUND: While children form an attachment to their abusive caregiver, they are susceptible to mental illness and brain abnormalities. To understand this important clinical issue, we have developed a rat animal model of abusive attachment where odor paired with shock paradoxically produces an odor preference. Here, we extend this model to a seminaturalistic paradigm using a stressed, "abusive" mother during an odor presentation and assess the underlying learning neural circuit. METHODS: We used a classical conditioning paradigm pairing a novel odor with a stressed mother that predominantly abused pups to assess olfactory learning in a seminaturalistic environment. Additionally, we used Fos protein immunohistochemistry to assess brain areas involved in learning this pain-induced odor preference within a more controlled maltreatment environment (odor-shock conditioning). RESULTS: Odor-maternal maltreatment pairings within a seminatural setting and odor-shock pairings both resulted in paradoxical odor preferences. Learning-induced gene expression was altered in the olfactory bulb and anterior piriform cortex (part of olfactory cortex) but not the amygdala. CONCLUSIONS: Infants appear to use a unique brain circuit that optimizes learned odor preferences necessary for attachment. A fuller understanding of infant brain function may provide insight into why early maltreatment affects psychiatric well-being.

Animals↗
PubMed2003

Effect of nicotine on the expression of leptin and forebrain leptin receptors in the rat.

We have previously reported that chronic nicotine administration (4.0 mg/kg/day by i.p. injection over 14 days) up-regulates orexin/hypocretin and neuropeptide Y (NPY) mRNA expression and peptide levels within the hypothalamus. Since there exists a coregulation between these neuropeptides and the protein leptin, the present study was undertaken to determine whether nicotine has a regulatory effect on leptin signaling. Under the same experimental regimen used previously, we found that nicotine down-regulates plasma leptin concentration by 48.8% (P<0.001) and leptin RNA level by 11.4% and 12.4%, respectively, in the perirenal and epididymal white adipose tissue (PWAT, EWAT) compared to the saline controls. We also measured an approximately 20% decrease in white and brown adipose tissue (BAT) by weight in nicotine-treated animals relative to saline controls (P<0.05). On the other hand, we found that chronic nicotine administration increased the expression levels of OB-Rb mRNA by 12% and OB-R mRNA by 25% in the medial basal hypothalamus compared to control rats. Subsequent radioligand binding assays indicated that nicotine also significantly increased leptin binding in ventromedial hypothalamic area (VMA), medial basal hypothalamic area (MBA), arcuate nucleus/median eminence, paraventricular nuclei and piriform cortex. Taken together, our results revealed that nicotine is involved in the regulation of leptin signaling, suggesting that leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body weight in rats.

Adipose Tissue↗
PubMed2005

Immunohistochemical localization of gastrin-releasing peptide receptor in the mouse brain.

Gastrin-releasing peptide (GRP) is a mammalian bombesin (BN)-like peptide that binds with high affinity to the GRP receptor (GRP-R). Previous behavioral studies using mice and rats showed that the GRP/GRP-R system mediates learning and memory by modulating neurotransmitter release in the local GABAergic network of the amygdala and the nucleus tractus solitarius (NTS). To date, the precise distribution of GRP-R in the brain has not been elucidated. We used a synthetic peptide derived from mouse GRP-R to generate affinity-purified antibodies to GRP-R and used immunohistochemistry to determine the distribution of GRP-R in the mouse brain. The specificity of anti-GRP-R antibody was confirmed in vitro using COS-7 cells transiently expressing GRP-R and in vivo using GRP-R-deficient and wild-type mouse brain sections. GRP-R immunoreactivity was widely distributed in the isocortex, hippocampal formation, piriform cortex, amygdala, hypothalamus, and brain stem. In particular, GRP-R immunoreactivity was observed in the lateral (LA), central, and basolateral amygdaloid (BLA) nuclei and NTS, which are important regions for memory performance. Double-labeling immunohistochemistry demonstrated that subpopulations of GRP-R are present in GABAergic neurons in the amygdala. Consequently, GRP-R immunoreactivity was observed in the GABAergic neurons of the limbic region. These anatomical results provide support for the idea that the GRP/GRP-R system mediates memory performance by modulating neurotransmitter release in the local GABAergic network.

Animals↗
PubMed2005

Alteration of kappa-opioid receptor system expression in distinct brain regions of a genetic model of enhanced ethanol withdrawal severity.

Abrupt withdrawal from chronic alcohol exposure can produce convulsions that are likely due to ethanol (EtOH) neuroadaptations. While significant efforts have focused on elucidating dependence mechanisms, the alterations contributing to EtOH withdrawal severity are less well characterized. The present studies examined the kappa-opioid receptor (KOP-R) system in Withdrawal Seizure-Prone (WSP) and Withdrawal Seizure-Resistant (WSR) mice, selected lines that display severe and mild convulsions upon removal from chronic EtOH exposure. Previous data demonstrated significant increases in whole brain prodynorphin (Pdyn) mRNA in WSP mice only during EtOH withdrawal. No significant effects of EtOH exposure or withdrawal were observed in WSR mice. The present study characterized Pdyn mRNA and the KOP-R in WSP and WSR mice during EtOH withdrawal using in situ hybridization (ISH) and KOP-R autoradiography. Analyses were performed in brain regions that express Pdyn mRNA and/or KOP-R and that might participate in seizure circuitry: the piriform cortex, olfactory tubercle, nucleus accumbens, caudate-putamen, claustrum, dorsal endopiriform nucleus, and cingulate cortex. ISH analyses confirmed previous findings; EtOH withdrawal increased Pdyn mRNA in multiple brain regions of WSP mice, but not WSR. Basal KOP-R binding was higher in WSR mice than in WSP mice, suggesting an anti-convulsant role for receptor activation. Finally, increased KOP-R density was present during EtOH withdrawal in WSP mice. These data suggest that differences in the KOP-R system among the lines might contribute to their selected difference in EtOH withdrawal severity.

Alcohol Withdrawal Seizures↗
PubMed2005

Activation of feeding-related neural circuitry after unilateral injections of muscimol into the nucleus accumbens shell.

Chemical inhibition of neurons in the nucleus accumbens shell (AcbSh) elicits intense, behaviorally specific, feeding in satiated rats. We have demonstrated previously that this treatment activates a number of brain regions, most significantly the lateral hypothalamus (LH). This activation could be elicited through a direct neural connection with the AcbSh or secondarily through changes in autonomic activity, stress, or circulating levels of orexigenic or satiety factors. In the present study, we used the immunohistochemical localization of Fos protein to map neuronal activation after unilateral muscimol injections into the AcbSh to determine whether AcbSh-mediated Fos expression remains lateralized in the circuit and whether secondary systemic changes in the rat can be excluded as primary factors in the activation of downstream component nuclei. Rats receiving only saline injections exhibited very little Fos immunoreactivity. In contrast, unilateral injections of muscimol into the AcbSh consistently increased Fos expression in several brain regions. Three distinct patterns of expression were observed. Fos synthesis in the LH was increased only on the side of the brain ipsilateral to the muscimol injection. Fos expression remained primarily ipsilateral to the injection site in the septohypothalamic, paraventricular hypothalamic (PVN), paratenial thalamic, and lateral habenular nuclei, and medial substantia nigra, but was increased bilaterally in the piriform cortex, supraoptic nucleus, central nucleus of the amygdala, and nucleus of the solitary tract. Smaller numbers of Fos-immunoreactive cells were seen unilaterally in the bed nucleus of the stria terminalis, medial ventral pallidum, arcuate nucleus, and ventral tegmental area and bilaterally in the supraoptic and tuberomammillary nuclei. The labeling in the LH, PVN, and other unilaterally labeled structures provides evidence that these brain regions are components of an AcbSh-mediated neural circuit and suggests that they may be involved in the expression of AcbSh-mediated feeding behavior.

Analysis of Variance↗
PubMed2006

Induction of CITED2 expression in the rat hippocampus following transient global ischemia.

CITED2 is implicated in the modulating the activity of HIF-1 which is a major transcription factor involved in ischemia-related gene expression. Following transient forebrain ischemia, we found that CITED2 was induced in a subset of brain regions including dentate gyrus of the hippocampal formation and piriform cortex. Because CITED2 was not induced in cultured neurons exposed to oxygen-glucose deprivation, we concluded that hypoxia is not sufficient to trigger its induction.

Animals↗
PubMed2006

Unilateral lesion of the subthalamic nucleus enhances cortical fos expression associated with focally evoked seizures in the rat.

Reducing subthalamic nucleus (STN) activity has been proposed as an anti-epileptic procedure. Here we show that, on the contrary, a unilateral lesion of the STN causes slight (nonsignificant) increases in the severity of limbic seizures evoked by bicuculline infusion into the piriform cortex, associated with marked Fos expression throughout the cerebral cortex. Abolishing the STN control over the basal ganglia output may therefore play a facilitatory role on cortical activation associated with limbic seizures.

Animals↗