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PubMed2005

Neurohistochemical biomarkers of the marine neurotoxicant, domoic acid.

Domoic acid and its potent excitotoxic analogues glutamic acid and kainic acid, are synthesized by marine algae such as seaweed and phytoplankton. During an algal bloom, domoic acid may enter the food web through its consumption by a variety of marine organisms held in high regard as seafoods by both animals and humans. These seafoods include clams, mussels, oysters, anchovies, sardines, crabs, and scallops, among others. Animals, such as pelicans, cormorants, loons, grebes, sea otters, dolphins, and sea lions, which consume seafood contaminated with domoic acid, suffer disorientation and often death. Humans consuming contaminated seafood may suffer seizures, amnesia and also sometimes death. In addition to analytical measurement of domoic acid exposure levels in algae and/or seafood, it is useful to be able to identify the mode of toxicity through post-mortem evaluation of the intoxicated animal. In the present study, using the rat as an animal model of domoic acid intoxication, we compared histochemical staining of the limbic system and especially the hippocampus with degeneration-selective techniques (Fluoro-Jade and silver), a conventional Nissl stain for cytoplasm (Cresyl violet), a myelin-selective stain (Black-Gold), an astrocyte-specific stain (glial fibrillary acidic protein), early/immediate gene responses (c-Fos and c-Jun), as well as for heat shock protein (HSP-72) and blood-brain barrier integrity (rat IgG). The results demonstrate that the degeneration-selective stains are the biomarkers of domoic acid neurotoxicity that are the most useful and easy to discern when screening brain sections at low magnification. We also observed that an impairment of blood-brain barrier integrity within the piriform cortex accompanied the onset of domoic acid neurotoxicity.

Animals↗
PubMed2006

Nutritional homeostasis and indispensable amino acid sensing: a new solution to an old puzzle.

Indispensable amino acids are neither synthesized nor stored in animals and are rapidly depleted when not provided by the diet. To maintain homeostasis, organisms must sense deficiency of an indispensable amino acid and implement a repletion strategy. In rats and birds, the anterior piriform cortex houses the detector, but its mechanism has evaded description for >50 years. Recently, rapid detection of amino acid depletion was shown behaviorally when naïve animals, pre-fed a low nitrogen diet, terminated their first deficient meal within 20 min. The general amino acid control system of yeast, which is activated by amino acid deprivation via deacylated tRNA, was found to be active in rodent brain, showing conservation of amino acid sensory mechanisms across eukaryotic species.

Amino Acids, Essential↗
PubMed2005

Different types of status epilepticus lead to different levels of brain damage in rats.

We investigated a possible correlation between behavior during status epilepticus (SE) and underlying brain damage. Adult rats were electrically stimulated in the left amygdala to induce SE, which was stopped 2 hours later. We observed two different types of SE: (1) typical SE (TSE), with facial automatisms, neck and forelimb myoclonus, rearing and falling, and tonic-clonic seizures; (2) ambulatory SE (ASE), with facial automatisms, neck myoclonus, and concomitant ambulatory behavior. TSE was behaviorally more severe than ASE (P<0.05). Histology revealed neuronal loss in several brain areas. There was a positive correlation between SE type and amount of injured areas 24 hours and 14 days after SE (P<0.01). The areas more affected were piriform cortex and hippocampal formation. We suggest quality of seizures during SE may be considered in further SE studies, as our results indicate its influence on the severity of brain damage following this paradigm.

Amygdala↗
PubMed2003

Translocation of glutamate transporter subtype excitatory amino acid carrier 1 protein in kainic acid-induced rat epilepsy.

Glutamate excitotoxicity has been implicated in the pathophysiology of epilepsy. Systemic injection of kainic acid (KA) in the rat produces an animal model of human temporal lobe epilepsy. We examined the temporal expression of the sodium-dependent neuronal glutamate transporter, excitatory amino acid carrier 1 (EAAC1), in KA-induced rat epilepsy. As an early alteration, perinuclear deposits of EAAC1 protein were found mainly in the large pyramidal neurons at the hippocampus, neocortex, piriform cortex, and amygdala with the reduction of neuropil staining 6 hours after KA injection. Immunoelectron microscopic study revealed that the perinuclear EAAC1 immunoreactivity corresponded to the translocation to the Golgi complex. At this time point, EAAC1 mRNA was down-regulated. The intracellular aggregation of EAAC1 primarily disappeared by 24 hours. In vitro studies indicated that internalization of EAAC1 from the plasma membrane to the intracellular compartment by KA treatment was associated with the reduction of electrogenic transporter currents. Our results suggest that the transient EAAC1 internalization participates in the modulation of the transporter function preventing excessive glutamate uptake to pyramidal neurons during the early stage of epilepsy.

Amino Acid Transport System X-AG↗
PubMed2000

Effects of threonine injections in the lateral hypothalamus on intake of amino acid imbalanced diets in rats.

Previous work from this laboratory suggests that animals decrease their intake of an amino acid imbalanced diet (IMB), due in part to a drop in the concentration of the dietary limiting amino (DLAA) in the anterior piriform cortex (APC). Administration of the DLAA, but not of a non-limiting amino acid into the APC, blocks the anorectic response to IMB. To our knowledge, the effects of DLAA injections on intake of a diet devoid of the DLAA (DEV), have not been examined in areas outside the APC. We hypothesized that the LH is a potential chemosensory area for DLAA. Our objectives were: (1) to determine whether injections of the DLAA threonine into the lateral hypothalamus (LH) alter intake of a threonine-devoid diet (DEV); and (2) to examine the dose-response effects of threonine injections into the LH on intake of threonine-corrected diet (COR). Administration of threonine into the LH stimulated DEV intake during the first 6 h at the 0.25 and 1-nmol doses by approximately 26 and 24%, respectively. Threonine (0.25, 2.5 nmol) did not alter COR intake at any time during the first 12 h. Our results suggest that: (1) the LH, along with the APC, likely acts as a chemosensory brain area for indispensable amino acids; and (2) both the APC and LH are part of a circuit that is involved in the short term anorectic response to amino acid imbalanced diets.

Amino Acids↗
PubMed2001

Immunohistochemical localization of the neuropeptide Y Y1 receptor in rat central nervous system.

The diverse effects of neuropeptide Y (NPY) are mediated through interaction with G-protein coupled receptors. Pharmacological analysis suggests the Y1 receptor mediates several of NPY's central and peripheral actions. We sought to determine the distribution of Y1 protein throughout the rat central nervous system by means of indirect immunofluorescence using the tyramide signal amplification method and a novel, amino terminally-directed Y1 antisera. This antisera was verified as specific for Y1 by solution-phase competition ELISA, Western blot and in situ blocking experiments. High concentrations of Y1 immunoreactivity were found in the claustrum, piriform cortex (superficial layer), arcuate hypothalamic nucleus, interpeduncular nucleus, paratrigeminal nucleus, and lamina II of the spinal trigeminal nucleus and entire spinal cord. Moderate levels of Y1 immunoreactivity were found the in the main olfactory bulb, dorsomedial part of suprachiasmatic nucleus, paraventricular hypothalamic nucleus, ventral nucleus of lateral lemniscus, pontine nuclei, mesencephalic trigeminal nucleus, external cuneate nucleus, area postrema, and nucleus tractus solitarius. Low levels of Y1 immunostaining were distributed widely throughout layers II-III of the cerebral cortex (i.e., orbital, cingulate, frontal, parietal, insular, and temporal regions), nucleus accumbens core, amygdalohippocampal and amygdalopiriform areas, dentate gyrus, CA1 and CA2 fields of hippocampus, principal and oral divisions of the spinal trigeminal nucleus, islands of Calleja and presubiculum. These findings are discussed with reference to previously reported receptor autoradiography, immunohistochemistry and mRNA analyses to further support the role of Y1 in NPY-mediated biology.

Amino Acid Sequence↗
PubMed2002

Differential induction of p53 in immature and adult rat brain following lithium-pilocarpine status epilepticus.

Activation of the tumor suppressor gene, p53, has been strongly implicated in selective neuronal cell death. This study investigated p53 expression in the immature and adult rat brain following status epilepticus induced by the administration of lithium-pilocarpine (LPSE). Both p53 mRNA and protein were examined in relation to neuronal degeneration using in situ hybridization and immunohistochemistry, respectively. Injured cells with eosinophilic cytoplasm with increased p53 mRNA were observed in hippocampal subfields, piriform cortex, amygdala and thalamus. p53 mRNA levels reached a peak by 8 h and returned to baseline by 24 h after the onset of LPSE. The magnitude of p53 mRNA induction was greatest in 21-day-old rats. In contrast to the cellular expression pattern of p53 mRNA, immunohistochemistry demonstrated that p53 protein was increased in all of the eosinophilic cells. Further, double-labeling studies revealed that p53 protein was elevated in neurons that were degenerating. This was supported by colocalization of activated caspase 3 in some cells with damaged DNA. These results provide additional evidence for a critical role for the p53 pathway in excitotoxic neuronal cell death due to status epilepticus.

Aging↗
PubMed2002

Immunohistochemical study of p53-associated proteins in rat brain following lithium-pilocarpine status epilepticus.

Activation of the p53-stress response pathway has been implicated in excitotoxic neuronal cell death. Recent studies have demonstrated an age-dependent induction of both p53 mRNA and protein in the rat brain following lithium-pilocarpine-mediated status epilepticus (LPSE). We investigated whether other proteins that have been shown to participate in the p53 cascade are induced by LPSE. We used immunohistochemistry to examine the expression of Mdm2, Bax, CD95/Fas/APO-1, ATM, Ref-1 and ubiquitin. A significant increase in nuclear Mdm2 immunoreactivity, which colocalized with p53, was observed in cells within hippocampal pyramidal cell layers, dentate gyrus, piriform cortex, amygdala and thalamus. Dual immunofluorescence microscopy revealed a reduction in free ubiquitin expression in cells with p53 and Mdm2 accumulation. Increased immunoreactivity for CD95/Fas/APO-1 and Bax was also detected in the same p53-positive cells. Moreover, expression of Ref-1 and ATM, which are involved in the response to oxidative stress-induced DNA damage and regulation of p53 function, were increased. Colocalization of Ref-1 and p53 suggests that Ref-1 might activate p53 function in LPSE-induced neurodegeneration. In contrast, ATM immunoreactivity was predominantly cytoplasmic suggesting that ATM may not directly modulate p53 activity in injured neurons. These results extend our previous observations with regard to activation and stabilization of p53 in injured central nervous system neurons. The data indicate that p53 induction following LPSE may activate downstream pro-apoptotic genes leading to neurodegeneration.

Animals↗
PubMed2002

Spatio-temporal dynamics of brain activated regions during drinking behavior in rats.

Spatio-temporal dynamics of activated brain areas induced by drinking were investigated and visualized in behaving rats using functional magnetic resonance imaging (fMRI). The rats were trained to drink in the magnet bore, and the images were taken during and after drinking glucose and distilled water. During glucose ingestion, the signal intensity was increased continuously and maximally in the lateral hypothalamic area (LHA) and the ventromedial hypothalamus (VMH). Somewhat less intense activation in the central nucleus of the amygdala (AMc), and transient activation in the piriform cortex and the mediodorsal nucleus of the thalamus were observed. The signal intensities of other regions measured were largely unchanged. During post-ingestive periods, the signals re-increased in the hypothalamic areas and AMc. When water was given, LHA and VMH were similarly activated, however, the signal intensity in the amygdala was not significantly increased. The results indicate that these brain regions are activated differentially during drinking behavior, and that LHA and VMH play a central role in the control of not only feeding but also drinking. The regional activities in LHA and VMH are not principally related to the gustatory sensation, and the reactivation after drinking may be related to satisfaction or post-ingestive nutritional information. Also, the responses of AMc are probably due to reward value difference. To the best of our knowledge, this is the first report of mapping of brain areas using fMRI in behaving rats. The improved method described in this study for collecting fMRI data in behaving animals will be useful for studying functional network during animal behavior.

Animals↗
PubMed2002

Retrograde tracing of zinc-enriched (ZEN) neuronal somata projecting to the olfactory bulb.

Zinc ions seem to be important to several neurological functions and have been connected to the pathophysiology of epilepsy, neuronal cell death after seizure or stroke, and Alzheimer's disease. Both epilepsy and Alzheimer's disease are clinical conditions believed to involve the olfactory bulb. The mammalian olfactory bulb is densely innervated by zinc-enriched (ZEN) neurons, and the distribution of the ZEN terminals in the mouse olfactory bulb has previously been described. The aim of this study was to describe the origins of ZEN terminals projecting into the main olfactory bulb of the rat. Selective labeling of ZEN terminals was accomplished by intracerebral infusion of sodium selenide, whereby zinc selenium clusters are created in the ZEN terminals. Some of these clusters move by retrograde axonal transport to the somata where they can be silver-enhanced by autometallography (AMG). After infusion of sodium selenide into the main olfactory bulb, retrogradely labeled ZEN somata were found (1) ipsilaterally in all anterior olfactory nuclei, taenia tecta, piriform cortex and lateral entorhinal cortex, and (2) contralaterally in anterior olfactory nuclei except the external division. The ipsilateral anterior olfactory nucleus had the densest population of ZEN somata, and it was found that these somata originated mainly from pyramidal neurons in layers II and III of each area. The olfactory-related centrifugal afferents to the main olfactory bulb are discussed.

Afferent Pathways↗
PubMed2003

Localization of orexins and their receptors in the rat olfactory system: possible modulation of olfactory perception by a neuropeptide synthetized centrally or locally.

Orexin-A and -B, also known as hypocretins, are two neuropeptides acting on feeding and sleep. They are specific ligands for two different receptors belonging to the G-protein coupled receptors family. Orexin fibers and orexin receptor neurons have been previously described in the forebrain olfactory system. Using immunocytochemistry, we showed that both orexin-A and -B as well as their receptors were present at different levels of the olfactory system, from the nasal mucosa to nuclei of the amygdala. A punctuated staining for orexins and their receptors was detected at the apical part of the olfactory epithelium; in the lamina propria of the mucosa, the staining was localized around olfactory nerves. At the ultrastructural level, olfactory neurons and supporting cells were found immunoreactive for orexins and their receptors. The labeling was localized in dendritic knobs and cilia of neurons, in the apical part and microvilli of supporting cells. The finding of immunolabeled cisternae of reticulum strongly suggests a local synthesis of both peptides and receptors, confirmed by RT-PCR experiments. In forebrain and amygdala regions, we detected numerous orexin fibers. Orexin receptors were present in mitral-tufted cells of the bulb and in many neuronal perikarya in the anterior olfactory nuclei, piriform cortex and amygdala nuclei. Altogether, these results show that orexins and their receptors are present at all levels of the olfactory system, from cilia where odors bind to their receptors to central regions where integration of olfactory signals occurs. They suggest a possible modulation of olfactory perception by these neuropeptides.

Amygdala↗
PubMed2003

Effects of chronic exercise and imipramine on mRNA for BDNF after olfactory bulbectomy in rat.

We examined the effects of chronic activity wheel running and antidepressant treatment on brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) in multiple brain regions-hippocampal formation (HF), ventral tegmental area/substantia nigra (VTA/SN), nucleus accumbens (NAc), and piriform cortex (PFx)-after bilateral olfactory bulbectomy (OBX). Male, Long-Evans rats (n=72) underwent either sham or OBX surgery and were randomly divided into eight experimental groups in a 2 (sham vs. OBX) x 2 (sedentary vs. activity wheel)x2 (saline vs. imipramine) factorial design. Animals were killed after 21 days of treatment. Drug x exercise interaction effects were observed for HF (P=0.006-0.023) and VTA/SN (P=0.021); exercise increased BDNF mRNA in the saline treated animals but not in the imipramine treated animals. OBX did not affect BDNF mRNA in the HF or VTA/SN (P>0.05). BDNF mRNA levels in the PFx were not altered by exercise, drug, or OBX (P>0.05). These results suggest that the effect of exercise on BDNF mRNA extends beyond the HF to the mesolimbic ventral tegmental area and that the potentiation of BDNF mRNA by exercise and antidepressant pharmacotherapy, reported by other investigators, is time limited.

Animals↗
PubMed1994

Limbic system fos expression associated with paternal behavior.

Axon-sparing lesions of the medial nucleus of the amygdala (MeA) decrease male parental behavior in the highly social prairie vole. To assess further the role of the amygdala in paternal behavior, male and female prairie voles were exposed to a pup or a non-social olfactory stimulus for 3 hours, and cells expressing Fos peptide were labelled using immunocytochemistry. Compared to controls, males exposed to a pup showed an increase in Fos expression in the MeA, as well as in several areas with connections to it: the accessory olfactory bulb, lateral septum, medial preoptic area, medial bed nucleus of the stria terminalis, nucleus reuniens and paraventricular nucleus of the thalamus. There was no increase in Fos immunoreactivity in the paraventricular nucleus of the hypothalamus or piriform cortex. The same pattern of Fos expression was found in female voles, with the exception of the thalamic paraventricular nucleus, where there was an increase in the pup-exposed group that was not statistically significant (P = 0.11). In addition, the magnitude of induction in females was markedly less than that in males in the medial preoptic area. These results provide further evidence that the MeA is involved in paternal behavior, and suggest certain other areas previously implicated in meternal behavior may also be involved in the control of paternal behavior in this species.

Animals↗
PubMed1997

Methamphetamine exposure can produce neuronal degeneration in mouse hippocampal remnants.

Neuronal cell death in hippocampal remnants was seen after methamphetamine (METH) exposure. Two techniques (Fluoro-Jade labeling and argyrophylia) showed that neuronal degeneration occurred in the indusium griseum, tenia tecta and fasciola cinerea within 5 days post-METH exposure in 70% of the mice. Neurodegeneration also occasionally occurred in the piriform cortex, hippocampus and frontal/parietal cortex. This cell death, unlike striatal neurotoxicity, was not dependent on magnitude of hyperthermia occurring but did correlate with behavioral seizure activity during METH exposure. Excitotoxic mechanisms may be underlying the neuronal degeneration since co-administration of phenobarbital blocked cell death.

Animals↗
PubMed1997

Distribution of pancreatic polypeptide receptors in the rat brain.

Pancreatic polypeptide (PP) is a regulatory peptide that modulates gastrointestinal function. Previously we demonstrated PP receptors in the brainstem and interpeduncular nucleus, and the PP receptors in the brainstem appear to modulate gastric motility and pancreatic exocrine secretion. The purpose of this study is to extend our understanding of the distribution of PP receptors in the rat brain in order to determine the systems that are potentially modulated by PP. Rat brains were studied using 125I-PP receptor autoradiography on cryostat sections of the entire brain cut in three planes (horizontal, sagittal, and coronal). Brain regions exhibiting PP binding sites were confirmed when identified in all three planes of section. Saturable PP binding was identified in the hypothalamus (arcuate and paraventricular n), the rostral forebrain (medial preoptic area, anterior olfactory nucleus, islands of Calleja, the dorsal endopiriform n, piriform cortex, and the bed n of the stria terminalis), medial amygdaloid n; the thalamus (anteromedial thal. n; reuniens thal. n; and paraventricular thal n), the interpeduncular red nucleus, substantia nigra, parabrachial n; locus coeruleus, mesencephalic trigeminal n, dorsal motor n of the vagus, the n solitary tract, and the area postrema. We conclude that PP receptors are distributed widely throughout the rat brain. The distribution of many of these PP binding sites corresponds to brain regions regulating digestion and autonomic function. We speculate, based on the patterns of binding in the olfactory and limbic systems, that PP receptors might be involved in positive reinforcement of ingestion behavioral as well as modulation of gastrointestinal function.

Animals↗
PubMed1997

Immunohistochemical and RT-PCR detection of Na+-dependent inorganic phosphate cotransporter (NaPi-2) in rat brain.

Expression of a renal Na+-dependent inorganic phosphate (Pi) cotransporter (NaPi-2) was studied in rat forebrain with reverse transcription and polymerase chain reaction (RT-PCR) and immunohistochemistry. RT-PCR analysis for total RNA from whole brain and sequencing of the PCR products showed expression of NaPi-2 mRNA in the brain. Immunohistochemical analysis revealed NaPi-2 staining in many nonpyramidal neurons of all six layers throughout neocortical areas and in neurons of proisocortical and periallocortical areas. NaPi-2-immunoreactive neurons were also detectable in the piriform cortex, hippocampal formation, caudate-putamen, amygdaloid nuclei and lateral geniculate nucleus. Furthermore, NaPi-2 staining was shown in ependymal cells and microvascular endothelial cells. The present results suggest that NaPi-2 is synthesized within the brain and involved in maintaining Pi homeostasis of certain neurons and/or the entire brain.

Animals↗
PubMed1998

Increased corticotropin-releasing factor immunoreactivity in select brain sites following kainate elicited seizures.

The literature has focused on the localization, regulation and function of corticotropin-releasing factor (CRF) expressing neurons localized in the paraventricular nucleus (PVN) of hypothalamus. However, less information is available on the expression, regulation, and function of CRF at extrahypothalamic sites. The current study examined the induction of CRF in extrahypothalamic brain sites following generalized clonic seizures induced by kainic acid. At 24 h post seizure onset, there was a marked increase of CRF immunolabeled perikarya in select brain areas, which contained little, if any, CRF in control brains. This CRF-like labeling was observed in olfactory structures such as the main olfactory bulb (internal granular layer), anterior olfactory nucleus, and deep layers of piriform cortex. Other sites of increased CRF-like immunoreactivity included the tenia tecta, inner layers of cingulate cortex, lateral septum, dorsal endopiriform nucleus, fundus striatum, and nucleus of the lateral olfactory tract. Additionally, CRF-like labeling was atypically increased in the amygdala (lateral and basolateral amygdaloid nuclei) and hippocampal formation (pyramidal cells of regions CA1/CA3 and polymorph cells within the dentate hilus). An association between the increased CRF immunoreactivity and neuropathological processes, characteristic of this seizure model, is hypothesized and discussed.

Animals↗
PubMed1997

Tissue-specific mRNA expression of a calcitonin receptor-like receptor during fetal and postnatal development.

The distribution of calcitonin receptor-like receptor (CRLR) mRNA in developing rats was investigated by in situ hybridization. Signals were found in the piriform cortex, the central and basolateral amygdala and the amygdalostriatal transition area. Among peripheral organs, the CRLR was predominantly expressed in the lung. mRNA expression in blood vessels, liver, midgut, rectum and urethra was restricted to gestational days 16 and/or 20. The CRLR was thought to be a calcitonin gene-related peptide (CGRP) type 1 receptor (Aiyar et al., J. Biol. Chem., 271 (1996) 11325-11329). This contrasts with previously reported evidence that the CRLR is an orphan receptor with no identifiable interactions with CGRP and other related ligands (Flühmann et al., Biochem. Biophys. Res. Commun., 206 (1995) 341-347). In situ hybridization signals have not been detected in the cerebellum and the spleen known to present a high density of CGRP binding sites. The different regional distribution of CGRP receptor binding sites and CRLR mRNA implies the latter encoding a different CGRP receptor subtype.

Aging↗