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PubMed1995

The N-methyl-D-aspartate antagonists phencyclidine, ketamine and dizocilpine as both behavioral and anatomical models of the dementias.

Phencyclidine (PCP) and ketamine can induce a model psychosis in drug addicts and exacerbate the symptoms of chronic schizophrenics. The model psychoses these drugs induce mimic a variety of schizophrenic symptoms, including flattened affect, dissociative thought disorder, depersonalization and catatonic states. These symptoms can persist for prolonged periods and chronic PCP and ketamine addicts have persisting memory deficits. Dizocilpine (MK-801) is a simpler drug than PCP or ketamine in its actions, but it shares with both the property of blocking in a non-competitive manner the N-methyl-D-aspartate (NMDA) ion-channel. Behavioral observations and drug-discrimination studies in animals indicate that PCP and dizocilpine are similar in their effects and they both have a neurotoxic effect on neurons in posterior cingulate cortex. Recent studies have indicated that both of these drugs, when given continuously for several days, further induce neuronal degeneration in other limbic structures. These include brain regions of rats related to olfaction, associated limbic structures such as piriform cortex and posterior regions of entorhinal cortex and in it's projections, through the perforant pathway, to dentate gyrus and other cells in ventral hippocampus. These degenerative consequences may be excitatory neurotoxic effects, for these compounds also induce an elevation in glucose metabolism maximal in just those structures where degeneration is observed and the degeneration involves entire cells, with all of their processes. It has been suggested these non-competitive NMDA antagonists induce an increase in firing rate in a limbic circuit which includes the perforant pathway. At least some competitive NMDA antagonists induce the same pattern of degeneration and altered glucose utilization. There is anatomical and functional evidence that alterations in these same limbic structures are present in the dementia syndrome manifested by some schizophrenics and most Alzheimer's patients. This suggests that these non-competitive NMDA antagonists may provide a more complete model of psychoses and memory disturbances than previously recognized, in that they can mimic both persisting symptomatology and neuroanatomical abnormalities. While the neurochemical underpinnings of this effect remain elusive, it appears to be both age and sex dependent. Further studies of the mechanisms by which NMDA antagonists induce increased glucose utilization and neurotoxicity in these limbic structures may clarify these alterations in this simplified Papez-like circuit.

Animals↗
PubMed1988

Localization of a family of muscarinic receptor mRNAs in rat brain.

A family of 4 rat muscarinic receptors (m1, m2, m3, and m4) have recently been cloned and sequenced (Bonner et al., 1987). Since pharmacological probes that are presently available do not appear to distinguish among 3 of these muscarinic receptors, we constructed oligonucleotide probes corresponding to the N-terminal sequences of the muscarinic receptors and used them to specifically localize m1, m2, m3, and m4 mRNA in sections of rat brain using in situ hybridization histochemistry. Northern analysis demonstrated a 3.1 kilobase (kb) m 1 mRNA, a 4.5 kb m3 mRNA, and a 3.3 kb m4 mRNA in cerebral cortex, striatum, hippocampus, and cerebellum. In situ hybridization histochemistry indicated a prevalence of m1 mRNA in the pyramidal cell layer of the hippocampus, the granule cell layer of the dentate gyrus, the olfactory bulb, amygdala, olfactory tubercule, and piriform cortex. Caudate putamen and cerebral cortex showed moderate levels of labeling. m2 mRNA was detectable in the medial septum, diagonal band, olfactory bulb, and pontine nuclei. m3 and m4 mRNA were also prevalent in the olfactory bulb and pyramidal cell layer of the hippocampus but were present only in low levels in the dentate gyrus. m3 mRNA was present in superficial and deep layers of the cerebral cortex, whereas m4 mRNA was more evenly distributed with a slightly more intense labeling evident in the midcortical layer. In addition, m3 mRNA was present in a number of thalamic nuclei and brain-stem nuclei, while m4 mRNA predominated in the caudate putamen. These data offer a new basis on which to interpret the heterogeneity of muscarinic actions in the CNS.

Animals↗
PubMed1993

Muscarinic receptor-mediated induction of Fos protein in rat brain.

Recent studies have shown that the centrally active muscarinic agonist pilocarpine induces c-fos mRNA in rat cortex. Here we describe the localization of muscarinic receptor-induced FOS protein, within the rat central nervous system (CNS), following administration of pilocarpine (25 mg/kg). High levels of FOS induction were apparent in many forebrain structures including the primary olfactory (piriform) cortex, nucleus accumbens, amygdala, hippocampus, neocortex and supra-optic nucleus of the hypothalamus. Within the neocortex FOS induction followed a laminar distribution being highest in layers 4 and 6 with lower induction seen in layers 2 and 5. Other areas showing FOS induction included the striatum, septum, inferior colliculus, thalamus, hypothalamus and several brainstem nuclei. Both atropine (10 mg/kg) and pirenzepine (100 mg/kg) reduced FOS induction suggesting that a pirenzepine-sensitive muscarinic receptor was involved. The possible significance of muscarinic-mediated FOS induction, to cholinergic kindling and the cholinergic hypothesis of learning and memory, is discussed.

Animals↗
PubMed2003

FMRI brain activation in response to odors is reduced in primary olfactory areas of elderly subjects.

Olfactory function is affected by aging and deficits often result in decreasing quality of life, health and safety. The present study investigated the cortical substrate of olfactory deficits related to aging with functional Magnetic Resonance Imaging (fMRI), with a retronasal olfactory stimulation protocol using flavored aqueous solutions presented to the mouth. Activation was found in young subjects in the piriform/amygdalar region and in the orbitofrontal cortex and in other areas previously found activated in neuroimaging studies using odorized air, including insula and cerebellum. Activation was seen in similar areas in old subjects but the degree of activation was significantly lower in regions receiving primary olfactory projections (piriform cortex, entorhinal cortex, and amygdala). This result supports the hypothesis of dysfunction and/or degeneration in areas critical to olfactory processing as a major cause of olfactory deficits in the older population.

Adult↗
PubMed1978

Histochemical labeling of beta-adrenergic receptors in the mouse central nervous system by 9-amino-acridin propranolol.

A new fluorescent beta-adrenergic antagonist, 9-amino-acridin propranolol (9-AAP), was administered intravenously to living mice. In the cerebral cortex, the highest concentration of 9-AAP was noted in the hippocampal formation, where it distinctly labeled the hippocampal pyramidal cell layer and the granule cell layer of the dentate gryus. High uptake occurred in the pyramidal cell layer of the piriform cortex. In the neocortex, fluorescence was less dense and more diffuse but confined to the basal layers. A similar pattern was observed in the basal layers of the cingulate cortex, but an additional high-density dotted fluorescence labeled its layer II. In the cerebellar cortex, 9-AAP was localized within the Purkinje cell layer. In the spinal cord, the highest density of fluorescence was observed in the nuclear collections of alpha-motoneurons. The findings were similar to those observed in the central nervous system of the rat and support the reproducibility of the method. 9-AAP may be used in vivo as a fluorescent probe to map out the central beta-adrenergic receptor system.

Acridines↗
PubMed2005

A field guide to the anterior olfactory nucleus (cortex).

While portions of the mammalian olfactory system have been studied extensively, the anterior olfactory nucleus (AON) has been relatively ignored. Furthermore, the existing research is dispersed and obscured by many different nomenclatures and approaches. The present review collects and assembles the relatively sparse literature regarding the portion of the brain situated between the olfactory bulb and primary olfactory (piriform) cortex. Included is an overview of the area's organization, the functional, morphological and neurochemical characteristics of its cells and a comprehensive appraisal of its efferent and afferent fiber systems. Available evidence suggests the existence of subdivisions within the AON and demonstrates that the structure influences ongoing activity in many other olfactory areas. We conclude with a discussion of the AON's mysterious but complex role in olfactory information processing.

Animals↗
PubMed1994

Regional expression of inducible heat shock protein-70 mRNA in the rat brain following administration of convulsant drugs.

Expression of inducible heat shock protein-70 mRNA (hsp-70 mRNA) was studied in the rat brain following systemic administration of different convulsant agents: an L-type voltage-dependent calcium channel agonist, (+/-)-BAY K 8644 (BAY-K); the excitotoxic glutamate agonists kainic acid and N-methyl-D-aspartic acid (NMDA); and the GABAA receptor complex antagonists pentylenetetrazole (PTZ) and lindane (gamma-hexaclorocyclohexane). BAY-K induced minimal hsp-70 mRNA expression in the hippocampus of convulsant rats, localized in the dentate gyrus and the pyramidal cell layer of Ammon's horn. Kainic acid treatment in rats, showing severe limbic convulsions, caused intense expression of hsp-70 mRNA and protein (HSP-70). Expression was localized in select cerebral regions, notably the pyramidal cell layer of the hippocampal CA3 field of Ammon's horn and the piriform cortex, and also the subicular complex and the amygdala, and, to a lesser extent, the entorhinal cortex, the pyramidal cell layer of CA1, several thalamic nuclei, and the parietal cortex. In contrast, systemic administration of NMDA, PTZ or lindane led to no detectable induction of hsp-70 mRNA in the rat brain, despite producing convulsions. Histological examination revealed cell injury only following kainic acid treatment. Damage was most apparent in the piriform and entorhinal cortices, pyramidal cell layer of the CA1 field, and cortical amygdaloid nuclei. BAY-K, NMDA, PTZ and lindane did not lead to any observable histopathological changes. These results show that convulsions of different aetiology do not inevitably induce hsp-70 mRNA expression or cell damage. Intense expression of hsp-70 mRNA was generally associated with regions that later showed variable degrees of nerve cell damage, although hsp-70 mRNA expression was not always predictive of subsequent cell death or survival.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2004

Cortical spreading depression activates and upregulates MMP-9.

Cortical spreading depression (CSD) is a propagating wave of neuronal and glial depolarization and has been implicated in disorders of neurovascular regulation such as stroke, head trauma, and migraine. In this study, we found that CSD alters blood-brain barrier (BBB) permeability by activating brain MMPs. Beginning at 3-6 hours, MMP-9 levels increased within cortex ipsilateral to the CSD, reaching a maximum at 24 hours and persisting for at least 48 hours. Gelatinolytic activity was detected earliest within the matrix of cortical blood vessels and later within neurons and pia arachnoid (> or =3 hours), particularly within piriform cortex; this activity was suppressed by injection of the metalloprotease inhibitor GM6001 or in vitro by the addition of a zinc chelator (1,10-phenanthroline). At 3-24 hours, immunoreactive laminin, endothelial barrier antigen, and zona occludens-1 diminished in the ipsilateral cortex, suggesting that CSD altered proteins critical to the integrity of the BBB. At 3 hours after CSD, plasma protein leakage and brain edema developed contemporaneously. Albumin leakage was suppressed by the administration of GM6001. Protein leakage was not detected in MMP-9-null mice, implicating the MMP-9 isoform in barrier disruption. We conclude that intense neuronal and glial depolarization initiates a cascade that disrupts the BBB via an MMP-9-dependent mechanism.

Animals↗
PubMed1996

Differential expression of oxytocin receptor mRNA in the developing rat brain.

The embryonic and postnatal localizations of oxytocin receptor mRNA in the developing rat brain were studied by in situ hybridization histochemistry. The hybridization signal was first detected at embryonic-day 13 in the primordium of the dorsal motor nucleus of vagus. Other positive regions progressively appeared after this time. The developmental profile of oxytocin receptor gene expression could be classified into two types; transient expression and constant abundant expression. The caudate putamen, cingulate cortex, the anterior thalamic nuclei, and the ventral tegmental area belonged to the first type. In these regions, oxytocin receptor mRNA was expressed intensely only during the early postnatal period. The regions such as the anterior olfactory nucleus, tenia tecta, some amygdaloid nuclei, piriform cortex, the ventromedial hypothalamic nucleus, subiculum, the prepositus hypoglossal nucleus and the dorsal motor nucleus of vagus showed constant expression of oxytocin receptor mRNA at high levels throughout development and in the adult. These findings concurred well with those of the ontogenic studies using receptor binding autoradiography with a ligand specific to oxytocin. Thus, the transient expression of oxytocin receptor during development was regulated at the transcriptional level in several brain regions, and oxytocin may play a role in brain development as well as in neural transmission in the mature brain.

Animals↗
PubMed2002

Cloning and localization of rgpr85 encoding rat G-protein-coupled receptor.

In an attempt to isolate genes involved in the brain development using ordered differential display PCR, we cloned rgpr85 which encodes rat G-protein-coupled receptor with high degree of identity to the amine-like neurotransmitter receptors. This gene was found to be localized at rat chromosome 4q21. In situ hybridization demonstrated that rgpr85 was predominantly expressed in the developing brain and spinal cord. Hybridization signal was especially abundant within the embryonic cortical plates where postmitotic cortical neurons are localized. In the cerebral cortex, the expression of rgpr85 was gradually decreased postnatally and became undetectable by P18. However, weak but significant expression of rgpr85 was maintained in the adult hippocampal formation, olfactory bulb, and cerebellum. Interestingly, rgpr85 expression was transiently induced in the adult hippocampal formation, piriform cortex, and amygdaloid complex by kainic acid (KA) treatment. Thus, dynamic regulation of rgpr85 expression suggests an importance of rgpr85-mediated signaling in the development of cerebral cortex and in the KA-induced responses in the adult brain.

Animals↗
PubMed2002

Mice with partial deficiency of c-Jun show attenuation of methamphetamine-induced neuronal apoptosis.

The regional distribution of c-Jun expression and of the number of apoptotic cells was compared in various brain areas after methamphetamine administration to mice. Our results showed that there was methamphetamine-induced overexpression of c-Jun in the cortex and striatum but not in the cerebellar cortex. There was an almost totally similar regional appearance of methamphetamine-induced apoptotic cells in the mouse brain; no apoptosis was present in the cerebellum. Additionally, in the neocortical area, more positive signals for c-Jun immunoreactivity were observed in the piriform cortex, an area that also showed more positive terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) signals than the frontal and parietal cortices. These observations suggested that c-Jun might be involved in methamphetamine-induced apoptosis. This idea was confirmed by using heterozygous c-Jun knockout mice that showed much less apoptosis than wild-type controls. In addition, we found that the majority of TUNEL-positive cells were also positive for c-Jun-like immunoreactivity in both genotypes. Moreover, methamphetamine-induced caspase-3 activity and PARP cleavage were also reduced in c-Jun heterozygous knockout mice. In contrast, methamphetamine-induced hyperthermia was essentially identical in the two genotypes. When taken together, our data support the hypothesis that c-Jun is involved in methamphetamine-induced apoptosis.

Animals↗
PubMed2004

Expression patterns of the novel imprinted genes Nap1l5 and Peg13 and their non-imprinted host genes in the adult mouse brain.

Recent work has implicated imprinted gene functioning in neurodevelopment and behaviour and defining the expression patterns of these genes in brain tissue has become a key prerequisite to establishing function. In this work we report on the expression patterns of two novel imprinted loci, Nap1l5 and Peg13, in adult mouse brain using in situ hybridisation methods. Nap1l5 and Peg13 are located, respectively, within the introns of the non-imprinted genes Herc3 and the Tularik1 (T1)/KIAA1882 homologue in two separate microimprinted domains on mouse chromosomes 6 and 15. These 'host' genes are highly expressed in brain and consequently we were interested in assessing their expression patterns in parallel to the imprinted genes. The brain expression of all four genes appeared to be mainly neuronal. The detailed expression profiles of Nap1l5 and Peg13 were generally similar with widespread expression that was relatively high in the septal and hypothalamic regions, the hippocampus and the cerebral cortex. In contrast, there was some degree of dissociation between the imprinted genes and their non-imprinted hosts, in that, whilst there was again widespread expression of Herc3 and the T1/KIAA1882 homologue, these genes were also particularly highly expressed in Purkinje neurons and piriform cortex. We also examined expression of the novel imprinted genes in the adrenal glands. Nap1l5 expression was localised mainly to the adrenal medulla, whilst Peg13 expression was observed more generally throughout the adrenal medulla and the outer cortical layers.

Animals↗
PubMed1999

Fjx1, the murine homologue of the Drosophila four-jointed gene, codes for a putative secreted protein expressed in restricted domains of the developing and adult brain.

The Drosophila gene four jointed (fj) codes for a secreted or cell surface protein important for growth and differentiation of legs and wings and for proper development of the eyes. Here we report the cloning of the mouse four-jointed gene (fjx1) and its pattern of expression in the brain during embryogenesis and in the adult. In the neural plate, fjx1 is expressed in the presumptive forebrain and midbrain, and in rhombomere 4, however a small rostral/medial area of the forebrain primordium is devoid of expression. Expression of fjx1 in the neural tube can be divided into three phases. (1) In the embryonic brain fjx1 is expressed in two patches of neuroepithelium: in the midbrain tectum and the telencephalic vesicles. (2) In fetal and early postnatal brain fjx1 is expressed mainly by the primordia of layered telencephalic structures: cortex (ventricular layer and cortical plate), olfactory bulb (subependymal layer and in the mitral cell layer). In addition expression is observed in the superior colliculus. (3) In the adult, fjx1 is expressed by neurones evenly distributed in the telencephalon (isocortex, striatum, hippocampus, olfactory bulb, piriform cortex), in the Purkinje cell layer of the cerebellum, and numerous medullary nuclei. In the embryo, strong expression can further be seen in the apical ectodermal ridge of fore- and hindlimbs and in the ectoderm of the branchial arches.

Amino Acid Sequence↗
PubMed2002

Appetitive and aversive olfactory learning in humans studied using event-related functional magnetic resonance imaging.

We combined event-related functional magnetic resonance imaging (fMRI) with olfactory classical conditioning to differentiate the neural responses evoked during appetitive and aversive olfactory learning. Three neutral faces [the conditioned stimuli (CS+)] were repetitively paired with pleasant, neutral, or unpleasant odors [the unconditioned stimuli (UCS)] in a partial reinforcement schedule. A fourth face was never paired to odor [the nonconditioned stimulus (CS-)]. Learning-related neural activity, comparing unpaired (face only) CS+ stimuli with CS-, showed valence-independent activations in rostral and caudal orbitofrontal cortex (OFC). Medial OFC responded to the appetitive (app) CS+, whereas lateral OFC responded to the aversive (av) CS+. Within nucleus accumbens, neural responses showed divergent activation profiles that increased with time in response to the appCS+ but decreased in response to the avCS+. In posterior amygdala, responses were elicited by the appCS+, which habituated over time. In temporal piriform cortex, neural responses were evoked by the avCS+, which progressively increased with time. These results highlight regional and temporal dissociations during olfactory learning and imply that emotionally salient odors can engender cross-modal associative learning. Moreover, the findings suggest that the role of human primary (piriform) and secondary olfactory cortices transcends their function as mere intermediaries of chemosensory information processing.

Adult↗
PubMed2000

Consolidation of passive avoidance learning is associated with transient increases of polysialylated neurons in layer II of the rat medial temporal cortex.

Within the rat medial temporal lobe, transient modulations of neural cell adhesion molecule (NCAM) polysialylation have been observed to follow spatial learning. These have been attributed to neuroplastic events associated with the processing of information destined for long term memory consolidation. To determine if similar events are associated with avoidance learning, we investigated change in polysialylated cell number in the entorhinal, perirhinal, and piriform cortex, following acquisition of a passive avoidance task in the rat. Direct quantification of polysialylated neurons in layer II of these cortical regions revealed a significant increase in polysialylated cell frequency at 12 h following passive avoidance training. Unlike spatial learning, the increased expression of polysialylated neurons persisted for up to 24-48 h following training. In the more dorsal aspect of the perirhinal/entorhinal cortex, this increase was found to be specific to learning, as it was not observed in animals rendered amnesic with scopolamine. By contrast, change in polysialylated cell frequency in the ventral aspect of the medial temporal lobe was only partially reduced by amnesic doses of scopolamine. The persisting activation of NCAM polysialylation in the more dorsal aspects of the perirhinal and entorhinal cortex is suggested to reflect the need for more extensive synaptic alterations, as compared to those required for the consolidation of spatial learning. Moreover, the neuroplastic modulations observed in the more ventral regions of the entorhinal and perirhinal cortex appear to be a unique aspect of avoidance conditioning that reflects the activation of alternative learning strategies associated with motivational and/or contextual parameters of the task.

Animals↗
PubMed1984

8-Hydroxy-2-(di-n-propylamino) tetralin is devoid of activity at the 5-hydroxytryptamine autoreceptor in rat brain. Implications for the proposed link between the autoreceptor and the [3H] 5-HT recognition site.

Experiments have been carried out to provide direct evidence for the proposed presynaptic 5-HT autoreceptor agonist activity of 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) a compound with selectivity for the 5-HT1A subtype of the 5-HT1 binding site. Rat brain frontal cortex slices were preincubated with [3H] 5-hydroxytryptamine and continuously stimulated with Krebs solution containing paroxetine and elevated K+ ions (25 mmol/l). The elevated efflux of tritium caused by exposure to K+ Krebs was inhibited in a dose related manner by 5-hydroxytryptamine and this inhibition was attenuated in the presence of quipazine and methiothepin. In slices of the rat frontal cortex, 8-OH-DPAT was without agonist or antagonist activity at the 5-HT autoreceptor at concentrations up to 1 mmol/l. Higher concentrations caused an increase in basal efflux of tritium. 8-OH-DPAT (1 mumol/l) was also without inhibitory activity in the piriform cortex, striatum and the hippocampus. These experiments have therefore failed to provide direct evidence for agonist activity of 8-OH-DPAT at the 5-HT autoreceptor and alternative explanations must be sought for its biochemical and behavioural effects in vivo. Moreover, the fact that 8-OH-DPAT is inactive at the autoreceptor at concentrations selective for the 5-HT1A recognition site suggests that this subtype of the 5-HT1 binding site may not correspond to the 5-HT autoreceptor.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

The topographical organization of neurons in the rat medial frontal, insular and olfactory cortex projecting to the solitary nucleus, olfactory bulb, periaqueductal gray and superior colliculus.

In 19 rats two different retrograde tracers (Fast Blue, Diamidino Yellow, Rhodamine-labeled latex microspheres, or wheat germ agglutinin conjugated with HRP) were injected into the solitary nucleus (NTS) and either the olfactory bulb (OB), periaqueductal gray (PAG) or superior colliculus (SC). The pattern of retrogradely labeled neurons in the medial frontal, insular and olfactory cortices was examined to determine the topographical organization of the cell populations projecting to these subcortical targets and the extent to which they overlapped. In the medial frontal cortex (MFC) SC projections originated most dorsally, while NTS and OB projections originated most ventrally and exhibited slight overlap. PAG projections originated from virtually the entire MFC and overlapped with cells projecting to the OB, NTS and SC. These results are consistent with the role of dorsal MFC as the rat's frontal eye field and the ventral MFC as a visceral motor area. Laterally, in the insular cortex there was virtually complete overlap between cells projecting to the NTS and PAG. The extensive overlap of PAG projections with NTS projections medially and laterally and with SC projections medially suggests the PAG is involved in a variety of brain visceral and somatic functions. In the piriform cortex there was overlap between cells projecting to the OB and cells projecting to the SC; the cells projecting to the SC were located in the endopiriform nucleus, and may provide a substrate for orienting responses to odors.

Animals↗
PubMed1981

Cholecystokinin in the central nervous system.

We have used high performance liquid chromatography and radioimmunoassay to characterize the CCK-like molecules in the central nervous system. The major form of CCK is the sulfated octapeptide. This molecule is distributed unevenly among various brain regions; the highest levels are found in the cortex and striatum. We have focused our attention on three areas in particular, the posterior pituitary, the caudate nucleus, and the hippocampus. The first of these receives its CCK-containing fibers from the hypothalamic magnocellular nuclei, the second appears to be innervated by the claustrum (or piriform cortex). The CCK in the hippocampus, on the other hand, is in intrinsic neurons. These structures and others in the brain have CCK binding sites.

Animals↗