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PubMed2000

Effects of antipsychotic drugs on cholecystokinin and preprotachykinin (substance P) mRNA expression in the rat hippocampal formation.

To assess the involvement of substance P (SP) and cholecystokinin (CCK) in the effects of antipsychotic drugs, preprotachykinin-A (PPT-A) and CCK mRNA expression was studied in the hippocampal formation using in situ hybridisation following 21 daily i.p. injections with the typical antipsychotic drug haloperidol (1 mg/kg) and the atypical drug clozapine (15 mg/kg). PPT-A mRNA levels were increased in the hippocampal CA3 subregion and in the entorhinal cortex after haloperidol, whereas a decrease was observed in the CA1 after clozapine. CCK mRNA levels increased in the CA1, the entorhinal cortex and in hilus, following both haloperidol and clozapine. It is suggested that earlier findings of increased SP levels in the hippocampal formation of schizophrenics may be a consequence of haloperidol treatment and that reduced hippocampal CCK and CCK mRNA levels found earlier in schizophrenics do not result from antipsychotic drug treatment. These results are consonant to the hypothesis that increased cortical CCK transmission may be beneficial in the treatment of psychosis.

Animals↗
PubMed1997

Zinc transport in the rat olfactory system.

To study zinc (Zn) mobility in the rat olfactory tract, brain distribution of 65Zn after injection into the olfactory bulb or amygdaloid nuclei was analyzed by autoradiography. Twenty-four hours after 65Zn injection into the olfactory bulb, 65Zn was distributed in the ipsilateral piriform cortex, amygdaloid nuclei and the anterior commissure. Moreover, in the case of injection of a higher level of 65Zn into the olfactory bulb, 65Zn was distributed in the ipsilateral entorhinal cortex in addition to the above regions. Twenty-four hours after 65Zn injection into the amygdaloid nuclei, 65Zn was distributed in the ipsilateral piriform and entorhinal cortex. These results suggest that Zn is intraneuronally transported along the olfactory tract. Zn may be taken up by the piriform neurons after release from the secondary olfactory neuron terminals and transported to the entorhinal area.

Amygdala↗
PubMed1976

An electron microscopic study of lesion-induced synaptogenesis in the dentate gyrus of the adult rat. I. Magnitude and time course of degeneration.

Synapses in the rat dentate gyrus are rapidly lost after removal of the primary input from the entorhinal cortex. In this paper we describe the extent and time course of degeneration and in the subsequent paper the nature of the reinnervation processes. They synapses of entorhinal afferents are remarkably concentrated in their zone of termination. Unilateral removal of the rat entorhinal cortex results in the loss of about 86% of all synapses in the outer three-fourths of the molecular layer of the epsilateral dentate gyrus. Entorhinal synapses are all asymmetric (Gray type I) and terminate on dendritic spines. Analysis of the degeneration reaction provides a means to examine the characteristics of the loss of a relatively homogeneous afferent on a single cell type. The morphological characteristics of the the degenerating terminals showed some heterogeneity; both the electron lucent and electron dense types of degenerating terminals were identified. The electron lucent type was observed only at short survival times. The time course of the loss of degenerating terminals was resolvable into two components, each of which followed first order decay kinetics. Thus degenerating entorhinal terminals behaved as a population which disappeared randomly at a rate dependent on the fraction of terminals present at any time. The loss of degenerating terminals was accompanied by the loss of postsynaptic sites. At short survival times the majority of postsynaptic sites (defined by the presence of a postsynaptic density) had disappeared. There was also a loss of complex spines and some shrinkage of the molecular layer.

Animals↗
PubMed2005

Remembering one year later: role of the amygdala and the medial temporal lobe memory system in retrieving emotional memories.

The memory-enhancing effect of emotion can be powerful and long-lasting. Most studies investigating the neural bases of this phenomenon have focused on encoding and early consolidation processes, and hence little is known regarding the contribution of retrieval processes, particularly after lengthy retention intervals. To address this issue, we used event-related functional MRI to measure neural activity during the retrieval of emotional and neutral pictures after a retention interval of 1 yr. Retrieval activity for emotional and neutral pictures was separately analyzed for successfully (hits) vs. unsuccessfully (misses) retrieved items and for responses based on recollection vs. familiarity. Recognition performance was better for emotional than for neutral pictures, and this effect was found only for recollection-based responses. Successful retrieval of emotional pictures elicited greater activity than successful retrieval of neutral pictures in the amygdala, entorhinal cortex, and hippocampus. Moreover, in the amygdala and hippocampus, the emotion effect was greater for recollection than for familiarity, whereas in the entorhinal cortex, it was similar for both forms of retrieval. These findings clarify the role of the amygdala and the medial temporal lobe memory regions in recollection and familiarity of emotional memory after lengthy retention intervals.

Adult↗
PubMed1999

Semaphorin D acts as a repulsive factor for entorhinal and hippocampal neurons.

We analysed the effects of semaphorin D on axons from the developing rat entorhinal-hippocampal formation. Explants from superficial layers of the entorhinal cortex and of the hippocampus anlage were obtained from various developmental stages and co-cultured with cell aggregates expressing semaphorin D. Neurites extending from entorhinal explants that had been isolated from early embryonic stages (E16 and E17) were not affected by semaphorin D, but were repelled at later stages (E20 and E21). Axons from hippocampal neurons explanted at E21 were also repelled by semaphorin D. In situ hybridization studies revealed expression of the semaphorin D receptor neuropilin-1 in the entorhinal cortex from stage E17 to stage P7, and in the dentate gyrus and CA1-3 regions between E17 and adulthood. These data suggest that semaphorin D is involved in the formation of the perforant pathway and acts, via the neuropilin-1 receptor, as a repulsive signal that prevents entorhinal fibres from growing into the granular layer of the dentate gyrus. These data also suggest a role for semaphorin D in the development of intrahippocampal connections.

Animals↗
PubMed1990

The differential activities of R (+)- and S(-)-zacopride as 5-HT3 receptor antagonists.

R(+)- and S(-)-zacopride were assessed as potential 5-HT3 receptor antagonists in behavioural and biochemical tests. The S(-)isomer was more potent than the R(+)isomer to antagonise the hyperactivity induced by the injection of amphetamine or the infusion of dopamine into the nucleus accumbens in the rat. In contrast, the R(+)isomer was more potent to reduce the aversive behaviour of mice to a brightly illuminated environment and in a marmoset human threat test, to facilitate social interaction in rats, to increase performance in a mouse habituation test and prevent a scopolamine-induced impairment, and to antagonise the inhibitory effect of 2-methyl-5-hydroxytryptamine to reduce [3H]acetylcholine release in slices of the rat entorhinal cortex. In binding assays, [3H]S(-)-zacopride and [3H]R(+)-zacopride labelled homogenous populations of high-affinity binding sites in the rat entorhinal cortex, R(+)-zacopride compete for a further 10 to 20% of the binding of [3H]R(+)/S(-)-zacopride or [3H]R(+)-zacopride in excess of that competed for by (S)(-)-zacopride. It is concluded that both isomers of zacopride have potent but different pharmacological activities, with the possibility of different recognition sites to mediate their effects.

Animals↗
PubMed2002

Evidence that synaptically released beta-amyloid accumulates as extracellular deposits in the hippocampus of transgenic mice.

A neuropathological hallmark of Alzheimer's disease is the deposition of amyloid-beta (Abeta) peptides in senile plaques in the hippocampus and cerebral cortex. Abeta is derived from larger integral membrane proteins termed amyloid precursor proteins (APP). We demonstrated previously that APP, synthesized by neurons in the entorhinal cortex, is transported via the perforant pathway to presynaptic terminals in the dentate gyrus. We reported that, although full-length APP and membrane-tethered, C-terminal APP derivatives (APP-CTFs) accumulate at terminal fields, the production of Abeta peptides at these sites was indeterminate. To test the hypothesis that APP-CTFs, generated from axonally transported APP, are further metabolized to Abeta peptides that are subsequently released and deposited proximal to nerve terminals, we created unilateral knife lesions of the perforant pathway of transgenic mice that exhibit hippocampal amyloid deposits. We observed pronounced reductions in amyloid burden in the ipsilateral dentate gyrus, findings that lead us to conclude that axonally transported APP gives rise to Abeta peptides that are released from presynaptic sites in the dentate gyrus and deposited in extracellular plaques. Moreover, our findings are consistent with the view that Abeta deposits are dynamic structures and that the perforant path lesion alters the equilibrium between Abeta production-deposition toward clearance as a consequence of blocked axonal transport of APP from the entorhinal cortex to terminal fields in the hippocampus.

Alzheimer Disease↗
PubMed2003

Gray matter features of schizotypal disorder patients exhibiting the schizophrenia-related code types of the Minnesota Multiphasic Personality Inventory.

OBJECTIVE: Previous studies have suggested that several code types of the Minnesota Multiphasic Personality Inventory (MMPI) are useful markers for identifying schizophrenia. We hypothesized that schizotypal disorder (STD) patients with such schizophrenia-related code types have the morphological brain abnormalities associated with schizophrenia. METHOD: Voxel-based morphometric analysis with statistical parametric mapping (SPM) 99 software was used to investigate the differences in brain morphology between 14 STD patients with the schizophrenia-related code types of the MMPI and 28 normal individuals. RESULTS: The STD patients showed significantly decreased gray matter volume in the insular regions bilaterally and in the left entorhinal cortex, compared with the controls. CONCLUSION: Our findings suggest that STD patients with the schizophrenia-related code types have volume reductions in these regions as an endophenotype that overlaps with schizophrenia.

Adolescent↗
PubMed1996

A novel entorhinal projection to the rat dentate gyrus: direct innervation of proximal dendrites and cell bodies of granule cells and GABAergic neurons.

Entorhinal fibers to the fascia dentata originating from layer II stellate neurons are known to terminate exclusively in the outer two thirds of the molecular layer, where they innervate distal dendritic portions of dentate neurons. Using anterograde tracing with Phaseolus vulgaris leucoagglutinin, we unraveled a previously unknown entorhinal projection that directly innervates proximal dendritic portions and somata of granule cells and GABAergic neurons. This projection originates from neurons located in entorhinal layers IV-VI of the medial entorhinal area. These fibers enter the outer two thirds of the molecular layer, traverse the inner molecular layer (IML) and granule cell layer, where they form numerous boutons, and finally arborize subjacent to the granule cells. Correlated light and electron microscopy revealed that the boutons formed by these fibers establish asymmetric synapses on dendrites in the IML, on spines and somata of granule cells, and on spineless dendrites subjacent to the granule cell layer. Postembedding immunogold staining indicates that this entorhino-dentate projection is not GABAergic and that it also terminates on GABAergic inhibitory neurons. These data demonstrate that not all entorhino-dentate fibers display a similar high laminar specificity for the outer molecular layer (OML). Although fibers from the superficial layers of the entorhinal cortex terminate exclusively in the OML, entorhinal fibers arising from deeper layers are not confined to laminar boundaries. Finally, the possibility that these supposedly excitatory entorhinal afferents may monosynaptically activate proximal dendrites and somata of dentate neurons needs to be incorporated into contemporary concepts of the hippocampal network.

Animals↗
PubMed2002

GABABR1 receptor protein expression in human mesial temporal cortex: changes in temporal lobe epilepsy.

Immunocytochemistry was used to examine gamma-aminobutyric acid beta (GABA)(B)R1a-b protein expression in the human hippocampal formation (including dentate gyrus, hippocampus proper, subicular complex, and entorhinal cortex) and perirhinal cortex. Overall, GABA(B)R1a-b immunostaining was intense and widespread but showed differential areal and laminar distributions of labeled cells. GABA(B)R1a-b-immunoreactive (-ir) neurons were found in the three main layers of the dentate gyrus, the most intense labeling being present in the polymorphic layer, whereas the granule cells were moderately immunoreactive. Except for slight variations, similar distribution patterns of GABA(B)R1a-b immunostaining were found along the different subfields of the Ammon's horn (CA1-CA4). The highest density of GABA(B)R1a-b-ir neurons was localized in the stratum pyramidale, where virtually every pyramidal cell was intensely immunoreactive, including the proximal part of the apical dendrites. Within the subicular complex, a more intense GABA(B)R1a-b immunostaining was found in the subiculum than in the presubiculum or parasubiculum, especially in the pyramidal and polymorphic cell layers. In the entorhinal cortex, distribution of GABA(B)R1a-b immunoreactivity was localized mainly in both pyramidal and nonpyramidal cells of layers II, III, and VI and in the superficial part of layer V, with layers I, IV, and deep layer V being less intensely stained. In the perirhinal cortex, the most intense GABA(B)R1a-b immunoreactivity was located in the deep part of layer III and in layer V and was mainly confined to medium-sized and large pyramidal cells. Thus, the differential expression, but widespread distribution, of GABA(B)R1a-b protein found in the present study suggests the involvement of GABA(B) receptors in many circuits of the human hippocampal formation and adjacent cortical structures. Interestingly, the hippocampal formation of epileptic patients (n = 8) with hippocampal sclerosis showed similar intensity of GABA(B)R1a-b immunostaining in the surviving neurons located within or adjacent to those regions presenting neuronal loss than in the controls. However, surviving neurons in the granule cell layer of the dentate gyrus displayed a significant reduction in immunostaining in 7 of 8 patients. Therefore, alterations in inhibitory synaptic transmission through GABA(B) receptors appears to affect differentially certain hippocampal circuits in a population of epileptic patients. This reduction in GABA(B)R1a-b expression could contribute to the pathophysiology of temporal lobe epilepsy.

Adult↗
PubMed1993

Effects on visual recognition of combined and separate ablations of the entorhinal and perirhinal cortex in rhesus monkeys.

Performance on visual delayed nonmatching-to-sample was assessed in rhesus monkeys with combined and separate ablations of the perirhinal and entorhinal cortex, as well as in unoperated controls. Combined (i.e., rhinal cortex) lesions yielded a striking impairment on this task, one almost as severe as that seen after combined amygdalohippocampal removals that included some of this subjacent cortex (Mishkin, 1978; Murray and Mishkin, 1984). Ablations of the perirhinal cortex alone produced a deficit nearly as severe as that found after rhinal cortex lesions, whereas ablations of the entorhinal cortex alone produced only a mild deficit. Contrary to the conclusion from an earlier study (Murray and Mishkin, 1986), the present results demonstrate not only that damage limited to the rhinal cortex is sufficient to produce a severe loss in visual recognition, but also that such damage leads to a far greater loss than damage to any other single structure in the medial part of the temporal lobe.

Animals↗
PubMed2000

Identifying cortical inputs to the rat hippocampus that subserve allocentric spatial processes: a simple problem with a complex answer.

A consideration of the cortical projections to the hippocampus provides a number of candidate regions that might provide distal sensory information needed for allocentric processing. Prominent among the input regions are the entorhinal cortex, the perirhinal cortex, the postrhinal cortex, and the retrosplenial cortex. A review of these sites reveals the surprising fact that in spite of their anatomical connections, removal of the perirhinal and postrhinal cortices has little or no effect on spatial tasks and hence does not functionally disconnect the hippocampus. Extensive retrosplenial lesions have only mild effects, and even lesions of the entorhinal cortex only partially mimic the effects of hippocampal lesions upon tests of spatial memory. In contrast, studies using c-fos imaging support the involvement of the entorhinal, postrhinal, and retrosplenial cortices, but not the perirhinal cortex. It is argued that there exist multiple aspects of spatial memory, and this is reflected in the multiple routes by which cortical information can reach the hippocampus. One consequence is that lesions in a single site often have surprisingly mild effects on standard spatial tests.

Afferent Pathways↗
PubMed1987

Monoamines and metabolites in cortex and subcortical structures: normal regional distribution and the effects of thiamine deficiency in the rat.

The present study measured the concentration of monoamines, metabolites and estimates of turnover rate in eighteen separate brain regions from controls and a rat model of Korsakoff's disease induced by a two week bout of pyrithiamine and thiamine deficient diet (PTD). A behaviorally tested control (n = 12) and PTD (n = 17) group, and a non-behaviorally tested PTD group (n = 8) were sacrificed 7 months after recovery from treatment. The brains were dissected into nine cortical areas and nine subcortical regions. In behaviorally tested PTD animals, a significant reduction of NE was observed in entorhinal cortex. Diminished norepinephrine (NE) concentration was also observed in entorhinal, hippocampal, septal and olfactory areas of the non-behaviorally tested PTD group. Serotonin and 5-hydroxyindoleacetic acid (5-HIAA) levels were increased in several brain areas, particularly midbrain-thalamus, striatum, of both groups of recovered PTD animals. These findings are discussed with respect to results and hypotheses presented in our previous study of this animal model. Significant differences in monoamine, metabolite and turnover estimates were also observed among cortical areas of the control animals. Entorhinal cortex contained the highest concentration of NE and 5-hydroxytryptamine (5-HT), while DA was highest in somatosensory cortex. The distribution of 5-HT and 5-HIAA were more homogeneous and displayed a rostral-caudal decline in concentration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Widespread cortical projections of the hippocampal formation in the cat.

Efferent projections from the hippocampal formation to the cat's cortex were traced with the retrograde horseradish peroxidase technique. Different areas of the cortex of 31 cats were injected with small amounts of horseradish peroxidase. All subregions of the hippocampal formation were screened for labeled cells. It was found that, with the exception of the entorhinal injections, only subicular areas of the hippocampal formation contain labeled neurons. When HRP was injected into the entorhinal cortex, labeled cells are also found in the hippocampus proper. The most dense projection from the subicular cortex is directed to the medial part of the cortical hemisphere. Here, cingulate, retrosplenial and medial prefrontal fields receive a substantial number of subicular efferents. Furthermore, the entorhinal cortex is reached by a number of axons originating in the subicular area. Scarce projections from the subicular cortex terminate in the dorsal prefrontal, temporal, parietal and prepiriform cortex. It is suggested that the projection from the subicular cortex to the neocortical areas of the frontal pole (medial prefrontal cortex) is of special importance as it may constitute a link between the association areas of the neocortex and those regions of the limbic system thought to play a role in memory (subicular cortex, mamillary bodies, anterior thalamus, cingulate gyrus).

Animals↗
PubMedDate not supplied

Complement mRNA in the mammalian brain: responses to Alzheimer's disease and experimental brain lesioning.

This study describes evidence in the adult human and rat brain for mRNAs that encode two complement (C) proteins, C1qB and C4. C proteins are important effectors of humoral immunity and inflammation in peripheral tissues but have not been considered as normally present in brain. Previous immunocytochemical studies showed that C proteins are associated with plaques, tangles, and dystrophic neurites in Alzheimer's disease (AD), but their source is unknown. Combined immunocytochemistry and in situ hybridization techniques show C4 mRNA in pyramidal neurons and C1qB mRNA in microglia. Primary rat neuron cultures also show C1qB mRNA. In the cortex from AD brains, there were two- to threefold increases of C1qB mRNA and C4 mRNA, and increased C1qB mRNA prevalence was in part associated with microglia. As a model for AD, we examined entorhinal cortex perforant path transection in the rat brain, which caused rapid increases of C1qB mRNA in the ipsilateral, but not contralateral, hippocampus and entorhinal cortex. The role of brain-derived acute and chronic C induction during AD and experimental lesions can now be considered in relation to functions of C proteins that pertain to cell degeneration and/or cell preservation and synaptic plasticity.

Aged↗
PubMed1992

Cortical transynaptic activation of tyrosine kinase receptor trkB messenger RNA expression in rat hippocampus.

The trkB gene encodes a tyrosine kinase receptor which is an essential component of the high-affinity cell surface receptor for the neurotrophin brain-derived neurotrophic factor. In this report we have used quantitative in situ hybridization to study the expression of trkB messenger RNA in the rat hippocampus following stimulation of afferents in the entorhinal cortex. A bilateral three-fold increase of trkB messenger RNA levels in the hippocampus was seen 4 h after quisqualate injection into the left entorhinal cortex. The increase was confined to the granule layer of the dentate gyrus. A small increase, however, was also seen bilaterally in the pyramidal cell layer. The increases in all hippocampal areas were completely prevented by pretreatment of the animals with systemic injection of diazepam but not with scopolamine. We suggest that glutamate release from cortical afferents to the hippocampus has the capacity to increase neuronal expression of trkB messenger RNA within the hippocampus. The results from the present study extend the interpretation of our previous evidence of cortical transynaptic activation of brain-derived neurotrophic factor messenger RNA and indicate the presence of a concomitant activation of trkB messenger RNA expression in the hippocampus.

Animals↗
PubMed1992

Basic fibroblast growth factor mRNA increases in specific brain regions following convulsive seizures.

Basic fibroblast growth factor (bFGF) is a trophic factor synthesized in the central nervous system (CNS), where it is believed to play a role in neuronal maintenance and repair. Little is known about the regulation of this growth factor in the CNS. To determine whether the expression of the bFGF gene in the brain of adult animals changes in response to alterations of neuronal activity, we examined bFGF mRNA levels in several brain regions of rats experiencing focally-evoked convulsive seizures. Seizures were induced by microinjecting bicuculline unilaterally into an epileptogenic site within the deep prepiriform cortex, area tempestas (AT). By 5 h after initiation of brief limbic motor seizures from AT, there was a four fold increase in the levels of bFGF mRNA in the entorhinal cortex, hippocampus and olfactory bulb, but not in the caudate-putamen. The maximal expression of bFGF mRNA was reached by 10 h after seizure onset. In the same animals, the mRNA encoding nerve growth factor (NGF) was increased in entorhinal cortex and hippocampus, but not in the olfactory bulb. Our results demonstrate that neuronal activity can influence bFGF expression in an anatomically selective fashion and that acute changes in bFGF can occur in the uninjured mature brain. The increase in bFGF expression in response to excessive activation of specific neuronal circuitry may represent an adaptive response to protect against potential injury in those circuits.

Animals↗
PubMed1986

Functional relations of the rodent claustral-entorhinal-hippocampal system.

Electrophysiological studies of the claustrum of rat demonstrate functional connections with the limbic system (dentate gyrus, hippocampus) via the entorhinal cortex. The pathways show reciprocal connectivity, a degree of topological organization and the capacity for a long-term response potentiation in the claustral projection to entorhinal cortex. The hypothesis that claustrum acts to functionally link neocortical regions with components of the limbic system is considered.

Animals↗