Novel genes expressed in the developing medial cortex.
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Two cDNAs, M1 and M2, recently isolated by the differential display method from embryonic rat cerebral hemisphere were characterized and their patterns of spatiotemporal expression analysed in developing rat forebrain by in situ hybridization histochemistry and correlative immunocytochemistry. Neither gene bears any sequence homology to other known genes. Both genes are particularly expressed in medial regions of the cerebral hemisphere and M2 in the roof of the adjacent diencephalon. M1 expression is highly localized and confined to the neuroepithelium of the hippocampal rudiment from embryonic day (E) 12 onward. Its location corresponds to the fimbrial anlage, and immunocytochemical localization of M1 protein indicates its expression in radial glial cells. M2 expression at E12 is more extensive in the medial cerebral wall, extending into the preoptic region and beyond the hippocampus into dorsal hemisphere and into the dorsal diencephalon, with caudal extension along the dorsal midline and in the zona limitans intrathalamica. Later, M2 expression is found in association with the corpus callosum, hippocampal commissure, fimbria, optic nerve, stria medullaris, mamillothalamic tract and habenulopeduncular tract. M1 and M2 expression domains corresponding to the locations of fiber tracts are present prior to the arrival of the earliest axons, as identified by neuron specific markers. These findings suggest M1 and/or M2 genes are involved in early regional specification of the hippocampus and related structures in paramedian regions of the forebrain, and that cell populations expressing these genes in advance of developing axonal pathways may be involved in the early specification of tract location. (+info)
9-16 Hz oscillation precedes secondary generalization of seizures in the rat tetanus toxin model of epilepsy.
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Unilateral intrahippocampal injection of tetanus toxin results in a chronic syndrome of intermittent epileptic seizures. During some of these seizures, rats develop a stereotypic, pathological motor behavior that indicates secondary generalization of epileptic activity. We report that secondary generalization was preceded by a 9-16 Hz oscillation of field potentials which was synchronized between the right and left dorsal hippocampi. The oscillation was associated with increased synchrony of population spike firing in right and left CA1 subregions which form the major output of the hippocampi. Cutting the ventral commissure abolished synchrony across the hippocampi and reduced the probability that the 9-16 Hz activity would be followed by secondary generalization. We concluded that a bilaterally synchronous 9-16 Hz hippocampal oscillation played a role in the secondary generalization of focal seizures in this chronic model of limbic epilepsy. (+info)
Amnesia due to fornix infarction.
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Background and Purpose-The fornix connects various structures involved in memory. We report a patient with anterograde amnesia after an acute ischemic infarct in the anterior fornix. Case Description-A 71-year-old female with acute-onset amnesia had neuroimaging studies showing ischemic infarction of both columns and the body of the fornix and the genu of the corpus callosum. Neuropsychological evaluation revealed anterograde amnesia without evidence of callosal disconnection. The patient showed marked improvement in her memory function on the follow-up visit. Conclusions-Amnesia in this case is likely due to infarction of the anterior fornix structures. (+info)
Using fos imaging in the rat to reveal the anatomical extent of the disruptive effects of fornix lesions.
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Activity of the immediate early gene c-fos was compared across hemispheres in rats with unilateral fornix lesions. To engage Fos production, rats first performed a radial arm maze task that is severely disrupted by bilateral fornix lesions. Using immunohistochemical techniques, Fos-positive cells were visualized and counted in 39 sites in both hemispheres. Fornix lesions led to a significant reduction in Fos in all ipsilateral hippocampal subfields, as well as the entorhinal cortex and most of the subicular complex. Other sites that showed reduced activity included the ipsilateral retrosplenial, anterior cingulate, and postrhinal cortices. Subcortical regions showing significant Fos decreases included the anterior thalamic nuclei, supramammillary nucleus, diagonal band of Broca, and lateral septum. Thus, the effects of fornix lesions extended beyond the hippocampal formation and included sites not directly innervated by the tract. These changes were nevertheless selective, as shown by the lack of hemispheric difference in any of the preselected control sites, the perirhinal cortex, or nucleus accumbens. Furthermore, there were no hemispheric differences in an additional group of animals with unilateral fornix lesions that were killed directly from the home cage. The location of Fos changes closely corresponded to those brain regions that when lesioned disrupt spatial working memory. Moreover, there was a correspondence between those brain regions that show increased Fos production in normal animals performing the radial arm maze task and those affected by fornix lesions. These results show that fornix transection has widespread, but selective, effects on a network of structures normally activated by spatial memory processes, with these effects extending beyond the hippocampal formation. (+info)
Impaired recognition memory in rats after damage to the hippocampus.
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Rats with radio-frequency or ibotenic acid lesions of the hippocampus and rats with radio-frequency lesions of the fornix were tested on the visual paired comparison task (VPC), a test of recognition memory. Memory was assessed at five different delay intervals ranging from 10 sec to 24 hr. All operated groups performed normally at the shorter delays (10 sec and 1 min). Across longer delays, the two groups with hippocampal damage were impaired. Rats with fornix lesions performed well on the VPC task but were impaired on a spatial task (spontaneous alternation). The results show that the hippocampus is essential for normal recognition memory. Moreover, fornix lesions need not mimic the effects of direct damage to hippocampal tissue. The findings are discussed in the context of the contribution of the hippocampus to recognition memory. (+info)
Fornix and hippocampal atrophy in traumatic brain injury.
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This study compared a fornix cross-sectional-area measurement and hippocampal volume in 86 traumatic brain injury (TBI) subjects with 46 normal controls. The TBI group showed a significant reduction in fornix area and hippocampal volume. It was also shown that initial injury severity was related to the degree of atrophy in both structures. Although fornix size and hippocampal volume correlated, such a modest correlation between these two structures suggests differential and potentially independent mechanisms of injury. The General Memory Index score from the Wechsler Memory Scale-Revised was shown to be significantly correlated with hippocampal volume following TBI. (+info)
Fornix-dependent induction of hippocampal CCAAT enhancer-binding protein [beta] and [delta] Co-localizes with phosphorylated cAMP response element-binding protein and accompanies long-term memory consolidation.
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The cAMP response element-binding protein (CREB) is an evolutionarily conserved transcription regulator essential for long-term memory formation. It is not known, however, whether the molecular events downstream of CREB activation are also conserved. An early, cAMP-dependent event necessary for learning-related long-term synaptic plasticity in the invertebrate Aplysia californica is the induction of the transcription factor CCAAT enhancer-binding protein (C/EBP). Here we show that two homologs in the rat, C/EBPbeta and C/EBPdelta, are induced at discrete times after inhibitory avoidance learning and co-localize with phosphorylated CREB in the hippocampus. This induction is blocked by fornix lesions, which are known to disrupt activation of CREB in the hippocampus and to impair memory consolidation. These results indicate that C/EBPs are evolutionarily conserved components of the CREB-dependent gene cascade activated in long-term memory. (+info)
A quantitative MR measure of the fornix in schizophrenia.
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Some cognitive disturbances accompanying schizophrenia may be due to abnormalities in the thalamus and components of the limbic system. The fornix is an important white-matter relay pathway connecting these structures and is likely to be affected in schizophrenia as well.Magnetic resonance images of the fornix were analyzed in 15 schizophrenic patients and 15 matched comparison group subjects. Fornix volume was compared between the two groups and was also correlated with the volumes of other neuroanatomical structures, as well as with illness presentation, clinical status, and cognitive/psychological measures. There was no significant difference in fornix volume between the two groups. Of note, fornix volume correlated significantly with the volumes of the hippocampus, parahippocampus, and the superior temporal gyrus in the schizophrenic subjects, but not in the controls. Moreover, the correlation between fornix and parahippocampal gyrus volumes differed significantly between the two groups. No association was found between fornix volume and illness presentation or between fornix and cognitive/clinical measures.Results suggest that there are no marked changes in fornix volume in schizophrenia by MRI. The fornix, however, may be part of a network of structures affected in schizophrenia, as indicated by correlated volumetric changes. (+info)