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At least 433 records · Page 24Linked to original sources
PubMed1994

Amyotrophic lateral sclerosis and parkinsonism-dementia from Guam: differences in neurofibrillary tangle distribution and density in the hippocampal formation and neocortex.

Amyotrophic lateral sclerosis/parkinsonism-dementia complex is a highly prevalent neurodegenerative disorder among the native Chamorro population of Guam, and is characterized by widespread formation of neurofibrillary tangles. In the present study, the distribution of neurofibrillary tangles was quantitatively assessed in the cerebral cortex of cases presenting with either predominant amyotrophic lateral sclerosis or parkinsonism-dementia symptomatology. Results show that although the regional and laminar lesion distribution is qualitatively similar in both groups, cases with predominant parkinsonism-dementia generally have higher lesion densities than cases with amyotrophic lateral sclerosis. Interestingly, layer II of the entorhinal cortex was affected to the same degree in both conditions. In both groups, the CA1 field of the hippocampus, subiculum, and entorhinal cortex were the most affected areas. In the neocortex, the perirhinal and inferior temporal cortex consistently had higher lesion densities than the frontal, parietal, and cingulate cortex, whereas the visual cortex was practically devoid of lesions. Also, most of the neurofibrillary tangles were located in the supragranular layers of the neocortex, with relatively low densities in the infragranular layers, in both brain groups. Interestingly, the primary motor cortex contained more neurofibrillary tangles in parkinsonism-dementia than in amyotrophic lateral sclerosis cases. It is possible that the differences in regional neurofibrillary tangle densities reflect the variable severity of the dementing process observed between the two groups of patients. Several studies on Alzheimer's disease and related disorders indicate that the regional and laminar cortical localization of neurofibrillary tangles may parallel the degeneration of specific corticocortical projections. The present data suggest that the population of corticocortical projections involved in Guamanian cases differs substantially from that affected in Alzheimer's disease. The differential distribution and densities of the lesions may contribute to the differences in symptomatology and severity of dementia among Alzheimer's disease and Guamanian cases, although these neurodegenerative disorders as well as related illnesses may share certain etiopathogenetic mechanisms.

Adult↗
PubMed1994

A developmental study of cyclic AMP-response element binding protein (CREB) by in situ hybridization histochemistry and immunocytochemistry in the rat neocortex.

Cyclic AMP (cAMP) mediates the hormonal stimulation of a number of eukaryotic genes by directing the protein kinase A (PK-A)-dependent phosphorylation of the transcription factor CREB. Somatostatin is one such gene known to be transcriptionally activated by cAMP via CREB. In view of the role somatostatin plays in the regulation of neocortical development, we examined the early expression of CREB mRNA and protein (from E10 to E14) in the rat neocortex by in situ hybridization and immunocytochemistry. mRNA for CREB was detected in all layers of the developing neocortex from E10 to E14. CREB immunoreactivity (CREB-IR) was also observed in most cortical cells by E10. However, the number of CREB-immunoreactive nuclei decreased thereafter, and on E14 there were immunoreactive cells only in the preplate. A moderate amount of somatostatin mRNA was observed on E16 in layer I, which is produced from the preplate. This stage specific expression of the CREB protein in the developing neuroepithelium suggests that by regulating transcription of some peptides including somatostatin, CREB plays a role in cortical development.

Animals↗
PubMed1995

Medial forebrain bundle stimulation in rats activates glycogen phosphorylase in layers 4, 5b and 6 of ipsilateral granular neocortex.

Functional activation in human brain produces an increase in glycolytic metabolism. Animal studies suggest activation-induced glycolysis is coupled to brain glycogenolysis. Medial forebrain bundle (MFB) stimulation activates the release of neurotransmitters which promote neocortical glycogenolysis in vitro. In the present study, active glycogen phosphorylase (GP), an index of glycogenolysis, is assessed histochemically in rat brain after 15 min of MFB self-stimulation. Active GP increased significantly in layers 4, 5b and 6 of granular neocortex ipsilateral to MFB self-stimulation. Restriction of increased glycogenolysis to granular neocortex suggests an important functional interaction between sensory neocortical processing and ascending MFB systems.

Animals↗
PubMed1995

Post-activation potentiation in the neocortex. III. Kindling-induced potentiation in the chronic preparation.

Previous experiments have shown the neocortex to be very resistant to the induction of long-term potentiation in chronic preparations. We show here that kindling-induced potentiation effects can be reliably produced in the neocortex of awake, freely moving rats. These effects develop rather slowly. In sites contralateral to the stimulation electrode, potentiation effects did not become clear until the animals had received about 5 days or more of stimulation. Ipsilateral sites required even longer (approximately 10 days), and both sites required more than 13 days to reach asymptotic levels of potentiation. Both monosynaptic and polysynaptic components were present in the neocortical field potentials. When population spikes were absent, the surface negative monosynaptic EPSP component tended to show a potentiation effect. If population spikes were present, they were generally enhanced while the monosynaptic population EPSP tended to be depressed. Consequently, the apparent depression may have been due to competing field currents. The later polysynaptic components (15-28 ms latency to peak) always showed a potentiation effect with 5 or more kindling stimulations and is presumed to result from activation of cortico-cortical associational fibers. All of these effects were long-lasting, showing little decay over a period of several weeks.

Animals↗
PubMed1995

Post-activation potentiation in the neocortex. IV. Multiple sessions required for induction of long-term potentiation in the chronic preparation.

The neocortex in chronically prepared rats is very resistant to the induction of long-term potentiation (LTP). In the first of two experiments described in this paper, we tried unsuccessfully to induce neocortical LTP within one session by coactivating basal forebrain cholinergic and cortical inputs to our neocortical recording site. In the second experiment, we tested a new procedure which involved the application of repeated conditioning sessions over several days. This procedure was suggested by our finding that kindling-induced potentiation (KIP) of cortical field potentials could be reliably triggered but was slow to develop. We administered 30 high frequency trains per day to the corpus callosum for 25 days. LTP in callosal-neocortical field potentials became clear after about 5 days of stimulation and reached asymptotic levels by about 15 days. After the termination of treatment, LTP persisted for at least 4 weeks, the duration of our post-stimulation test period. As in previous experiments on kindling-induced potentiation, the potentiation effects were clear in both early population spike components and in a late (probably disynaptic) component. The monosynaptic EPSP component was often depressed, but this may have been due to competing field currents generated by the enhanced population spike activity. We discuss these results in the context of theories emphasizing slower but more permanent memory storage in neocortex compared to the hippocampus.

Animals↗
PubMed1988

Evidence for dual serotonergic projections to neocortex: axons from the dorsal and median raphe nuclei are differentially vulnerable to the neurotoxin p-chloroamphetamine (PCA).

Previous studies have shown that there are morphologically dissimilar serotonergic (5-HT) axon types in rat cerebral cortex which are differentially sensitive to the neurotoxic effects of certain psychotropic drugs: methylenedioxyamphetamines (MDA and MDMA) and p-chloroamphetamine (PCA) cause degeneration of fine 5-HT axon terminals in cortex, while sparing beaded axons. Moreover, a recent anterograde transport study suggests that fine and beaded 5-HT axons arise from the dorsal raphe (DR) and median raphe (MR) nuclei, respectively. These data led us to propose that the DR projection to neocortex is selectively vulnerable to the neurotoxic effects of PCA, while the MR projection is resistant; this hypothesis was tested in the present study by comparing retrograde axonal transport of the fluorescent tracer Fluoro-Gold in PCA-treated and control rats. Using this method, only axons that survive PCA treatment can take up and transport the injected label back to the cell bodies of origin, thus allowing us to determine which raphe-cortical projections remain intact after PCA. The results show that PCA administration produces a loss of fine 5-HT axon terminals in neocortex and a concomitant reduction in the number of retrogradely labeled neurons in the DR (77% decrease), when compared to controls. In contrast, beaded 5-HT axon terminals are spared and the number of labeled neurons in the MR remains unchanged after PCA. These results demonstrate that DR and MR projections to cortex are differentially vulnerable to PCA: fine axon terminals arise from neurons in the DR and are highly sensitive to the neurotoxic effects, whereas beaded axons from the MR are resistant. We therefore propose that there are two anatomically and functionally separate 5-HT projections to cortex having different (1) nuclei of origin, (2) axon morphology, (3) regional distributions, and (4) pharmacological properties. Since the mood-altering substances MDA, MDMA, and PCA act specifically upon 5-HT axon terminals from the dorsal raphe nucleus, DR neurons may be preferentially involved in the control of affective state.

Amphetamines↗
PubMed1988

Cholinergic grafts in the neocortex or hippocampus of aged rats: reduction of delay-dependent deficits in the delayed non-matching to position task.

Aged (24 month) rats have previously been shown to manifest delay-dependent deficits in the performance of an operant delayed non-matching to position task. In the present experiment, cholinergic-rich grafts implanted into either the neocortex or the hippocampus of aged rats are shown to reinnervate the host neocortex and hippocampus, respectively, and to provide a significant amelioration of the host animals' short-term memory impairments. The results are discussed in light of the cholinergic hypothesis of geriatric memory dysfunction.

Aging↗
PubMed1990

Development of layer I and the subplate in the rat neocortex.

Development of layer I and the subplate of the rat neocortex was examined with [3H]thymidine autoradiography. The experimental animals used for neurogenesis were the offspring of pregnant females injected with [3H]thymidine on 2 consecutive days: Embryonic Day (E) 13-E14, E14-E15, . . . E21-E22, respectively. On Postnatal Day 5, the proportion of layer I and subplate cells originating during 24-h periods were quantified at three anteroposterior levels. Presumptive Cajal-Retzius cells (large horizontal cells) are generated mainly on E14 and subplate cells on E14 and E15 ("outside-in" gradient). Both populations are generated earlier than cells in the cortical plate, which has an "inside-out" gradient. The subplate also has a ventrolateral/older to dorsomedial/younger neurogenetic gradient. The small- to medium-sized horizontal cells in layer I have an extensive period of neurogenesis with an "outside-in" gradient. To study morphogenesis, pregnant females were given single injections of [3H]-thymidine during gestation and embryos were removed in successive 24-h intervals (sequential-survival). On E15 and E16, cells accumulate outside the neuroepithelium in the primordial plexiform layer with older presumptive Cajal-Retzius cells superficial and younger presumptive subplate cells deep. The Cajal-Retzius cells permanently settle superficially among a first system of extracellular channels that appears on E14. Before reaching their final settling sites, subplate cells form the incipient cortical plate in the ventrolateral neocortex on E16. On E17, a seocnd system of extracellular channels appears below the cortical plate. On E18 and E19, subplate cells leave the cortical plate and permanently settle among the deep extracellular channels in a separate layer.

Animals↗
PubMed1992

Persistent innervation of the rat neocortex by basal forebrain cholinergic neurons despite the massive reduction of cortical target neurons. I. Morphometric analysis.

In Alzheimer's disease, a characteristic neurochemical abnormality is the loss of cholinergic enzymes in the neocortex, reflecting the degeneration of basal forebrain neurons responsible for cholinergic innervation of the neocortex. It is hypothesized that basal forebrain neuronal degeneration results from a reduction in the level of trophic factors synthesized by neurons in the target regions of cholinergic projections. Data from a large number of animal lesioning studies tend to support this theory; however, most of these lesions also induce widespread, nonspecific injury responses in the CNS. To directly test the dependence of basal forebrain cholinergic neurons on target-derived neurotrophic support, pregnant Sprague-Dawley rats were injected with moderate doses of methylazoxymethanol acetate (MAM) on Gestational Days 14 and 15. Extensive morphometric analysis of offspring reveals that the prenatal administration of MAM during this period of neurogenesis results in the ablation of 40-70% of cortical neurons, without significant effects on the hippocampus or the genesis of basal forebrain cholinergic neurons. Examination of MAM-treated animals at several ages reveals no significant differences in neuronal density of cholinergic neurons as compared to controls. Extensive analysis of animal brains at several time points has failed to reveal any evidence of classical injury responses which might be responsible for preservation of basal forebrain neurons. These results contradict the theory that mature basal forebrain cholinergic neurons are critically dependent on the availability of target-derived neurotrophic factors and are therefore unlikely to be the major etiological factor in basal forebrain neuronal degeneration characteristic of Alzheimer's disease.

Acetylcholine↗
PubMed1992

Neuronal loss or replacement in the injured adult cerebral neocortex induces extensive remodeling of intrinsic and afferent neural systems.

The question of how the cerebral cortex responds over time to changes in cortical neuronal number was addressed by inducing excitotoxic cortical neuronal loss, either alone or followed by homotypic fetal cortical cell suspension grafts, in adult rats. Following neuronal cell loss, rapid gliosis and inflammation temporarily maintained tissue volume. As gliosis subsided, tissue shrinkage occurred until the ratio of glia to neurons approached that of normal neocortex. After neuronal loss, total cortical glutamate uptake and glutamic acid decarboxylase activity dropped markedly and remained low, and there was a gradual but considerable reduction in the total size of afferent fiber networks. However, when expressed as concentrations per unit of tissue or protein, histological and neurochemical cortical markers showed increases during the phase of tissue shrinkage and in the long-term equilibrated to near normal levels. Retrograde tracing studies showed that the reduction in total afferent fiber network is accompanied by the atrophy of afferent neuronal cell bodies. Grafts of fetal cortical cells placed after excitotoxic lesions provided long-term reconstitution of cortical tissue mass, maintained afferent fiber systems, and prevented both the atrophy and surrounding cellular gliosis of some afferent neuronal cell bodies for over a year, but were unable to innervate the main cortical target regions in the host. Thus after neuronal loss or replacement, the adult cerebral neocortex and its afferent systems remodel to a density of neurons, glia, and afferent fibers similar to that found in intact tissue, illustrating structural plasticity toward a dynamic equilibrium.

Afferent Pathways↗
PubMed1994

An extensive network of PHF tau-rich dystrophic neurites permeates neocortex and nearly all neuritic and diffuse amyloid plaques in Alzheimer disease.

Previous studies demonstrated paired helical filament tau (PHF tau) in neuritic but not diffuse beta-amyloid (A beta) plaques in Alzheimer's disease (AD). Re-examination of amyloid deposits with antibodies to A beta and PHF tau by conventional and confocal microscopy using double label immunohistochemistry showed that PHF tau is a component of both diffuse and neuritic plaques in AD. Unlike controls, a dense network of PHF tau positive dystrophic neurites extended throughout the AD neocortex permeating nearly all neuritic and diffuse plaques. Thus, PHF tau-rich dystrophic neurites are common components of neuritic and diffuse plaques in AD neocortex.

Aged↗
PubMed1978

N-ethyl-N-nitrosourea-induced teratogenesis of brain in the rat. A cellular and cytoarchitectural analysis of the neocortex.

N-Ethyl-N-nitrosourea (ENU) was administered intravenously to pregnant Wistar-albino rats on days 14--21 of gestation in order to study the teratological effects of the carcinogen on the developing brain. Offspring were killed 60 days postnatally, and the brains examined histologically by cresyl violet staining and Golgi-Cox preparations. Macroscopic examination of the brains revealed a graded pattern of microcephaly. Injection of ENU on day 14 of gestation gave the most severe effects and injection on day 21 the least effects. Microscopic examination of the neocortex revealed a graded reduction in the lateral and sagittal lengths, thickness, and the number of cells in a sample slab of the cortex. In the Golgi-Cox preparations the pyramidal neurons of cortical layers III and V, as well as neurons of other layers, were seen to have fewer secondary and tertiary dendrites, and the length of their dendrites appeared stunted. These characteristics also were graded in relation to the day of injection of ENU. Altered cytology and cytoarchitecture of the neocortex and possible underlying mechanisms are discussed.

Animals↗
PubMed1991

Parvalbumin immunoreactive neurons in normal human temporal neocortex and in patients with Alzheimer's disease.

Parvalbumin-immunoreactive (PARV-ir) neurons were studied in the temporal neocortex of 4 normal subjects and in 7 patients with Alzheimer's disease (AD) whose brains were removed from the skull between 1 and 4 h after death and immediately fixed by perfusion through the carotid arteries to minimize pitfalls related to delayed tissue processing. Freezing microtome sections were immunostained free-floating for PARV using a well characterized monoclonal antibody diluted at 1:5000 and the peroxidase-antiperoxidase method. PARV-ir cells predominated in layers III, IV and V and were classified as bitufted cells and small, medium and large multipolar neurons according to their dendritic arbors. Immunoreactive cell processes surrounding the soma of neighbouring cells and immunoreactive vertical strings of buttons were consistent, respectively, with terminal axons of basket cells and chandelier neurons. The number of PARV-ir cells in the superior (T1), middle (T2) and inferior (T3) temporal gyri was variable from one case to another in both normal and pathological cases. Only 1 of 7 patients with AD had significantly reduced numbers of PARV-ir neurons, thus suggesting that PARV-ir cells in the neocortex are relatively resistant to degeneration in Alzheimer's disease.

Aged↗
PubMed1991

The use of microwave tissue fixation to demonstrate the in vivo phosphorylation of an acidic 80,000 molecular weight protein in the rat neocortex following treatment with soman.

Studies were conducted to determine if soman, a cholinesterase inhibitor, could activate the protein kinase C system in the rat neocortex. Using microwave radiation for rapid tissue fixation, it was demonstrated that treatment with soman increased 32P incorporation into an acidic 80,000 molecular weight, heat-stable protein in vivo. Based on relative molecular weight and isoelectric point this protein appears to be identical to a protein identified as a substrate for protein kinase C. Additionally, a protein of the same molecular weight and isoelectric point could be phosphorylated in tissue slices prepared from the neocortex by cholinergic dependent mechanisms. Also, treatment with soman decreased protein kinase C in the soluble fraction of this brain region; however, no corresponding increase was observed in the particulate fraction. These results suggest that soman can activate protein kinase C in vivo, and demonstrate the utility of using microwave tissue fixation to study protein phosphorylation events in vivo.

Acetylcholine↗
PubMed1988

Effect of minaprine on synaptic transmission in the neocortex of the rat in vivo.

The effects of minaprine and/or excitatory amino acid antagonists on transcallosal responses were examined in urethane-anesthetized rats. The transcallosal response was recorded from the surface of the anterior neocortex, following electrical stimulation of the contralateral corpus callosum. The transcallosal response consisted of a biphasic positive-negative waveform. Intravenously-administered minaprine increased the amplitude of the positive- and negative-waves, in a dose-dependent manner. Intracortical injection of (+/-)-2-amino-5-phosphonovalerate (APV) and gamma-D-glutamylglycine (DGG) reduced the amplitude of the negative-wave, with no effects on the amplitude of the positive-wave. L-Glutamate diethylester (GDEE) had no effect on the transcallosal response. The minaprine-induced increase in the amplitude of the negative-wave was completely antagonized by simultaneous intracortical injections of APV and DGG which, per se, did not affect that transcallosal response. In contrast, APV and DGG had no effect on the increase in the amplitude of the positive-wave induced by minaprine. The enhancing effect of minaprine on the transcallosal response remained unaltered in case of an intracortical injection of GDEE. These findings indicate that the negative-wave of the transcallosal response may be related to receptors for excitatory amino acids. The possibility that the pharmacological action of minaprine on synaptic transmission in the neocortex may be linked to the excitatory amino acid receptors warrants further attention.

2-Amino-5-phosphonovalerate↗
PubMed1987

Functional heterogeneity of the right and left cerebral neocortex in the modulation of the immune system.

The cerebral neocortex is now known to modulate the immune system but this modulation is hemispherically asymmetrical. It was previously reported that large ablation, including the anterior prefrontal part of the left cortex decreased whereas symmetrical right lesions enhanced B and T cell-mediated responses. However, the neocortex is an heterogeneous structure from anatomical and physiological points of view and it could be speculated that different aspects of the immune system could be regulated by various cortical areas. In these experiments, restricted neocortical lesions involving the parieto-occipital lobes were performed in C3H/He mice. Animals with right lesions showed depressed mitogen-induced lymphoproliferation and enhanced antibody production to sheep erythrocytes as compared to that of animals with bilateral lesions. Left lesions appeared not to modify these reactions. Furthermore, the percentage of suppressor/cytotoxic T lymphocytes was depressed more in animals with bilateral lesions as compared to any of the other groups. None of the lesions performed appeared to modify the natural killer cell activity. These results confirm that connections between left and right cortex are involved in the modulation of the immune system and suggest that the immunomodulatory functions of the cortex depend upon the specific regions within the right cortex.

Animals↗
PubMed1978

Steroidogenic activity of hACTH and related peptides on the human neocortex and fetal adrenal cortex in organ culture.

Explants prepared from the neocortex and the fetal zone of the human fetal adrenal (gestational age 13 to 18weeks) were maintained under conditions of organ culture for 7 to 9 days during which time they were exposed to hACTH and various related peptides. Corticotrophic activity was monitored by the daily release of dehydroepiandrosterone sulfate (3beta-hydroxy-5-androsten-17-one, 3-sulfate; DHA-S) and cortisol as quantified by radioimmunoassay, hACTH (2.2 x 10(-9) - 2.2 x 10(-8)M) was the most active in sustaining steroidogenesis by both neocortical and fetocortical cells. alpha-MSH possessed similar properties but not at concentrations lower than 10(-6)M, whereas CLIP (4.4 x 10(-9) - 1.1 x 10(-7)M), the 18-39 C-terminal moiety of ACTH, was devoid of activity. Corticotrophic activity with respect to fetocortical explants appeared to be that of maintenance of function best illustrated by dehydroepiandrosterone sulfate biosynthesis, while enhancement of steroidogenesis was observed in the neocortex as manifested by cortisol release. Although not eliminating the possible existence of a specific fetal corticotrophin related to ACTH1-39, the data indicate that hACTH is capable of regulating steroidogenesis in the fetal zone which is primarily geared to the formation of dehydroepiandrosterone sulfate.

Adrenal Cortex↗
PubMed1984

Involvement of brain neocortex and liver in the regulation of T cells: the mode of action of sodium diethyldithiocarbamate (imuthiol).

Sodium diethyldithiocarbamate ( imuthiol ), a non-antigenic and non-carcinogenic compound, devoid of toxic effects at immunostimulant doses, shows distinctive properties in recruitment and activation of T cells. Studies on its mode of action disclosed unsuspected links between the immune system, the endocrine liver and the central nervous system. Evidence was obtained indicating that the brain neocortex modulates T-cell mediated events, most likely via control of specific hormonal synthesis by the liver. The influence of imuthiol is determined at the level of the brain neocortex.

Animals↗