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PubMed1978

Autoradiographic study of early neurogenesis in rat neocortex.

The early neurogenesis of rat neocortex was analysed by means of light and electron microscopic autoradiography. It was found that the very first preneurons originate probably as early as ED 11. They are the horizontal cells of Cajal-Retzius. The peak of their formation is on ED 13 (surface index estimated on ED 17 after injection of 3H-thymidine on ED 13:21, after injection on ED 12:4, after injection on ED 15:5), WHereas no Cajal-Retzius cells could be found to have originated after ED 15. Theses cells are the developmentally most advanced of the neocortex. The cells second in date of origin and maturation are preneurons which presumably correspond to the presumptive neurons of Layer VII (VI b), and begin to originate on ED 12. The end of their formation could not be defined owing to a lack of ultrastructural differences to other, younger preneurons in later gestational stages. These two cell types are the first cellular components of the primordial plexiform layer (Marin-Padilla, 1978) or pallial anlage (Rickmann, 1977), demonstrating an outside-in gradient within this layer, and are separated by the formation of the cortical plate. This could be proven by their simultaneous labelling above and below the cortical plate after administration of 3H-thymidine before ED 15. These results confirm the hypothesis of a dual origin of the mammalian neocortex (Marin-Padilla, 1978).

Animals↗
PubMed1991

Empirical comparison of the MEG and EEG: animal models of the direct cortical response and epileptiform activity in neocortex.

This review directly addresses the appropriateness of the dipole model as a physical representation of neocortical sources produced by evoked and spontaneous epileptiform activity in neocortex. Three dimensional electrical measurements of cellular currents in rat sensory neocortex are compared to the extracranial magnetic fields these currents produce. Comparisons are performed for the direct cortical response (DCR) evoked by electrical stimulation of the cortical surface, and for evoked and spontaneous interictal and ictal discharge of the penicillin focus in the same animal preparation. Our data support the hypothesis that evoked and epileptiform magnetic fields result from intradendritic currents oriented perpendicular to the cortical surface. Furthermore, magnetic fields can be detected from epileptic foci smaller than 3 x 3 mm2. This work provides an empirical foundation for physical models with which to interpret noninvasive neuromagnetic recordings of epileptic discharge in human focal seizure disorders. The dipole approximation appears to be appropriate for the interpretation of magnetic field phenomena in neocortex.

Animals↗
PubMed1976

[The predominantly unilateral influence of the posterior hypothalamus on the neocortex].

High-frequency electrical stimulation of the-posterior hypothalamus applied 10-20 days after the sectioning of the brain stem at the level of the anterior frontal margins of the anterior coliculus results in the preferential activation of the ipsilateral neocortex. When unilateral lesions are placed in the posterior hypothalamus, the predominance of synchronous activity in the ipsilateral neocortex is observed. In the premesencephalic preparations, weak single electrical stimulation of the posterior hypothalamus provokes spindles in the ipsilateral portions of the frontal cortex. At more intensive single stimulation of the posterior hypothalamus there occurs diffuse appearance of spindles in different neocortical areas. Besides the preferential unilateral effect, the influence of the posterior hypothalamus is more prominent in the frontal than in the occipital regions of the cortex. It is suggested that the posterior hypothalamus exerts its influence on the neocortex through the thalamic nuclei.

Animals↗
PubMed1992

Effect of ACTH, adrenalectomy and the combination treatment on the density of 5-HT2 receptor binding sites in neocortex of rat forebrain and 5-HT2 receptor-mediated wet-dog shake behaviors.

The effect of ACTH and/or adrenalectomy on serotonin (5-HT)2 receptor binding sites was evaluated in the neocortex of rat forebrain. One day after the adrenalectomy or sham operation, ACTH (50 micrograms/day) was injected subcutaneously into adult male SD rats for 10 consecutive days. Saturation analysis showed that subchronic ACTH treatment significantly increased the Bmax values for 3H-ketanserin binding without any change in the Kd values. Moreover, this ACTH-induced increase in the Bmax values was prevented by adrenalectomy. The concentrations of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) measured by HPLC-ECD were not altered by these manipulations. Ten-day administration of corticosterone (20 and 50 mg/kg) also increased 5-HT2 receptor density in the neocortex of rat forebrain. 5-HT2 (and 5-HT1C) receptor agonist, (+/-)DOI-induced wet-dog shakes in ACTH and/or adrenalectomy-treated rats were also examined. Ten-day administration of ACTH enhanced (+/-)DOI-induced wet-dog shakes and this increase was prevented by adrenalectomy. These results indicate that subchronic adrenocorticotropin-adrenal axis activation of rats increases both the number of 5-HT2 receptors in neocortex of forebrain and the wet-dog shake responses induced by (+/-)DOI.

Adrenalectomy↗
PubMed1994

Redistribution of glutamate and GABA in the cerebral neocortex and hippocampus of the Mongolian gerbil after transient ischemia. An immunocytochemical study.

The redistribution of glutamate and GABA in postischemic brains was examined immunocytochemically using the gerbil model of unilateral 1 h cerebral ischemia. In the cerebral neocortex, the majority of neurons underwent recovery processes after 5 h of recirculation, while neurons in the hippocampus were irreversibly damaged. Glutamate-like immunoreactivity (LI) was highly increased in the degenerating hippocampal CA3 pyramidal cells after recirculation, while in the neocortex and the hippocampal CA1 sector, the pyramidal cells showed only slightly increased glutamate-LI. GABA-LI-positive punctae in the neuropil, corresponding to neuronal processes of GABAergic neurons, were accentuated after recirculation both in the cerebral neocortex and the hippocampus. Although the astrocytes on the nonischemic side showed neither glutamate-LI nor GABA-LI, the swollen astrocytes and their foot processes, which were observed after recirculation, often showed strong glutamate-LI and GABA-LI. These data suggest (1) the accumulation of glutamate or glutamate-like substances, especially in the CA3 pyramidal cells, (2) the excitation of the GABAergic neurons and their subsequent uptake of GABA, and (3) the sequestration of the extracellular neurotransmitters by astrocytes in the postischemic period.

Animals↗
PubMed1999

Does the perireticular thalamic nucleus project to the neocortex?

This study defines several features of the early connections of the developmentally transient perireticular thalamic nucleus of rats. The neocortex of developing rats was injected with either DiI, biotinylated dextran, WGA-HRP (wheatgerm agglutinin conjugated-horseradish peroxidase), fluorescent latex beads or cholera toxin subunit B (CTB) and their brains were processed for tracer detection with standard methods. In general, tracer injections into various regions of the developing neocortex revealed no labelled neurones within the perireticular nucleus, although some of these tracers (WGA-HRP, dextran) labelled many of the amoeboid microglial cells that are found within this nucleus. There were, however, many retrogradely labelled neurones in a region adjacent to the perireticular nucleus, within the nucleus basalis of the basal forebrain (medial edge of globus pallidus). Their identity was confirmed as neurones of the nucleus basalis since they were all were similar in morphology and somal size to neurones that were immunoreactive to NGFr (nerve growth factor receptor), an antigen found only among neurones of the nucleus basalis and basal forebrain. Moreover, double labelling experiments revealed that most, if not all, of the cortically labelled neurones were NGFr-immunoreactive also. Thus, in conclusion, our results suggest that the perireticular nucleus does not project to the neocortex; the only neurones in the general vicinity of the perireticular nucleus that have a cortical projection form part of the nucleus basalis.

Animals↗
PubMed1979

Histological and neurochemical effects of fetal treatment with methylazoxymethanol on rat neocortex in adulthood.

Forebrain microencephaly results when developing rats are exposed to methylazoxymethanol acetate (MAM) at 15 days of gestation (DG). This potent alkylating agent is selectively cytotoxic for dividing cells. Since distinct neuronal populations in neocortex vary greatly with respect to timing of mitotic activity during gestation, it was predicted that some groups would be differentially reduced by treatment. Histological examination of neocortex from treated rats grown to adulthood revealed major losses of laminae II--IV with relative preservation of deeper layers. The atrophic adult neocortex was further characterized by assay of several defined pre- and postsynaptic neurochemical markers. Total markers for GABAergic neurons were greatly reduced (glutamate decarboxylase -71%, [3H]GABA synaptosomal uptake -63% and endogenous GABA -59%). Total [3H]GABA binding to cortical membranes was reduced 67%. Total [3H]glutamate synaptosomal uptake and endogenous glutamate were reduced 71% and 65% respectively. In contrast, total presynaptic markers for noradrenergic innervation were minimally altered but concentration of tyrosine hydroxylase, [3H]norepinephrine synaptosomal uptake and endogenous norepinephrine were increased by 275%, 130% and 133%, respectively. Concentration of cholinergic presynaptic markers was also increased (choline acetyltransferase +97%, endogenous acetylcholine +64%) in atrophic cortex, but to a lesser degree than for noradrenergic innervation. Specific binding of muscarinic cholinergic antagonist [3H]quinuclidinyl benzilate and the beta-adrenergic receptor antagonist [3H]dihydroalprenolol was reduced 25% and 29% respectively in treated cortex. Thus, MAM treatment at 15 DG severely reduces intrinsic neuronal populations including GABAergic and glutamatergic neurons, and produces a shrunken cortex relatively hyperinnervated by noradrenergic and cholinergic neurons. MAM-induced microencephaly is a useful model system for producing relatively selective lesions of telencephalic neurons and for study of altered neurochemical relationships following developmentally incurred brain damage.

Acetylcholine↗
PubMed1981

Spreading depression induced by microinjection of enkephalins into the hippocampus and neocortex.

The opioid peptides Leu-enkephalin, Met-enkephalin and D-Ala2-Met-enkephalinamide were injected at various concentrations into the neocortex and hippocampus of rats to examine their effects on EEG activity and DC potentials. All three compounds were found to elicit spreading depression (SD) in both structures. Higher doses of Met-enkephalin were required to elicit SD as well as seizure activity. In the hippocampus the wave of SD was frequently preceded by seizure activity which was antagonized by naloxone pretreatment (40 mg/kg i.p.). Naloxone also prevented Leu-enkephalin-induced SD in the neocortex (but not in the hippocampus) and Met-enkephalin-induced SD in the hippocampus (but not in the neocortex). It failed to block SD elicited by D-Ala2-Met-enkephalinamide in both structures. Some of the various reported behavioral effects of intracranial injections of enkephalins could be artefacts of hippocampal and/or cortical spreading depression.

Animals↗
PubMed1983

The evoked release of endogenous amino acids from tissue prisms of human neocortex.

The K+-evoked release of 13 amino acids has been determined from tissue prisms of neocortex from patients of various ages, and from rats. Prisms were prepared from various regions of human neocortex obtained at neurosurgery. Upon depolarization aspartate, glutamate and gamma-aminobutyrate (GABA) were shown to be preferentially released. The efflux of glutamate was calcium-dependent. Prisms prepared from human neocortex obtained shortly after death also exhibited preferential K+-induced release of putative amino acid transmitters. Absolute concentrations released into the media were similar to those found for neurosurgical samples. Comparison of the release data for rat and human samples revealed that the efflux of aspartate, glutamate and GABA occurred to a greater extent from rat brain preparations. The K+-evoked release of glutamate from human samples showed a significant linear increase from 12 to 68 years of age.

Aged↗
PubMed1985

Basal forebrain innervation of rodent neocortex: studies using acetylcholinesterase histochemistry, Golgi and lesion strategies.

Acetylcholinesterase (AChE)-rich projections from basal forebrain to neocortex cerebri were characterized in the present study. The purpose was to investigate 3 aspects of these projections in rats and mice that have been incompletely described in previous work: intracortical organization of the fibers, subcortical pathways and axonal branching patterns of individual basal forebrain neurons. AChE histochemistry, lesions and Golgi impregnations were the principal strategies employed in this light microscopic study. The moderately dense, AChE-stained innervation of neocortex can be altered by intracortical lesions. The results depended on the region involved and the orientation of the lesion. Sagittal knife cuts had barely detectable effects, regardless of sites. Coronal knife cut lesions in medial cortex resulted in substantial loss of staining in cingulate and medial occipital fields. In contrast, coronal lesions of lateral or anterior cortex produce only small zonal reductions in staining. The interpretation of the latter findings that we favor is that AChE-rich basal forebrain fibers enter lateral/anterior cortex and branch densely there, but in tangentially limited and overlapping terminal domains. Observations on the topography and targets of AChE-rich basal forebrain cortical afferents revealed that the fibers could be grouped based on certain characteristics. Three sets of fibers were distinguishable: anterior pathway innervating cortex of the frontal pole. These fibers were traceable to the region of the substantia innominata/nucleus basalis. They crossed the neostriatum and external capsule in the sagittal plane, forming in 3 dimensions an orderly sheet-like array of fibers bridging the anteroventral surface of the neostriatum with nearby polar cortex medial pathway innervating cingulate and medial occipital cortex. Emerging predominantly from the region of the diagonal band, the fibers run caudally as a triangular bundle in deep layer VI of cingulate cortex. lateral pathway innervating most of remaining lateral neocortex. The fibers radiate out from substantia innominata/nucleus basalis with a complex 3-dimensional organization. In all pathways, fibers enter and initially run within layer VI before ascending pialward, although the intracortical course in layer VI differs between pathways. These fibers primarily terminate in layer V with a secondary concentration in layer I. However, the latter appears to receive substantial AChE-stained inputs from other sources, possibly intracortical, as well. The pathways overlap at their respective boundary zones. This system is comparably organized in rats and mice.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1989

Antibodies directed against tyrosine hydroxylase differentially recognize noradrenergic axons in monkey neocortex.

In previous immunohistochemical studies of monkey neocortex, we found that antisera directed against tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) appeared to label distinct populations of neocortical axons, which presumably were dopaminergic and noradrenergic, respectively. In the present study, we further evaluated the apparent selectivity of this rabbit anti-TH antiserum for cortical dopaminergic fibers in monkeys by comparing it with two other anti-TH antibodies, a mouse monoclonal and a sheep polyclonal. In addition, the latter two anti-TH antibodies were used in double-labeling studies with a rabbit anti-DBH antiserum. In both single- and dual-label studies, each anti-TH antibody visualized a similar population of cortical axons, although the number of labeled fibers differed across antibodies. That is, in some cortical regions and layers, both the sheep and mouse anti-TH antibodies labeled more cortical fibers than did the rabbit anti-TH antiserum. Thus, the former two antibodies appeared to identify a subpopulation of TH-containing fibers that the latter antibody did not. Dual-label experiments, involving the rabbit anti-DBH antiserum and either the sheep or mouse anti-TH antibodies, demonstrated numerous neocortical DBH-immunoreactive axons in which TH was not detectable immunohistochemically. The percentage of DBH-immunoreactive fibers that were single-labeled differed across cortical regions and with the anti-TH antibody employed. For example, in primary motor cortex the mouse anti-TH antibody did not label 99.4% of the DBH-positive fibers, whereas in primary visual cortex, 76.4% of the DBH-immunoreactive axons were identified by the sheep anti-TH antibody. The results of these studies indicate that many DBH-immunoreactive, presumably noradrenergic, axons in monkey neocortex are not visualized by anti-TH antibodies, and that the ability of anti-TH antibodies to identify noradrenergic cortical axons in monkeys differs substantially among anti-TH antibodies and across cortical regions. These findings may be consistent with previous reports suggesting that the TH molecule is present in different concentrations or molecular forms in dopaminergic and noradrenergic cortical fibers. Finally, this study demonstrates that the labeling characteristics of a particular anti-TH antibody must be carefully evaluated, particularly in studies of primate neocortex, in order to properly interpret the results of those studies.

Adrenergic Fibers↗
PubMed1989

Unlike hypoxia, hypoglycemia does not preferentially destroy GABAergic neurons in developing rat neocortex explants in culture.

We tested whether hypoglycemia, like hypoxia, would preferentially destroy GABAergic nerve cells in the neocortex. To this end, rat neocortex explants dissected from 6-day-old rat pups and cultured up to a developmental stage approximately comparable to that of the newborn human neocortex, were exposed to hypoglycemia for different periods. Quantitative light microscopic and immunocytochemical evaluation of the cultures demonstrated that hypoglycemia does not preferentially destroy GABAergic but rather non-GABAergic neurons, a finding quite opposite to what was found after hypoxia. Recent biochemical data from other laboratories which seem to support this difference in neuronal vulnerability are discussed. It is concluded that perinatal hypoglycemia may not form such a serious threat with respect to the genesis of epilepsy as does hypoxia.

Animals↗
PubMed1990

Posthoc phosphorylation of proteins derived from ischemic rat hippocampus, striatum and neocortex.

Disruption of the brain's protein phosphorylation system by ischemia may cause irreversible metabolic and structural alterations leading eventually to cell death. To examine the effect of ischemia on the phosphorylation state of brain proteins, tissue homogenates derived from the hippocampus, striatum and neocortex of normal rats and rats subjected to severe forebrain ischemia were phosphorylated with [gamma-32P]ATP. The phosphorylated proteins were separated by two-dimensional polyacrylamide gel electrophoresis and changes were assessed by autoradiography. Cerebral ischemia caused marked alterations of the phosphorylation state of many brain proteins; phosphorylation of some proteins was increased while phosphorylation of others was decreased. Despite differences in the sensitivity of the hippocampus, striatum and neocortex to ischemic injury the direction and approximate magnitude of protein phosphorylation changes caused by ischemia were similar in all three regions. Since the pattern of protein phosphorylation in the ischemia-vulnerable hippocampus was identical to that in the ischemia-resistant paramedian neocortex we conclude that abnormalities of protein phosphorylation may be necessary for ischemic injury to neurons but none are sufficient to explain the selective vulnerability of certain brain regions to ischemic damage.

Animals↗
PubMed1990

Electrophysiological properties of embryonic neocortex transplants replacing the primary visual cortex of adult rats.

Solid pieces of the occipital neocortex derived from 17-day rat fetuses were placed in a cavity formed by complete unilateral aspiration of the primary visual cortex in adult rats. Vital labeling of the brain with bisbenzimide was used to differentiate grafts from the host brain tissue. 2 to 10 months after operation electrophysiological experiments were performed in which neuronal activity and field potentials in transplants were recorded in response to sensory and electrical stimulation of the host brain. This study shows that in a large portion of the transplants (14 out of 25): (1) the majority of neurons (183/270) are controlled by visual stimuli and many of them respond to electrical stimulation of the lateral geniculate body (53/62) and the homotopic sites of the contralateral neocortex (28/62); latencies of these responses are within the ranges typical of the normal visual cortex; (2) there is a topical representation of the visual field on the transplants; (3) receptive field sizes, the preference to stationary flashes or to moving visual stimuli and the temporal response pattern of the grafted neurons are similar to those of the primary visual cortex. However, the field potentials evoked visually were recorded only in part of the transplants (8/14) which revealed clear neuronal visual responses, and field potential depth profile differed from that in visual cortex in situ. The functional organization of the transplants remained unchanged throughout the long-time testing. Taken together, these results suggest that after primary visual cortex removal, fetal neocortex transplants may be able to replace functionally the damaged neural circuitries of the host brain.

Animals↗
PubMed1992

Somatotopic maps within the zona incerta relay parallel GABAergic somatosensory pathways to the neocortex, superior colliculus, and brainstem.

Neurons located in the zona incerta (ZI) of the ventral thalamus project to several regions of the central nervous system, including the neocortex, superior colliculus, and brainstem. However, whether these projections are functionally segregated remains unknown. This issue was addressed here by combining neuroanatomical tracers with immunohistochemical staining for gamma-aminobutyric acid (GABA) and/or parvalbumin, coupled with neurophysiological mapping. GABAergic projection neurons were found in four distinct subregions of the ZI including: (1) the rostral pole of the ZI, from which neurons project to the supragranular layers of the neocortex (especially layer I); (2) the dorsal subregion of the ZI, where both ascending projections to the neocortex and descending projections to the pretectal area were observed; (3) the ventral subregion of the ZI, whose neurons project to the superior colliculus; and 3) the caudal pole of the ZI, from which descending projections to the lower brainstem and spinal cord were observed. Somatotopic representations of the contralateral cutaneous periphery were also identified in the dorsal and ventral subregions of ZI, both of which were found to receive dense direct afferent projections from the trigeminal complex, and dorsal column nuclei. These results suggest that the rat ZI is a major somatosensory relay in the ventral thalamus, carrying feed-forward inhibitory signals to neocortical and subcortical targets, in parallel with the excitatory somatosensory pathways.

Afferent Pathways↗
PubMed1994

Microzonal decreases in the immunostaining for non-NMDA ionotropic excitatory amino acid receptor subunits GluR 2/3 and GluR 5/6/7 in the human epileptogenic neocortex.

Potential alterations in glutamate-utilizing excitatory circuits in resected human epileptogenic frontal and temporal neocortex were investigated by using immunocytochemical methods to visualize receptor subunits which comprise the AMPA/kainate (GluR2/3) and kainate (GluR5/6/7) receptor subtypes. Examination of the patterns of immunostaining in regions of neocortex that were identified as spiking and non-spiking based on intraoperative electrocorticography revealed dramatic, microzonal decreases in immunoreactivity for the receptor subunits examined. The patches of decreased immunostaining for GluR2/3 and for GluR5/6/7 were often coincident with respect to each other. However, such abnormal regions were not necessarily correlated with any particular electrocorticographically defined regions nor any overtly abnormal cytoarchitectural features in adjacent Nissl-stained sections. Moreover in many but not all cases, the focal regions of decreased receptor subunit immunoreactivity coincided with small patches of decreased parvalbumin immunoreactivity a calcium-binding protein which labels a subpopulation of powerful inhibitory GABAergic interneurons. These results indicate that in the human epileptogenic neocortex there may be alterations in particular excitatory and/or inhibitory synaptic systems at small, multiple neocortical foci, and that these alterations are found mostly in the same regions. We suggest that these alterations may contribute to the initiation and/or propagation of seizure activity.

Adolescent↗
PubMed1988

Hypoxia preferentially destroys GABAergic neurons in developing rat neocortex explants in culture.

The hypothesis that hypoxic ischemia before or during the human birth process preferentially destroys GABAergic nerve cells, particularly in the neocortex, was tested in a tissue culture model system. To that end, rat neocortex explants dissected from 6-day-old rat pups and cultured to a developmental stage approximately comparable to that of the newborn human neocortex were exposed to hypoxia for different periods. Quantitative light microscopic and immunocytochemical evaluation of the cultures demonstrated that GABAergic neurons were indeed the first neurons to die during hypoxia.

Animals↗
PubMedDate not supplied

Lymphocyte homing after left or right brain neocortex ablation.

The cerebral neocortex is known to modulate the immune system in an asymmetrical way. Ablations of the left cortex decrease, whereas symmetrical right lesions have no effect, or enhance, T cell functions measured 6-8 weeks after lesioning. However, modifications of immune responses induced by lesions of the brain neocortex could result from a lymphocyte redistribution mediated by glucocorticoids, like that observed during stress. We tested this possibility in the present experiments. Cortical lesions modulated concanavalin A-induced proliferation of both lymph node and spleen lymphocytes in a similar way. Cortical lesions of either side modified neither the lymphocyte distribution of 51Cr-labelled injected lymph node cells, nor the percentage of blood cell subsets. These results show that cortical lesions do not affect lymphocyte homing, and suggest that the brain neocortex immunomodulatory effects are not mediated by glucocorticoids.

Animals↗