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At least 1,585 records · Page 88Linked to original sources
PubMed1989

Long-term effects of cholinergic basal forebrain lesions on neuropeptide Y and somatostatin immunoreactivity in rat neocortex.

The effect of cholinergic basal forebrain lesions on immunoreactivity to somatostatin (SOM-i) and neuropeptide-Y (NPY-i) was investigated in the rat parietal cortex, 16-18 months after multiple bilateral ibotenic acid injections in the nucleus basalis complex. As a result of the lesion, the cholinergic fiber density in the cortex decreased by 66% with a concurrent increase in SOM-i fibers by more than 50% and a 124% increase in NPY-i fiber innervation. The neuropeptidergic sprouting response on cholinergic denervation does not match the concurrent cholinergic and peptidergic decline in Alzheimer's disease and as such does not support the cholinergic lesion alone as an animal model for this neurodegenerative disorder.

Animals↗
PubMed1990

Interaction between raphe dorsalis and nucleus basalis magnocellularis in the regulation of high-voltage spindle activity in rat neocortex.

In the present study we compared the effects of an ibotenic acid lesion of the nucleus basalis magnocellularis (NBM), a 5,7-dihydroxytryptamine lesion of the raphe dorsalis (RD) and a combined RD and NBM lesion on the regulation of neocortical electrical activity in freely moving rat. NBM lesions (choline acetyltransferase decrease: frontal cortex 29%, occipital cortex 23%) increased both slow wave amplitudes and waking immobility-related high-voltage spindles (HVS). Although RD lesions (serotonin decrease: frontal cortex 67%, occipital cortex 68%) alone did not affect neocortical electrical activity, the lesion aggravated the increase of HVSs induced by an NBM lesion. The present results demonstrate an interaction between the RD and NBM in regulating cortical functions.

Analysis of Variance↗
PubMed1990

The electrophysiological basis of epileptiform magnetic fields in neocortex.

Electrical measurements of epileptiform cellular currents in a penicillin model of focal epilepsy were directly compared to the extracranial magnetic fields these currents produce. Our data support the hypothesis that epileptiform magnetic fields result from intradendritic currents oriented perpendicular to the cortical surface. Furthermore, magnetic fields could be detected from epileptic foci smaller than 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.

Animals↗
PubMed1990

Pirenzepine-insensitive muscarinic autoreceptors regulate acetylcholine release in human neocortex.

The release of [3H]acetylcholine ([3H]ACh) and its modulation mediated by autoreceptors were investigated in synaptosomes prepared from fresh human cerebral cortex prelabelled with [3H]choline ([3H]Ch) and depolarized in superfusion with 15 mM KCl. The K(+)-evoked release of tritium was almost totally accounted for by unmetabolized [3H]ACh and was largely calcium-dependent. Exogenous ACh decreased the depolarization-evoked release of [3H]ACh in a concentration-dependent manner (EC50 = 1.5 microM). The inhibitory effect of ACh on [3H]ACh release was counteracted by the non-selective muscarinic antagonist atropine. In contrast, the selective M1 receptor antagonist pirenzepine was ineffective. It is concluded that muscarinic autoreceptors regulating the release of ACh are present on cholinergic nerve terminals of human cerebral cortex and appear to belong to a pirenzepine-insensitive subtype.

Acetylcholine↗
PubMed1991

Valproate suppresses N-methyl-D-aspartate-evoked, transient depolarizations in the rat neocortex in vitro.

Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1-1 mM) in a dose-related manner suppressed the characteristic transient depolarizations induced by N-methyl-D-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5-10 mM) also reduced L-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.

Animals↗
PubMed1991

Perforated and non-perforated synapses in rat neocortex: three-dimensional reconstructions.

Perforated and non-perforated synapses in the molecular layer of rat parietal cortex have been assessed morphologically and quantitatively using three-dimensional reconstructions of the postsynaptic terminal. Perforated synapses were analyzed at nine ages, ranging from 0.5 to 22 months of age, and non-perforated synapses at three ages--0.5, 12, and 22 months. Examination of the reconstructions shows that perforated synapses increase in size and complexity with increasing age. This increasing complexity is reflected in a break-up of the postsynaptic density, which is punctuated by larger, branched perforations. In the most extreme cases the result is the appearance of isolated islands of postsynaptic density separated by, and also surrounded by, a synaptic contact zone. Spinules are especially prominent at around 12 months of age in perforated synapses, and the overall negative curvature of the young junctions is replaced by positively curved junctions from 4 months onwards. The non-perforated synapses are relatively small and show few changes with increasing age. Using the measurement option in the reconstruction program, the following trends emerged. All parameters of perforated synapses increased in size with increasing age, whereas the corresponding parameters of non-perforated synapses remained relatively unchanged over this age range. In addition, the percentage of the synaptic contact zone surface area occupied by the postsynaptic density decreased with increasing age in perforated synapses, but increased in non-perforated synapses. The total postsynaptic density surface area of non-perforated synapses per unit volume of molecular layer was double that of perforated synapses at 0.5 months, but the situation was reversed at 12 months. This parameter was similar in the 2 populations at 22 months. This suggests that perforated synapses contribute more to the total surface area of the postsynaptic density in mid- to late-adulthood than do non-perforated synapses, despite non-perforated synapses outnumbering perforated by 2-3:1 at these ages. These data provide more specific evidence that perforated and non-perforated synapses constitute separate synaptic populations from early in development, and that perforated synapses are responsible for the maintenance of neuronal postsynaptic density surface area from mid-adulthood onwards.

Animals↗
PubMed1991

Re-entry waves of Leao's spreading depression between neocortex and caudate nucleus.

About 40% of spreading depression (SD) waves elicited from the parieto-occipital cortex of anesthetised rats penetrated through the temporal lobe structures (amygdala) into the caudate nucleus. Almost 70% of these SD waves did not terminate in the caudate but returned to the cortex and spread through it toward the site of SD initiation. Longer cortico-caudate (5.9 +/- 0.1 min) than caudate-cortical (4.7 +/- 0.2 min) conduction times suggest that SD enters and leaves caudate through routes of different length. SD waves elicited by KCl microinjection into the caudate reached frontal and parieto-occipital cortical electrodes with latencies indicating that the transit point is 5 mm closer to the rostral than to the caudal electrode. The region best satisfying this condition corresponds to rostral claustrum. The directionally biased SD conduction through the transit zone provides a re-entry path for cortico-caudate-cortical SD propagation and forms thus a natural reverberator the small dimensions of which preclude generation of repetitive SD waves.

Animals↗
PubMed1991

Differential distribution of a neurofilament protein epitope in acetylcholinesterase-rich neurons of human cerebral neocortex.

The majority of acetylcholinesterase-rich pyramidal neurons in neocortical layers III and V of the human brain displayed intense immunostaining with SMI-32, a monoclonal antibody which recognizes a non-phosphorylated epitope of neurofilament proteins. In contrast, very few of the heteromorphic acetylcholinesterase-rich perikarya embedded in the white matter of the cerebral hemispheres are associated with this type of immunostaining. These two groups of acetylcholinesterase-rich cortical neurons can thus be differentiated not only on the basis of morphology and location but also on the basis of cytochemical signature. The concurrent visualization of SMI-32 immunoreactivity and acetylcholinesterase enzyme activity also showed that SMI-32 immunoreactive neurons can be subdivided into several subgroups on the basis of their perikaryal acetylcholinesterase activity.

Acetylcholinesterase↗
PubMed1992

Numerous SP-positive pyramidal neurons in cat neocortex are glutamate-positive.

An immunocytochemical technique that allows visualization of two antigens in the same neuron was used to verify the possibility that some neocortical pyramidal neurons contain both glutamate (Glu) and substance P (SP) immunoreactivity. The results show that a large fraction of SP-positive pyramidal neurons are also Glu-positive, and indicate that in a small population of cortical neurons a fast excitatory synaptic transmitter and a slow peptidic modulator coexist.

Animals↗
PubMed1993

Thalamocortical patches in auditory neocortex.

Thalamocortical afferents to the primary auditory cortex of the rabbit were labeled by the iontophoretic injection of the anterograde tracers PHA-L or biocytin into the ventral division of the medial geniculate body (vMGB). Single injections of either tracer into the vMGB labeled multiple "patches" of afferent axons in lamina III/IV of the ipsilateral auditory cortex. Serial section analysis revealed that single patches were elongated in the rostral-caudal axis forming bands of approximately 2 mm in length. The orientation of the bands was similar to the isofrequency contours of the tonotopic maps derived from prior electrophysiological experiments. Within the coronal plane, the topography of the patches is remarkably similar to the intermittent distribution of binaural interaction subclasses described in physiological studies. Our results are consistent with a model of vMGB organization containing functionally distinct, parallel anatomical pathways to AI.

Afferent Pathways↗
PubMed1993

Binaural vs. monaural auditory evoked potentials in rat neocortex.

High spatial resolution epicortical recording techniques and numerical modeling were used to investigate laterality effects on the middle latency auditory evoked potential (MAEP) complex. Our data confirm previous reports that auditory stimulus laterality has a consistent effect on the amplitude, timing, and spatial distribution of the MAEP complex. The earliest temporal components (P1a, P1b and N1) show the greatest sensitivity, and are absent during ipsilateral stimulation. The later positive slow wave (P2) is present at the same amplitude during all stimulation conditions. Generation of the P2 appears to be independent of prior activation of areas 36 and 41 reflected in the early components, suggesting its generation by a more diffuse thalamocortical pathway, possibly from the medial division of the medial geniculate. Serial vs. parallel activation of rodent auditory cortex is discussed in the context of laterality-sensitive MAEP components.

Animals↗
PubMed1993

Chromogranin A, a soluble synaptic vesicle protein, is found in cortical neurons other than previously defined peptidergic neurons in the human neocortex.

Neuropeptides in the cerebral cortex have previously been identified in non-pyramidal neurons only. By comparing the location of chromogranin A (CgA), a soluble protein of large dense-core synaptic vesicles, with that of SMI-32, neuropeptide Y (NPY), parvalbumin (PV) and calbindin (CaBP) using double label immunohistochemistry, we demonstrate that CgA is present in pyramidal neurons as well as in several subtypes of non-pyramidal neurons.

Adult↗
PubMed1993

Alterations in delta opioid receptor levels in discrete areas of the neocortex and in the globus pallidus of the aging guinea pig: a quantitative autoradiographic study.

The effect of aging on delta opioid receptors was examined in the brains of guinea pigs aged 1, 6, 24 and 36 months. Quantitative autoradiography was used to monitor the concentrations of delta receptors in various anatomical regions at five rostro-caudal levels. delta opioid receptor populations were found to be remarkably stable throughout the life span of this species. We have, however, discovered anatomical areas which offer striking exceptions. In the globus pallidus, progressive age-related losses of delta receptors reached 50% in the senescent animal. In contrast, laminae I, II of the lateral agranular frontal cortex and laminae I, II and III, IV of the primary somatosensory cortex demonstrated age-related increases in the concentrations of delta receptors ranging from 30 to 45%. These changes are discussed with the view to their being functionally related components of motor circuitry involving pyramidal and extrapyramidal elements.

Aging↗
PubMed1995

GABA-immunopositive neurons in rat neocortex with contralateral projections to S-I.

The callosal projection is traditionally believed to be exclusively excitatory in function. A new method combining lectin-conjugated colloidal gold for retrograde tracing with immunofluorescence for GABA was used to investigate this question. The large majority of neurons retrogradely labeled after injections of tracer into contralateral S-I were GABA-negative cells in layers II-VI. However, GABA-positive neurons projecting to contralateral S-I were also seen. The majority of double-labeled cells were only weakly labeled with tracer; they were located both in superficial and deep cortical layers and represented at least 1% of all retrogradely labeled neurons. Neurons double-labeled for both tracer and GABA in upper layers were found mainly within the central patch of callosally projecting neurons, whereas those in deep layers were scattered throughout contralateral cortex.

Animals↗
PubMed1995

GABAergic suppression prevents the appearance and subsequent fatigue of an NMDA receptor-mediated potential in neocortex.

We have investigated the regulation of an N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potential by gamma-aminobutyric acid (GABA)-mediated inhibition using extracellular and whole-cell voltage clamp recordings in rat auditory cortex in vitro. Single afferent stimulus pulses at low intensity elicited a slow extracellular negativity (Component C) that was mediated by NMDA receptors. At higher intensities, Component C was suppressed by recruitment of GABAergic inhibition. To understand the actions of GABAergic inhibition on Component C, we determined the effects of: (i) paired-pulse stimulation, which depresses GABAergic inhibition; (ii) pharmacological antagonism of GABA receptors; and (iii) afferent stimulation in slices from neonatal rats prior to the development of cortical inhibition. The results indicate that GABAergic inhibition prevents Component C from occurring, thereby preventing its reduction upon repeated stimulation. Whole-cell voltage clamp recordings were used to test the hypothesis that GABAergic suppression occurred by way of membrane hyperpolarization. At hyperpolarized holding potentials no NMDA receptor-mediated synaptic current was elicited, even with paired-pulse stimulation. At depolarized holding potentials a significant NMDA synaptic current was elicited despite the presence of GABAergic synaptic currents. We conclude that membrane hyperpolarization by GABAergic inhibition prevents the appearance and subsequent fatigue of an NMDA receptor-mediated synaptic potential. Reduction of inhibition can act as a 'switch' to fully release the NMDA potential as frequently as once every 10-20 s.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1996

Mild postischemic hypothermia limits cerebral injury following transient focal ischemia in rat neocortex.

Intraischemic mild hypothermia has been shown to attenuate cerebral infarction occurring after transient focal ischemia. In contrast, the capacity of mild hypothermia to provide a protective effect when administered postischemically has not been clearly defined for transient focal events such as occur in many types of stroke. The present study addressed this issue by investigating the influence of timing and duration of mild hypothermia on cerebral infarction in a rat model of reversible focal ischemia. Sprague-Dawley rats (n = 45) were subjected to 3 h of focal neocortical ischemia by occluding reversibly one middle cerebral artery and both carotid arteries. Mild hypothermia was established after reperfusion and maintained for brief (1 h) or prolonged (21 h) periods. Animals were sacrificed 24 or 48 h after ischemia. A significant reduction (32%) in the volume of infarction was obtained when hypothermia was established immediately after reperfusion and maintained for a prolonged (21 h) period. In contrast, immediate but brief (1 h) hypothermia did not reduce infarction volume. Delaying hypothermia until 30 min post reperfusion and maintaining it for 21 h reduced infarction volume by 22%; however, this effect did not achieve statistical significance. These findings demonstrate that mild postischemic hypothermia is capable of protecting against cerebral injury following transient focal ischemia but that prolonged hypothermia is required to achieve this effect. These findings are consistent with increasing evidence that the window of therapeutic opportunity after transient focal ischemia is rather brief and that critical mechanisms involved in this form of ischemic injury remain activated over a rather lengthy postischemic interval.

Animals↗
PubMed1983

Extracellular matrix during laminar pattern formation of neocortex in normal and reeler mutant mice.

The spatial and temporal distribution of extracellular matrix, which occupied the large extracellular spaces in the developing cerebral cortex, was studied during pre- and perinatal ontogenesis of normal and reeler mutant mice. Colloidal iron-staining material was localized principally in the marginal zone and subplate of normal mice, whereas in reeler mutants, most of the material was found in the outer layers of the cortex. Patterns of extracellular matrix localization in both genotypes followed the laminar pattern formation of cerebral cortex architecture. Histochemical ultrastructural visualization of this extracellular matrix and its susceptibility to enzymatic treatment suggested that the major components are glycosaminoglycans. Their possible role in relation to afferent axon targeting is discussed.

Animals↗