Estrogen binding in the neonatal neocortex.
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The effect of hyperphenylalaninemia on size and density of synapses in rat neocortex.
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Circulation of cortical spreading depression around electrically stimulated areas and epileptic foci in the neocortex of rats.
Spreading depression (SD) elicited in the cerebral cortex of anaesthetized rats does not penetrate into epileptic foci (penicillin) or cortical regions subjected to repetitive electrical stimulation (6--10 Hz, 0.05--0.01 msec). The extent of the SD block, monitored by the absence of the slow potential change and preservation of spontaneous and evoked EEG activity, can be varied in certain limits by changing the stimulus parameters. When the diameter of the block in the parietal cortex is reduced at a time when its temporal boundary is circumvented by an SD wave, propagating in the rostral direction, a strip of cortical tissue between the block and sagittal sulcus is opened for SD which spreads through this route from the frontal to the occipital cortex and starts reverberating around the block. Other methods for eliciting SD reverberation employ removal of an additional block in a section of the circular pathway and directionally biased propagation around the stimulation point. SD reverberation lasting for at least 3 cycles was observed 109 times (median number of completed cycles 5.2, average cycle duration 4.4 +/- 0.1 min). It is suggested that SD reverberation around an epileptic focus can account for slow oscillations of ictal and interictal discharge and for recurrent seizures.
Animals↗
Selective facilitation of synapses in the neocortex by heterosynaptic activation.
Heterosynaptic facilitation (HF) of different excitatory postsynaptic potentials (EPSPs) can be recorded in the motor cortex os anesthetized cats following repetitively applied EPSP-spike stimulus pairs. HF turned out to be synapse-specific in many cases, because not all of the stimulated inputs in the same neuron could produce it. Furthermore, membrane depolarization, increase in membrane resistance and firing activity, can appear with or without HF of a test EPSP.
Animals↗
Nitrous oxide alters oxidative metabolic activities of rat neocortex in situ.
Nitrous oxide was shown by dual wavelength reflection spectrophotometry to decrease the ratio of reduction/oxidation of cytochrome a,a3 and to increase local blood volume in the cerebral cortex of rats in situ. These changes were in contrast to the decreased local blood volume and increased reduction of cytochrome a,a3 produced by pentobarbital. These effects of nitrous oxide were similar to those produced by respiration of 95% O2 with 5% CO2 except that such inspiration resulted in hemoglobin oxygenation while N2O produced some disoxygenation of hemoglobin. We conclude that the N2O effect on metabolism is likely due to increased energy demand. These results also provide some indication that changes in oxidative functioning in brain tissues may occur without alteration in the concentrations of high energy phosphate compounds.
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Axolemmal infoldings bind calcium in nerve endings of the stimulated neocortex.
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Spiny stellates as cells of origin of association fibres from area 17 to area 18 in the cat's neocortex.
Neurons in the cat's area 17 were stained in Golgi-like fashion following injection of horseradish peroxidase into area 18. Such staining allows classification of neurons on the basis of dendritic morphology. The types of neurons found in area 17 are: pyramidal cells in layers 2, 3 and 4ab; spiny stellate cells in the lower part of layer 3, and in layer 4ab; and a few pyramidal and spindle cells in layer 5. The axons of the spiny stellate cells are finer than those of pyramidal cells; they give off collaterals in deeper cortical layers and may bifurcate when entering the white matter. Spiny stellates in area 17 do not project to area 19; after injections are made into area 17, these neurons are found neither in area 18 nor in area 19. The spiny stellate cell with a long axon is thus categorized as a projection neuron which takes part in the pathway from area 17 to ipsilateral and contralateral area 18.
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Spread of acetylcholine sensitivity in the neocortex following lesion of the nucleus basalis.
Neuronal responses to the iontophoretic application of acetylcholine, carbachol and nicotine were studied in rats, 2 or 3 weeks following bilateral lesions of the nucleus basalis region, and compared to those obtained in normal animals. The percentage of cortical neurons excited by acetylcholine and their individual sensitivity were higher in lesioned animals. Furthermore, the laminar distribution of the responses to acetylcholine and the proportion of responses to carbachol and nicotine were also modified.
Acetylcholine↗
Release of GABA from the guinea-pig neocortex induced by electrical stimulation of the 'locus coeruleus' or by norepinephrine.
GABA release from the cortical surface was measured in freely moving guinea-pigs using collecting cups and a mass-fragmentographic method. Stimulation of the locus coeruleus caused a prolonged sedation of the animals and a 60% increase of GABA output from their cerebral cortex. Similar results were obtained after intraventricular injections of norepinephrine. Phentolamine antagonized these effects. The results suggest that the noradrenergic innervation of the cortex modulates the function of cortical GABA neurons.
Animals↗
Locus coeruleus lesions and resistance to extinction of a classically conditioned response: involvement of the neocortex and hippocampus.
Bilateral electrolytic lesions of the locus coeruleus were made in rabbits prior to classical conditioning of the nictitating membrane (NM) response. After recovery, the animals received one session of unpaired training followed by 3 days of paired acquisition training and 4 days of unpaired training (extinction). At the end of extinction norepinephrine (NE) and dopamine (DA) levels were measured in several brain regions. Each lesioned animal was placed into one of two groups according to whether or not the animal exhibited a significant depletion of cortical/hippocampal NE. A third group was formed by non-lesioned controls. There were no significant differences between the 3 groups during acquisition; however, during days 3 and 4 of unpaired extinction the group with cortical/hippocampal NE depletion showed significantly larger NM responses on the conditioned stimulus-alone trials than either of the two control groups. This extinction deficit appeared mainly in the unconditioned stimulus-period component of the tone-alone conditioned responses. The magnitude of the extinction deficit was highly correlated with the depletion of NE in both cortical and hippocampal samples but not with the depletion of NE in the hypothalamus/mid-thalamus, or cerebellum.
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Evidence for high affinity choline transport in synaptosomes prepared from hippocampus and neocortex of patients with Alzheimer's disease.
Sodium-dependent, hemicholinium-sensitive choline transport was measured in purified synaptosomes prepared from fresh necropsy brain of patients with senile dementia of the Alzheimer type and from control subjects. Choline transport velocity was standardized in terms of the occluded lactate dehydrogenase activity of the various synaptosomal preparations, rather than in terms of the protein content, since this enzyme is more representative of the synaptosome content of the purified homogenates. A regional difference in high-affinity choline transport was observed in purified synaptosomes prepared from brains of mentally normal controls; the velocities of sodium-dependent and hemicholinium-sensitive choline uptake into synaptosomes from hippocampus were about twice as great as that into synaptosomes from frontal cortex, indicating a greater relative density of cholinergic innervation in the hippocampus. Hippocampal and neocortical cholinergic nerve cell endings, prepared as synaptosomes, from brains of patients with Alzheimer's disease, also accumulated choline by a high-affinity mechanism; however, the velocity of uptake into both brain areas was decreased in comparison with controls. Choline transport into synaptosomes from Alzheimer frontal cortex was reduced approximately 50%, while uptake into Alzheimer hippocampal synaptosomes represented only 20% of the control activity. The reduction in synaptosomal high-affinity choline transport in Alzheimer's disease could be indicative of degeneration of cholinergic nerve terminal boutons resulting from cholinergic nerve cell death, or could result from an overall decrease in the number of carrier sites per nerve terminal or in the carrier transport velocity.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Specific retrograde transport of nerve growth factor (NGF) from neocortex to nucleus basalis in the rat.
[125I]labeled NGF injected in very small quantities into the frontal or dorsal anterior occipital cortex of adult rats, was specifically taken up and transported retrogradely to large, presumably cholinergic neurons in the nucleus basalis region (lateral preoptic nucleus, anterior lateral hypothalamic nucleus, substantia innominata, ventral globus pallidus and internal capsule), as revealed by light microscopic autoradiography. Cells projecting to the injection site in the frontal cortex were localized ipsilaterally in the more caudal parts of the nucleus basalis region, whereas cells projecting to the dorsal anterior occipital cortex could be found throughout the entire extent of the nucleus basalis and also in the vertical and horizontal limb of the nucleus of the diagonal band of Broca. Other nuclei known to project to the cortex (locus coeruleus, substantia nigra, nucleus raphe, thalamus) were consistently found to be unlabeled. In contrast to [125I]NGF, injection of [125I]cytochrome C failed to label any cell bodies in the basal forebrain nuclei by retrograde transport. This high selectivity for uptake and retrograde transport of NGF indicates the presence of membrane receptors for NGF or a closely related molecule on these cholinergic neurons of the basal forebrain innervating the cerebral cortex.
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Glutamic acid decarboxylase activity decreases in mouse neocortex after lesions of the basal forebrain.
Glutamic acid decarboxylase (GAD) activity was measured in the cerebral cortex of animals after acute and chronic lesions to basal forebrain cholinergic nuclei. Such lesions were shown to result in an extensive depletion of cholinergic markers in parietal cerebral cortex. A statistically significant 30% decrease in GAD activity was first detected at 6 weeks postlesion and was still measurable 8 months after the lesion. These results suggest that cholinergic inputs to cortex indirectly or directly influence GABAergic transmission in cortex.
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The effects of serotonin on the morpho-functional development of rat cerebral neocortex in tissue culture.
The morpho-functional development of the visual area of the cerebral cortex of newborn rats and effects of serotonin (5-HT) on these processes were studied in long-term (up to 40 days) organotypic cultures. It was shown that systematic addition of 5-HT in physiological concentrations to the nutrient medium during cultivation of the explants stimulates glia proliferation, neuron differentiation, neuropil formation, axon myelination and synaptogenesis. Electrophysiological studies of cortical cells in 5-HT-treated cultures showed earlier exhibition of spontaneous activity, increased number (by 33%) of spontaneously firing neurons and prevalence of periodic (bursting) type of discharges. Cultivation of neurons in a medium with 5-HT approximates their sensitivity to 5-HT to that observed in situ. The data obtained are indicative of the stimulating effects of 5-HT on the morpho-functional development of the rat cerebral cortex in tissue culture.
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Morphologic features of embryonic neocortex grafts in adult rats following frontal cortical ablation.
Embryonic cortex from 19-day fetuses was transplanted in a medial frontal cortex wound cavity of 105-day-old male rats. Nissl-stained tissue revealed little internal laminar organization. Graft sections impregnated by the Loyez method exhibited bands of myelinated fibers surrounding implants as well as long-interconnecting and swirl-like fiber fascicles within the implant. Tissue processed histochemically for acetylcholinesterase and choline acetyltransferase revealed enzyme-positive fibers and cell bodies within the grafts. Cytochrome oxidase histochemistry revealed regional variations in the metabolic activity of the grafts. In summary, although our frontal cortex grafts exhibit many of the morphological features seen in intact frontal cortex, the organization of these components within the implant is dissimilar to normal cortical tissue.
Acetylcholinesterase↗
The role of basal forebrain in the primary cholinergic vasodilation in rat neocortex produced by systemic administration of cismethrin.
The pyrethroid insecticide cismethrin (9 mumol/kg) causes a large blood flow increase in cerebral cortex, without a parallel increase in metabolism. A unilateral lesion of the basal forebrain attenuated the blood flow increase in the cortex ipsilateral to the lesion but augmented that in the contralateral cortex. Cortical choline acetyltransferase was similarly affected. Atropine sulphate substantially reduced the flow increase and was additive to the lesion effects. Systemic cismethrin is thus capable of activating a cholinergic vasodilation in the cortex and, in the parietal cortex at least, a substantial proportion of the flow increase is mediated by extrinsic projections from the basal forebrain.
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Noradrenergic innervation does not affect chronic regulation of [125I]pindolol receptors in fetal rat brain transplants or host neocortex.
Fetal (E15-16) somatosensory cortex (n = 15) or cerebellum (n = 9) were placed into the somatosensory cortex (SmI) of adult rat hosts to study the relative importance of tissue origin versus host milieu on graft beta-adrenoceptor regulation. Autoradiographic studies of [125I]pindolol ([125I]pin) binding in the presence of 3 microM serotonin were performed as an index of beta-receptor binding in both intact hosts and those with ipsilateral locus coeruleus (LC) lesions and/or ipsilateral superior cervical ganglionectomy. [125I]pin binding within fetal grafts was highly variable with areas of highest specific binding in cortical grafts (Kd = 209 +/- 30 pM, Bmax = 106 +/- 7 (fmol/mg protein) being comparable to host cortex (Kd = 211 +/- 41 pM, Bmax = 111 +/- 9 fmol/mg protein). Average total binding in whole cortical grafts was 73% and in cerebellar grafts was 60% of that in comparable adult cortex. Host cortex had 66-73% and cerebellum had 4-8% beta 1-receptors while cortical grafts had 59% and cerebellar grafts had 43% beta 1-receptors as determined by competitive binding with ICI 89406 and 118551. Noradrenergic fibers derived from both the host LC and superior cervical ganglion grew into fetal cortical grafts. Binding to high affinity uptake sites ([3H]desmethylimipramine, [3H]DMI) on noradrenergic terminals in cerebellar grafts was 28% higher than that in cortical grafts; superior cervical ganglionectomy decreased [3H]DMI binding in cortical grafts by 37% but had no effect on cerebellar grafts. Neither ganglionectomy nor LC lesions affected total specific binding or binding to beta-receptor subtypes in the grafts or host cortex 3-6 months after removal. Therefore, anatomic site of origin appeared to be the predominant factor in determining the development of beta-adrenoceptors in fetal cortical tissue. In ectopically placed cerebellar grafts, beta-receptor subtypes did not develop comparably to host cerebellar receptors suggesting that host milieu may be of critical importance in receptor development in this tissue.
Adrenergic Fibers↗
Transient expression of Alz-50 immunoreactivity in developing rat neocortex: a marker for naturally occurring neuronal death?
Alz-50-immunoreactive neurons were evident in the subplate and cortical plate of the neonatal rat, but immunoreactivity was lost by the beginning of the second postnatal week. Many of these neurons were double-labeled by an injection of [3H]thymidine on gestational day (G) 12. Moreover, subplate neurons that were generated on G12 were eliminated from cortex by the end of the third postnatal week. Thus, Alz-50 immunoreactivity may be an early indicator of naturally occurring neuronal death.
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