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Direct connectivity between pontine taste areas and gustatory neocortex in rat.

Horseradish peroxidase histochemistry was used to determine the course and extent of neuronal projections from the pontine taste area (PTA) to the gustatory neocortex (GN) in rat. Two distinct findings were encountered: (1) thalamocortical projections from posterior ventromedial thalamus to GN were confirmed, and (2) direct projections from cells located in the PTA to the GN were described. This novel anatomical finding supports previous suggestions that some gustatory information may be relayed to forebrain areas without making synaptic connection in the diencephalon.

Animals↗

The neural circuitry of the neocortex examined in the in vitro brain slice preparation.

The in vitro brain slice technique has been applied to the study of the neocortex. Cortical blocks were removed from adult rats deeply anesthesized with halothane, sectioned coronally at 400-700 micrometer, and placed in a brain slice chamber. Cortical slices typically showed spontaneous and evoked potential activity and normal histology for 8 h or longer. Single units and evoked potential recordings were made from different layers of the cortex using micropipettes. The evoked potentials to electrical stimulation of differing intensity, frequency, and from different cortical layers were analyzed. Evoked potential from all but the most superficial layers of the cortex showed a characteristic 6-component response to stimulation of nearby white matter. This evoked potential closely resembled cortical responses recorded in vivo by other investigators following afferent stimulation. The response amplitude of all components increased as stimulus intensity was raised. Radial movement of the recording electrode showed that components 1-3 had their largest amplitudes in the deepest cortical layers, component 4 reached its greatest amplitude and shortest latency in layer IV, and components 5 and 6 reached their greatest amplitudes in layers IV to II. The frequency following for various components was measured showing greater decline in amplitude for components 4-6 than 1-3. This, together with the results of previous investigators, suggests that the first 3 components represent afferent fiber input, while component 4 represents the first cortical response (layer IV). Components 5 and 6 represent later, additional cortical responses. Further support for the intracortical origin of component 4 was provided by lateral intracortical stimulation within layer IV, giving an evoked potential composed mostly of component 4. With lateral movement of the recording electrode in layer IV the evoked potential disappeared in under 1 mm, suggesting a fairly restricted afferent input to the cortex. The present results encourage the use of the cortical brain slice preparation as an appropriate model system in which to study cortical neural circuitry.

Action Potentials↗

The projection of the basal nucleus of Meynert upon the neocortex in the monkey.

After injections of horseradish peroxidase into several areas of the neocortex in the macaque monkey longitudinal bands of labeled cells in the basal nucleus of Meynert related to areas of cortex in the frontal lobe have been found to overlap along their long axes with the bands related to widely separated but interconnected areas of the parieto-temporal cortex. The frontal and parietal lobes are related to the anterior and posterior halves respectively of the nucleus, the temporal cortex to the postero-lateral margin of the nucleus and the occipital lobe to its upturned posterior extension.

Animals↗

Amino acid release from biopsy samples of temporal neocortex from patients with Alzheimer's disease.

Tissue prisms prepared from neurosurgical samples of temporal neocortex of Alzheimer and control patients, upon depolarization preferentially released aspartate, glutamate and gamma-aminobutyrate (GABA). The Alzheimer and control samples did not significantly differ in the pattern of amino acid release, although acetylcholine synthesis by the Alzheimer tissue prisms was greatly reduced. There was no correlation between the efflux of any amino and acetylcholine synthesis. These observations suggest that in Alzheimer's disease there are no major changes in the extracellular concentrations of these putative amino acid transmitters.

Acetylcholine↗

Penicillin-induced epileptic phenomena in the rabbit's neocortex I. The development of interictal spikes after epicortical application of penicillin.

In an attempt to elucidate the generation mechanisms underlying interictal spikes in the neocortex, the temporal development of spikes after the epicortical penicillin (PNC) application was studied. Field potentials (FP) were recorded simultaneously within the 6 neocortical layers with a multielectrode consisting of 16 contacts (10 X 10 micron 2) in a row at spacings of 150 micron. A one-dimensional current-source-density (CSD) analysis yielded the positions of current, sink and source densities, so that the different electrical events during a spike could be more accurately located within the different neocortical layers. After the epicortical application of PNC a typical succession of events, which underly the development of spikes, was observed. These events are similar in the visual and the motor cortex: immediately after the epicortical PNC application negative transients occur in the two uppermost cortical layers as well as within layers V to III. Due to the diffusion of the drug a characteristic succession of different processes takes place. Fully developed spikes show a typical configuration of sources and sinks, a moderate sink in layer V initiates a massive, double-peaked sink within layers II, III. This configuration of sinks suggests that some sort of triggering mechanism takes place. Since similar events are observed during interictal spikes in the visual and the motor cortex, neuronal structures common to both cortical areas are supposed to be responsible for the generation of PNC spikes.

Animals↗

Subcellular distribution of neuropeptide Y-like immunoreactivity in guinea pig neocortex.

Neuropeptide Y-like immunoreactivity (NPY-LI) was enriched in synaptosomal fractions of neocortex, which on lysis yielded vesicle-rich fractions. The distribution of NPY-LI on a sucrose density gradient was similar to that of somatostatin, with a concentration in heavy vesicles. The peptides were not found in light vesicles in contrast to the distribution of noradrenaline. Both homogenate and vesicular NPY-LI coeluted with synthetic NPY on reverse-phase HPLC.

5'-Nucleotidase↗

Branched projections of pallidal and peripallidal neurons to neocortex and neostriatum: a double-labeling study in the cat.

Double-labeling of basal forebrain neurons by retrograde axonal transport of different markers demonstrated afferents shared by the neocortex and neostriatum. A considerable double-labeled complement of neurons located in the globus pallidus (lateral pallidal segment) and the adjacent interdigitating basal nucleus of Meynert (peripallidal region) had branched axonal collaterals projecting to the precruciate, cingulate and prorean gyri as well as to the head of the caudate nucleus.

Animals↗

Axonal branching of basal forebrain projections to the neocortex: a double-labeling study in the cat.

Double-labeling of basal forebrain neurons by retrograde axonal transport demonstrates divergent collateralization among undecussated axonal projections to the neocortex. These branched fibers originate from a considerable complement of large polymorphic cell bodies located mainly in the basal nucleus of Meynert. They terminate in multiple neocortical sites including the precruciate, postcruciate and/or cingulate gyri. This extensive intra- and intergyral axonal branching indicates that neurons in the basal forebrain of the cat have extensive axonal fields innervating adjacent neocortical gyri.

Animals↗

Postsynaptic potentials evoked in spiny neostriatal projection neurons by stimulation of ipsilateral and contralateral neocortex.

Postsynaptic potentials were evoked in neostriatal neurons by stimulation of the ipsilateral and contralateral medial agranular frontal cortical field (AGm) in the rat. This cortical region is known to project bilaterally to the dorsal lateral head of the caudate-putamen of rats. Ipsilateral stimulation of AGm should excite all types of corticostriatal neurons projecting to neostriatal neurons in the corresponding area in neostriatum, while stimulation of the same cortical area on the side contralateral to the recording should evoke synaptic potentials from a more restricted subpopulation of crossed corticostriatal neurons. Neostriatal neuronal responses were recorded intracellularly and spiny projection neurons identified by intracellular staining with horseradish peroxidase. The initial EPSP response to contralateral stimulation was similar to that evoked from the ipsilateral side, except for the absence of a relatively small short latency component responsible for the earliest part of the response to ipsilateral cortical stimulation. Comparison with previous findings indicated that this earliest EPSP component was due to activation of fast-conducting descending cortical efferents with collateral projections exclusively to the ipsilateral neostriatum. Stimulation of contralateral neostriatum evoked responses identical to those obtained using stimulation of contralateral neocortex. Analyses of these responses indicated that both EPSPs arise from activation of the same population of fibers. Stimulation of the contralateral internal capsule just caudal to neostriatum was not effective in evoking the EPSP. Chronic hemidecortication did not change the shape of the EPSP evoked from the intact contralateral side, but reduced its amplitude by approximately one half. These observations indicate that contralaterally projecting corticostriatal neurons in the rat project bilaterally in neostriatum, have axonal branches to the contralateral cerebral cortex as well as neostriatum, and converge onto neostriatal neurons that also receive input from the corresponding cortical region on the ipsilateral side.

Animals↗

Seizure-like discharges induced by lowering [Mg2+]o in the human epileptogenic neocortex maintained in vitro.

Seizure-like discharges were observed in slices of human epileptogenic neocortex maintained in vitro when [Mg2+]o was lowered near to zero. This type of epileptiform activity: (1) could occur spontaneously or following extracellular focal stimuli; (2) resembled the electrographic pattern associated with tonic-clonic seizures; (3) was accompanied by increases in [K+]o (maximally 6.2 mM from a baseline of 3.25 mM) and decreases in [Ca2+]o (maximally 0.23 mM from a baseline of 1.8 mM). Application of the selective antagonist of N-methyl-D-aspartate (NMDA) receptors, DL-2-amino-5-phosphonovalerate, suppressed in a reversible manner both spontaneous and stimulus-induced seizure-like discharges, suggesting that NMDA-activated conductances are important for the genesis of prolonged epileptiform discharges generated by human epileptogenic neocortical slices.

Epilepsies, Partial↗

Long-lasting potentiation of synaptic transmission requires postsynaptic modifications in the neocortex.

The mechanisms of associative long-lasting potentiation (LLP) of excitatory postsynaptic potentials (EPSPs) were studied in the motor cortex of anesthetized cats. Mono- and oligosynaptic EPSPs were evoked by stimulations of thalamic VL nucleus, pyramidal tract, callosal and somatosensory system and paired with orthodromic, antidromic or current-induced action potentials. EPSP-spike stimulus pairs with 0.1-0.2 Hz frequency and 0-200 ms interstimulus intervals induced increases in the amplitudes and durations of EPSPs for 40-60 min or longer after 20-50 pairings. The LLP was prevented when postsynaptic firing was blocked by intracellular current injection or by juxtasomatic application of gamma-aminobutyric acid. LLP was also prevented when the level of intracellular free calcium was lowered by the intracellular injection of the calcium chelator EGTA or when neuronal transport was blocked by the intracellular injection of colchicine. Neither EGTA nor colchicine blocked postsynaptic firing. Thus, these findings show that LLP in the neocortex is a postsynaptic phenomenon which requires conjunctive pre- and postsynaptic activity, adequate levels of intracellular free calcium, and functional intracellular transport.

Action Potentials↗

Mechanism of aminopyridine-induced ictal seizure activity in the cat neocortex.

Intracellular recordings were obtained from neurons in the motor cortex of anesthetized cats in order to examine membrane and synaptic processes involved in aminopyridine (AP)-induced ictal seizure activity. Depolarizing and hyperpolarizing membrane potential sequences which behaved as large, synchronized excitatory and inhibitory postsynaptic potentials, were found to accompany the ictal seizure potentials. After several repetitions of the seizure attack, partial responses, bursts and depolarizing plateaus with spike inactivation occurred. In layers IV and V we found non-pyramidal tract neurons showing endogenous bursting ability activated by AP. These neurons seemed to be the initiators of the rhythmic synchronous activity of the epileptic neuron population. Our results suggest that AP-induced epileptogenesis represents an adequate model of ictal events in the neocortex.

Action Potentials↗

Single thalamic dopaminergic neurons project to both the neocortex and spinal cord.

Cells in the rat subparafascicular thalamic nucleus (Spf) belonging to the diencephalic A11 cell group, were immunohistochemically stained with antibodies against tyrosine hydroxylase (TH) and dopamine itself. Employing a combination of retrograde fluorescent double-labeling and TH immunofluorescence techniques, we revealed the existence of dopaminergic Spf cells, giving rise to collateral projections to the neocortex and spinal cord.

Animals↗

Demonstration of glutamate-positive axon terminals forming asymmetric synapses in cat neocortex.

Electron microscopic examination of sections immunocytochemically processed with an anti-glutamate serum reveals that many asymmetric synapses in the cat neocortex contain elevated levels of immunodetectable glutamate. These labelled axon terminals are likely to use glutamate as neurotransmitter. Axon terminals forming symmetric contacts were never labelled. Since glutamate is known to exert potent excitatory effects on neocortical neurons, the present finding gives immunocytochemical evidence that asymmetric synapses are excitatory.

Animals↗

Correspondence between 5-HT2 receptors and serotonergic axons in rat neocortex.

The anatomic relationship between serotonergic (5-HT) axons and 5-HT2 receptors in the rat forebrain was determined by a combined analysis of transmitter immunocytochemistry and receptor autoradiography. High densities of 5-HT2 receptors, localized by the ligand N1-methyl-2-125I-LSD (125I-MIL), are found in neocortex and striatum; these regions also receive a dense serotonergic innervation. Regional variations in the density of 5-HT2 receptors and 5-HT axons correspond closely in most, but not all, areas of the forebrain. In somatosensory cortex (SI), the laminar distribution of 5-HT2 receptors closely matches that of 5-HT axons: in particular, a dense band of 5-HT2 receptors in layer Va of SI is in precise register with a dense plexus of fine 5-HT axons. We have also observed a close spatial relationship between 5-HT2 receptors and fine axons in other areas of the forebrain, suggesting that 5-HT2 receptors may be selectively linked to a particular type of 5-HT axon terminal. Since fine axons of this type have been reported to arise from the dorsal raphe nucleus, it appears likely that 5-HT2 receptors may mediate the effects of dorsal but not median raphe projections.

Animals↗

Basal forebrain lesions differentially alter galanin levels and acetylcholinergic receptors in the hippocampus and neocortex.

The basal forebrain contains two subpopulations of cholinergic cells: the medial septal area (MSA) has projections to the hippocampus, while the nucleus basalis magnocellularis (NBM) has projections to the entire neocortex. In the rat, galanin-like immunoreactivity (GAL-LI) may coexist with acetylcholine (ACh) in MSA neurons but not in NBM neurons. In the monkey, GAL-LI may coexist with ACh in neurons throughout the basal forebrain. The present study investigated the differential distribution of GAL-LI within these regions by placing discrete lesions in the MSA and NBM of rats. Endogenous levels of GAL-LI were decreased in the hippocampus but not in the cortex. This differential decrease is consistent with the coexistence of GAL-LI with ACh in neurons within the MSA but not within the NBM. Markers for nicotinic and muscarinic cholinergic receptors, i.e. binding for [3H]nicotine and [3H]pirenzepine, were unchanged in the cortex and hippocampus following these lesions. This suggests that these cholinergic receptor sites do not exist upon projections originating in the NBM or MSA. These results provide new information about the similarities and differences of these two subpopulations of basal forebrain cells, which in turn may have functional ramifications.

Animals↗

Brain neocortex immunomodulation in rats.

The influence of the cerebral neocortex on the immune system was studied in groups of male Wistar rats after lesioning the right or the left fronto-parietal cortex. In left-lesioned rats, mitogenesis of T-lymphocytes induced either by phytohemagglutinin or Urtica Dioca Agglutinin was depressed by about 25-40% as compared to controls. In contrast, T-cell mitogenesis in animals with right lesions, was enhanced by about 20-45% as compared to controls and by about 90% as compared to that observed in left-lesioned animals. Cortical lesions of either side were shown not to modify antibody synthesis and plasma levels of ACTH, or prolactin. These results, quite similar to those that we have previously observed in female mice, suggest that lateralization in brain cortex immunomodulatory functions may exist in both sexes and in several species of mammals.

Animals↗

Transplantation of embryonic ventral forebrain grafts to the neocortex of rats with bilateral lesions of nucleus basalis magnocellularis ameliorates a lesion-induced deficit in spatial memory.

Embryonic ventral forebrain grafts containing developing cholinergic cells were transplanted to the neocortex of rats with bilateral quisqualic acid lesions of the nucleus basalis magnocellularis. A lesion-induced deficit on performance of a spatial alternation test of memory was reduced by such transplants. When the same animals were treated with the acetylcholinesterase inhibitor physostigmine (0.05 mg/kg), however, performance on the behavioral task was not further promoted, and therefore, under these conditions, the cholinergic cortical transplants appear not to be subject to modulation by anticholinesterase drugs.

Acetylcholinesterase↗