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At least 973 records · Page 54Linked to original sources
PubMed1985

Ingestive responses to homeostatic challenges in rats with ablations of the anterolateral neocortex.

Because rats with either anterolateral neocortical or lateral hypothalamic (LH) damage initially display similar feeding and drinking deficits and recovery patterns, the possibility that anterolateral neocortical ablations would also produce similar chronic ingestive impairments to glucoprivic and hydrational challenges was examined. In general, rats with anterolateral neocortical ablations exhibited normal feeding responses to food deprivation and glucoprivation induced by insulin or moderate doses of 2-deoxy-D-glucose (2-DG), but their response to a high dose (500 mg/kg) of 2-DG was impaired. These animals also drank normally in response to hypertonic saline injections and following water deprivation, but only if food was available during the test session, results indicating that they drank prandially. Results indicate that although the anterolateral neocortex and LH are anatomically related, these brain regions appear to be functionally dissimilar in terms of the regulation of ingestion.

Animals↗
PubMed1985

Cortical substrates of taste aversion learning: involvement of dorsolateral amygdaloid nuclei and temporal neocortex in taste aversion learning.

The amygdaloid complex is functionally implicated in conditioned taste aversion (CTA) learning. Results of previous neurobehavioral studies have provided equivocal evidence concerning the involvement of specific amygdaloid nuclei in CTA learning. The present study was conducted to examine the involvement of the central (CE), lateral (LA), and basolateral (BL) amygdaloid nuclei and the temporal neocortices (area 20) in CTA learning. To that end, distinct groups of rats received bilateral electrolytic lesion placements in the CE, LA, BL, or the temporal neocortices. Control animals received scalp and meningeal incisions only. Following recovery, animals were habituated to a restricted drinking schedule with distilled water. Animals then received CTA conditioning, with LiCl used both as the conditioned stimulus and as the unconditioned stimulus. Anterograde degeneration histologies were performed on all brain tissue to evaluate relations between CTA learning deficits and axonal pathology induced by lesion placements. Results of behavioral manipulations indicated that destruction of the CE, LA, or temporal neocortex impaired CTA acquisition, but damage induced to the basolateral amygdaloid nucleus did not. Anatomical observations indicated that degeneration of amygdalofugal and/or corticofugal projections to the convolutions of the olfactory tubercle (medial), subthalamic nucleus, and the parabrachial complex is correlated with CTA learning deficits. These results indicate that destruction of the dorsolateral amygdaloid nuclei and/or the temporal neocortices may produce CTA learning deficits by affecting olfactory, gustatory, and/or gastrointestinal processing in various portions of the forebrain.

Amygdala↗
PubMed1982

Contribution of the rat's neocortex to ingestive control: I. Latent learning for the taste of sodium chloride.

Neocortical mechanisms do not directly contribute to the execution of taste discrimination, sodium appetite, or the acquisition of a taste aversion in the rat. Examination of previous studies led to the question of whether some permanent ingestive control deficit would be revealed if elements of these experimental paradigms were combined. A latent learning paradigm for the taste of salt was applied to decorticate rats. The ability of decorticate rats to associate how they obtained the taste of NaCl when sodium replete was assessed by examining bar presses during extinction when sodium depleted. Intact rats exposed to 4-6 hr of NaCl taste training retained the association after decortication; decorticate rats exposed to the same training acquired the association. What was most striking was that decorticate rats exposed to as little as 2 min of NaCl taste training demonstrated the ability to associate bar pressing with NaCl by their resistance to extinction. The association was specific to NaCl training; training with distilled water or KCl did not yield resistance to extinction during sodium depletion. Subcortical structures are therefore adequate for latent learning involving NaCl taste. Conversely, data of other investigators have revealed that the neocortex is required for the retention of taste aversion learning for the same taste.

Animals↗
PubMed1981

Synaptic facilitation requires paired activation of convergent pathways in the neocortex.

In associative learning, the activated neurones undergo a variety of concomitant functional alterations--increases or decreases of firing activity and modifications of membrane potential or resistance and of synaptic responsiveness. Synaptic transmission which can be strengthened only when there is paired activity in two pathways is of particular interest in relation to mechanisms for associative learning. For the neocortex, there are few observations of the plastic changes, induced by conditioning procedures, in the effectiveness of individual synapses. We now report that various regimes with joint stimulations of convergent excitatory pathways on to intracellularly recorded neurones in the motor cortex of the cat result in synaptic facilitation lasting for up to 30 min.

Action Potentials↗
PubMed1999

Two networks of electrically coupled inhibitory neurons in neocortex.

Inhibitory interneurons are critical to sensory transformations, plasticity and synchronous activity in the neocortex. There are many types of inhibitory neurons, but their synaptic organization is poorly understood. Here we describe two functionally distinct inhibitory networks comprising either fast-spiking (FS) or low-threshold spiking (LTS) neurons. Paired-cell recordings showed that inhibitory neurons of the same type were strongly interconnected by electrical synapses, but electrical synapses between different inhibitory cell types were rare. The electrical synapses were strong enough to synchronize spikes in coupled interneurons. Inhibitory chemical synapses were also common between FS cells, and between FS and LTS cells, but LTS cells rarely inhibited one another. Thalamocortical synapses, which convey sensory information to the cortex, specifically and strongly excited only the FS cell network. The electrical and chemical synaptic connections of different types of inhibitory neurons are specific, and may allow each inhibitory network to function independently.

Action Potentials↗
PubMed1993

Redistribution of glutamate and glutamine in slices of human neocortex exposed to combined hypoxia and glucose deprivation in vitro.

This study was undertaken to elucidate the roles of neurons and glial cells in the handling of glutamate and glutamine, a glutamate precursor, during cerebral ischemia. Slices (400-600 microns) from human neocortex obtained during surgery for epilepsy or brain tumors were incubated in artificial cerebrospinal fluid and subjected to 30 min of combined hypoxia and glucose deprivation (an in vitro model of brain ischemia). These slices, and control slices that had not been subjected to "ischemic" conditions, were then fixed and embedded. Ultrathin sections were processed according to a postembedding immunocytochemical method with polyclonal antibodies raised against glutamate or glutamine, followed by colloidal gold-labeled secondary antibodies. The gold particle densities over various tissue profiles were calculated from electron micrographs using a specially designed computer program. Combined hypoxia and glucose deprivation caused a reduced glutamate immunolabeling in neuronal somata, while that of glial processes increased. Following 1 h of recovery, the glutamate labeling of neuronal somata declined further to very low values, compared to control slices. The glutamate labeling of glial cells returned to normal levels following recovery. In axon terminals, no consistent change in the level of glutamate immunolabeling was observed. Immunolabeling of glutamine was low in both nerve terminals and neuronal somata in normal slices and was reduced to nondetectable levels in nerve terminals upon hypoxia and glucose deprivation. This treatment was also associated with a reduced glutamine immunolabeling in glial cells. Reversed glutamate uptake due to perturbations of the transmembrane ion concentrations and membrane potential probably contributes to the loss of neuronal glutamate under "ischemic" conditions. The increased glutamate labeling of glial cells under the same conditions can best be explained by assuming that glial cells resist a reversal of glutamate uptake, and that their ability to convert glutamate into glutamine is compromised due to the energy failure. The persistence of a nerve terminal pool of glutamate is compatible with recent biochemical data indicating that the exocytotic glutamate release is contingent on an adequate energy supply and therefore impeded during ischemia.

Brain Ischemia↗
PubMed1995

Mitochondrial hyperoxidation signals residual intracellular dysfunction after global ischemia in rat neocortex.

Reperfusion after global ischemia (10-60 min in duration) in rat neocortex most commonly provoked transient hyperoxidation of mitochondrial electron carriers, tissue hyperoxygenation, and CBF hyperemia. These responses were normally accompanied by recovery of K+ homeostasis and EEG spike activity. Goals of this research were to understand putative relationships among these postreperfusion events with special emphasis on determining whether mitochondrial hyperoxidation results from intracellular changes that may modulate residual damage. The amplitude of postischemic mitochondrial hyperoxidation (PIMHo) did not increase when CBF increased above an apparent threshold during reperfusion, and tissue hyperoxygenation was not required for PIMHo to occur or to continue. These findings suggest that PIMHo is not merely a response to increased CBF and tissue hyperoxygenation; rather, PIMHo is modulated, at least in part, by residual intracellular derangements that limit mitochondrial electron transport. This suggestion was supported by observations that NAD became hyperoxidized after reoxygenation in anoxic hippocampal slices. Also, PIMHo occurred and subsequently resolved in many animals, but K+o never was cleared fully to baseline and/or EEG spike activity never was evident. One suggestion is that PIMHo signals or initiates residual intracellular derangements that in turn impair electrical and metabolic recovery of cerebral neurons after ischemia; an alternative suggestion is that PIMHo and tissue hyperoxygenation are not the sole factors modulating the immediate restoration of electrical activity after ischemia. Present data also support the following: Decreased oxygen consumption, despite adequate oxygen delivery, likely contributes to tissue hyperoxygenation after ischemia; and mitochondrial hyperoxidation is modulated by a limitation in the supply of electrons to the mitochondrial respiratory chain.

Animals↗
PubMed1997

Pharmacologically distinct GABAB receptors that mediate inhibition of GABA and glutamate release in human neocortex.

1. The release of endogenous gamma-aminobutyric acid (GABA) and glutamic acid in the human brain has been investigated in synaptosomal preparations from fresh neocortical samples obtained from patients undergoing neurosurgery to reach deeply located tumours. 2. The basal outflows of GABA and glutamate from superfused synaptosomes were largely increased during depolarization with 15 mM KCl. The K(+)-evoked overflows of both amino acids were almost totally dependent on the presence of Ca(2+) in the superfusion medium. 3. The GABAB receptor agonist (-)-baclofen (1, 3 or 10 microM) inhibited the overflows of GABA and glutamate in a concentration-dependent manner. The inhibition caused by 10 microM of the agonist ranged from 45-50%. 5. The effect of three selective GABAB receptor antagonists on the inhibition of the K(+)-evoked GABA and glutamate overflows elicited by 10 microM (-)-baclofen was investigated. Phaclofen antagonized (by about 50% at 100 microM; almost totally at 300 microM) the effect of (-)-baclofen on GABA overflow but did not modify the inhibition of glutamate release. The effect of (-)-baclofen on the K(+)-evoked GABA overflow was unaffected by 3-amino-propyl (diethoxymethyl)phosphinic acid (CGP 35348; 10 or 100 microM); however, CGP 35348 (10 or 100 microM) antagonized (-)-baclofen (complete blockade at 100 microM) at the heteroreceptors on glutamatergic terminals. Finally, [3-[[(3,4-dichlorophenyl) methyl]amino]propyl] (diethoxymethyl) phosphinic aid (CGP 52432), 1 microM, blocked the GABAB autoreceptor, but was ineffective at the heteroreceptors. The selectivity of CGP 52423 was lost at 30 microM, as the compound, at this concentration, inhibited completely the (-)-baclofen effect on both GABA and glutamate release. 5. It is concluded that GABA and glutamate release evoked by depolarization of human neocortex nerve terminals can be affected differentially through pharmacologically distinct GABAB receptors.

Aged↗
PubMed1984

Histochemical changes of the developing human cerebral neocortex. Studies on two enzymes of energy metabolism in three cortical areas.

Developmental changes of two mitochondrial enzymes, succinate- and menadione-dependent alpha-glycerophosphate dehydrogenases (SDH, M alpha GPDH) have been studied by histochemical techniques in early autopsy material in the following areas of human neocortex: area 4 (motor cortex), area 17 (visual cortex) and area 40 (associative cortex). Each area studied revealed a special enzymatic architecture. SDH - a marker of oxidative activity - develops for several years after birth and in some areas (4 and 40) reaches its adult pattern only after 11 years. Considerable modifications occur during development in the relative activities of the different cortical layers. SDH activity initially appears in layers which send projections to subcortical relays or receive specific thalamocortical afferents. Layers which receive cortico-cortical projections mature later on. In contrast to SDH activity that of M alpha GPDH is elevated already before birth, increases until one month of age and decreases afterwards. This enzyme present in neuroblasts disappears from mature cortical neurons, except from those of the VIth layer. The distribution of this enzyme in cortical layers of the child is opposite to that of SDH. The developmental evolution of these two enzymes has been confirmed by biochemical assays.

Adult↗
PubMed1969

Studies on memory: evidence for a widespread memory trace in the neocortex after the suppression of recent memory by puromycin.

Intracerebral injections of puromycin in mice have provided evidence that the hippocampal area of the brain contains the memory trace of recently learned maze behavior and that, with time, the trace is also found in the neocortex. The present experiments were planned to determine whether this enlargement of locus would develop after the blockage of recent memory in the hippocampus by puromycin, i.e., whether the neocortical locus is established if hippocampal memory is suppressed. The experiments depend upon our earlier finding that the memory blockage caused by puromycin can be removed by small intracerebral injections of saline. Control experiments showed that saline injected into the frontal cortex three days after training did not release the puromycin blockage of memory in the hippocampal area. Injections of saline into the frontal cortex 6 and 11 days after training did, however, release memory in mice whose recent memory had been suppressed by puromycin; we interpret this result to mean that the memory trace appears widely in the cortex despite the suppression of recent memory in the hippocampus. The theoretical implications of this finding are briefly discussed.

Animals↗
PubMed1985

Cholinergic ventral forebrain grafts into the neocortex improve passive avoidance memory in a rat model of Alzheimer disease.

The memory dysfunction of Alzheimer disease has been associated with a cortical cholinergic deficiency and loss of cholinergic neurons of the nucleus basalis of Meynert. This cholinergic component of Alzheimer disease can be modeled in the rat by ibotenic acid lesions of the cholinergic nucleus basalis magnocellularis. The memory impairment caused by such unilateral lesions, as reflected in passive avoidance behavior, is reversed by grafts into the deafferented neocortex of embryonic neurons of the cholinergic ventral forebrain, but not by grafts of noncholinergic hippocampal cells.

Acetylcholinesterase↗
PubMed1987

Ontogeny of the serotonergic projection to rat neocortex: transient expression of a dense innervation to primary sensory areas.

The development of serotonergic innervation to rat cerebral cortex was characterized by immunohistochemical localization of serotonin combined with autoradiographic imaging of serotonin-uptake sites. In neonatal rat, a transient, dense, serotonergic innervation appears in all primary sensory areas of cortex. In somatosensory cortex, dense patches of serotonergic innervation are aligned with specialized cellular aggregates called barrels. The dense patches are not apparent after 3 weeks of age, and the serotonergic innervation becomes more uniform in adult neocortex. This precocious neonatal serotonergic innervation may play a transient physiologic role in sensory areas of cortex or may exert a trophic influence on the development of cortical circuitry and thalamocortical connections.

Aging↗
PubMed1991

Early ingrowth of thalamocortical afferents to the neocortex of the prenatal rat.

The initial ingrowth of thalamocortical afferents into the presumptive somatosensory cortex was examined in the fetal rat. Thalamic fibers were labeled in fixed brains with the carbocyanine dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI). On embryonic day 16, thalamocortical afferents arrive in the neocortex and course tangentially within the intermediate zone immediately underneath the cortical plate. By embryonic day 17, thalamocortical fibers have begun their radial growth into cortex and their arbors span the cell-sparse zone between layer VIb and the bottom of the cortical plate. By the day of birth (embryonic day 21), thalamocortical fibers from a dense plexus within layers VI and V below the dense cortical plate. Our observations indicate that in the rat thalamic afferents arrive in the cortex at a very early age and arborize within the forming cortical layers without an apparent "waiting" period.

Afferent Pathways↗
PubMed1996

Inhibitory neurons in the human epileptogenic temporal neocortex. An immunocytochemical study.

Immunocytochemical methods were used to study alterations in inhibitory neuronal circuits in human neocortex resected during surgical treatment of intractable temporal epilepsy associated or not with brain tumours. The epileptogenic cortex was characterized and divided into spiking or non-spiking zones by intraoperative electrocorticography (ECOG). The resected cortex was cut into blocks, sectioned and stained immunocytochemically for visualization of glutamic acid decarboxylase (GAD), the calcium-binding protein, parvalbumin (PV) and glial fibrillary acidic protein (GFAP). A variety of alterations in cortical neuronal circuits as revealed by immunocytochemical and histological methods were found. Similar alterations in inhibitory neuronal circuits appear to occur independently of the primary epileptogenic site and pathology associated with epilepsy, which suggests that there is possibly a common basic underlying mechanism that leads to seizure activity. These changes were apparently unrelated to ECOG findings at surgery, which bring into question the value of the use of interictal epileptic discharges recorded by ECOG to guide cortical resections. The most conspicuous and common change was the loss of chandelier cells. The finding that these cells are among the most vulnerable types of GABAergic interneurons in the epileptogenic temporal cortex indicates that they might be of great functional importance, since the axon terminals of chandelier cells are likely to exert powerful regulation of impulse generation in cortical pyramidal cells. Therefore, these cells might represent a key component in the aetiology of human epilepsy.

Adolescent↗
PubMedDate not supplied

Selective changes in the microorganization of the human epileptogenic neocortex revealed by parvalbumin immunoreactivity.

The microanatomy of the human lateral temporal cortex removed from patients with intractable temporal lobe epilepsy was studied using correlative light and electron microscopic immunocytochemical methods for the localization of the calcium-binding protein parvalbumin (PV). PV immunostaining was mainly used to label a subpopulation of powerful cortical inhibitory interneurons that have been shown to be lost at epileptic foci in certain animal models of epilepsy. In the human neocortex with normal appearance, we identified the same local neuronal circuitry as in the normal monkey cortex, but in some regions of the same cortex, a fine disorganization of neuronal circuits (loss of inhibitory neurons and presumptive thalamocortical terminals) was found. This abnormal circuitry may interfere with normal cerebral activity in epileptic patients. These results also indicate that PV immunoreactivity can be a useful tool to study normal and abnormal synaptic circuits in the human cerebral cortex.

Adolescent↗
PubMedDate not supplied

Functional interactions between the medial temporal lobes and posterior neocortex related to episodic memory retrieval.

We applied structural equation modeling to positron emission tomography data in humans to examine functional interactions between the right medial temporal lobe (MTL) and selected right neocortical regions in relation to visual recognition memory. Using a priori knowledge about anatomical connections between these regions as a guiding constraint, we modeled the pattern of interactions [i.e. covariances in regional cerebral blood flow (rCBF)] associated with episodic memory retrieval of spatial location and compared it with the pattern for retrieval of object identity. We also compared these patterns with those associated with perceptual matching of spatial location and object identity. Although displaying no difference in average rCBF across tasks, the right MTL showed domain-specific qualitative differences in interactions with posterior dorsal (parieto-occipital sulcus, supramarginal gyrus) and ventral regions (fusiform gyrus, superior temporal sulcus) but not with a prefrontal region. MTL interactions involving dorsal regions were positive in the spatial retrieval task but negative for object retrieval. Interactions involving ventral regions showed the reverse pattern. No comparable changes were observed during perceptual matching. Using control models, we demonstrated the neuroanatomical specificity of these results. Our results provide support for the notion that the nature of interactions between the MTL and posterior neocortex depends on the domain of information to-be-recovered.

Brain Mapping↗
PubMed1993

Changes in tyrosine phosphorylation in neocortex following transient cerebral ischaemia.

Growth factor receptors activate protein tyrosine kinases, which are important for cell growth and survival. The protein tyrosine kinase (PTK) activity and the levels of phosphotyrosine (Ptyr) containing proteins were studied in the rat neocortex exposed to 15 min of transient cerebral ischaemia. The levels of the Ptyr containing proteins increase during recovery in the synaptosomal fraction, while the changes in the light membrane fraction are less marked. Protein tyrosine phosphorylation in the cytosol decreases. The differential changes in the levels of phosphotyrosine proteins in the particulate and cytosolic fractions suggest that the signal cascade from membrane bound receptors through tyrosine phosphorylation in the cytosol may be interrupted following ischaemia. This may be of importance for the development of neuronal damage.

Animals↗
PubMed1994

DNA damage consistent with apoptosis in transient focal ischaemic neocortex.

Transient focal ischaemia was produced in rat right neocortex by temporary middle cerebral artery occlusion. DNA damage was visualized in situ in cells of this right hemisphere but not in the contralateral hemisphere. The extracted damaged DNA exhibited laddered fragmentation which is indicative of apoptotic degradation. The amount of DNA damage was quantified by an end-labelling technique and shown to increase with the duration of the ischaemic insult. We conclude that the neurodegeneration resulting from focal ischaemia has an apoptotic component.

Animals↗