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At least 1,711 records · Page 95Linked to original sources
PubMed1993

High-affinity kainate binding sites in living slices of rat neocortex: characterization and regulation.

We have characterized a high-affinity kainate binding site in in vitro living rat neocortical slices using [3H]kainate. [3H]Kainate labelled at least two binding sites, the higher affinity site with a Kd of 7.1 nM and a Bmax of 71.2 fmol/mg protein. This high-affinity binding site showed a pharmacology consistent with a kainate receptor with competition by kainate and domoic acid, as well as the (RS)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate antagonist 6-cyano-2,3-dihydroxy-7-nitroquinoxaline. Increases in cellular depolarization induced by 2-h preincubations in veratridine and glutamate led to a significant 55% average decrease in [3H]kainate binding in adult cortex. Similarly, preincubation in kainate led to a significant average 26% decrease in binding. In both instances, Eadie-Hofstee analysis of saturation binding data revealed that the decreased binding reflected changes in receptor number. At different postnatal ages, increases in cellular depolarization significantly decreased binding (< 20 days postnatal age, -86%; > 60 days, -48%). Kainate treatment also significantly decreased binding at all ages (-64% at < 20 days; > 60 days, -18%), with significant differences noted between ages. These age-dependent effects are unlike those previously described for either N-methyl-D-aspartate [Lanius and Shaw (1992) Anat. Rec. 232, 54(A)] or (RS)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate high affinity receptors [Shaw and Lanius (1992) Devl Brain Res. 68, 225-233].(ABSTRACT TRUNCATED AT 250 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Basal forebrain grafts in the rat neocortex restore in vivo acetylcholine release and respond to behavioural activation.

Acetylcholine release in the frontal cortex of awake rats after acute or chronic lesions of the nucleus basalis magnocellularis and grafting of cholinergic-rich basal forebrain tissue was studied by in vivo microdialysis. Three to four weeks and five months after a unilateral quisqualic acid lesion of the nucleus basalis, and five months after lesion and cortical implantation of a basal forebrain cell suspension, acetylcholine release was characterized during a range of pharmacological and behavioural manipulations. Neostigmine (5 microM) was added to the perfusion fluid in order to inhibit the degradation of acetylcholine. The extracellular levels of acetylcholine in normal animals increased three- to four-fold when KCl (100 mM) was added to the perfusion medium and was reduced by 80% after addition of tetrodotoxin (1 microM). The nucleus basalis lesion resulted in a 60% reduction in baseline acetylcholine levels compared to normal and the response to KCl-evoked depolarization was significantly reduced. There were no differences between the acute and chronic lesion groups during any of the manipulations performed. Rats with grafts showed baseline levels of acetylcholine about 70% higher than normal, and responded to both KCl (two-fold increased acetylcholine release) and tetrodotoxin (85% reduced levels). All groups showed lower acetylcholine levels during halothane anaesthesia (on average 70-85% reduction). Sensory stimulation by handling resulted in a two-fold increase in acetylcholine release in normal animals, whereas the absolute responses in the lesioned controls were significantly weaker. Rats with grafts increased their acetylcholine release after handling to an extent not different to normal or lesioned controls. Immobilization stress induced an almost two-fold increase in cortical acetylcholine levels in normal rats, whereas the effect in the lesion-only groups was very weak. The grafts responded to the immobilization with an enhanced acetylcholine overflow that was significantly higher than in lesioned controls. The results showed that the reduction in frontocortical acetylcholine release induced by excitotoxic lesions of the nucleus basalis did not recover spontaneously over several months. Intracortical cholinergic-rich grafts obtained from the fetal basal forebrain provided a source of acetylcholine release with firing-dependent properties which could be modulated by behaviourally stressful stimuli. The ability of the grafts to respond to behavioural manipulation strongly suggests that the host brain can functionally influence graft neuronal activity during ongoing behaviour. Host control of graft activity may play a role in the recovery of the lesion-induced deficits seen with these types of grafts.

Acetylcholine↗
PubMed1994

Growth-promoting interactions between the murine neocortex and thalamus in organotypic co-cultures.

The aim of this study was to assess whether developing cerebral cortex produces diffusible factors that can affect the growth of thalamic cells and, if so, what the role of these factors might be during the formation of thalamocortical connections. We studied interactions between cultured organotypic explants from mice maintained in defined serum-free medium. First, we cultured explants of embryonic dorsolateral thalamus in isolation from any other tissue; after culture, these explants were viewed intact and then sectioned. We estimated the numbers of healthy and pyknotic cells before and after culture, and the rates of mitosis in the explants during culture (using bromodeoxyuridine). Based on these data, we concluded that the majority of cells in the thalamic explants survived, although significant numbers of pyknotic cells did accumulate. Thalamic explants extended either very few or no neurites when cultured alone. We then cultured explants of embryonic thalamus near to explants from other tissues. A gap was always maintained between the explants, and we measured the length and density of neurite outgrowth from each thalamic explant. Slices of embryonic cortex promoted a small but significant increase in the amount of growth from thalamic explants. Postnatal cortex stimulated much more profuse neurite outgrowth; postnatal cerebellum had less of an effect, and postnatal medulla or liver had none. We showed that there was significantly more outgrowth from thalamic explants cultured in medium that had been preconditioned with cortical slices than from thalamic explants cultured in control medium, confirming that diffusible factors were produced by the cortex. The survival and mitotic rates of thalamic cells were unaffected by co-culture with the cortex. We conclude that the developing cortex releases diffusible factors that stimulate the growth of thalamic neurites and that other regions of the brain may also release the same substance(s). The lack of a specific source of thalamic growth promoting factor(s) argues against a role for these factors in guiding thalamic axons to specific targets; indeed, we were unable to demonstrate any chemotropic guidance of thalamic axons towards cortical explants in collagen gels. Since postnatal cortex has a more potent stimulatory effect than prenatal cortex, it seems possible that, in vivo, the cortical-derived factors act mainly on thalamocortical axons that have located their targets and are in the process of arborizing and refining their connections.

Animals↗
PubMed1995

Functional geometry of amino acid sensitive membrane of layer V neurons in the guinea-pig neocortex in vitro.

On guinea-pig neocortical slices the spatial organization of dendrites sensitive to excitatory amino acids was studied. Extracellular recording were obtained from the the soma of layer V neurons. Responses of 135 neurons to iontophoretically applied glutamate or aspartate have been analysed. An increased firing rate to somatic and most of dendritic applications were of short latency not exceeding 500 ms. Dendritic applications caused somatic responses with far longer latencies (up to 2-3 s) in 18% of cases. Latencies of responses to excitatory amino acids applied to several dendritic sites of the same neuron had similar values. The greatest reactions were obtained in response to excitatory amino acids imposed to the soma and proximal dendrites. At a distance of 100 microm beyond the soma in the basal region and region and further than 300 microm in the apical region excitatory amino acid applications produced two to three times less intensive somatic response. The area where dendritic activation gave rise to change in neuronal firing was confined to 350 and 800 microm for basal and apical dendrites, respectively. Topography of effective dendritic sites fell into the area corresponding to anatomically known outline of dendritic tree of pyramidal neurons. This fact implies that in our experiments we basically dealt with layer V pyramids. The results obtained suggest that local activation of distal dendrites may elicit spike generation in the soma. Different electrical properties of somatic and dendritic membranes are discussed.

Animals↗
PubMed1995

Properties of single axon excitatory postsynaptic potentials elicited in spiny interneurons by action potentials in pyramidal neurons in slices of rat neocortex.

In slices of adult rat somatomotor cortex, paired intracellular recordings determined the properties of a novel class of excitatory connection, that of presynaptic pyramidal axon collaterals onto burst firing, spiny inhibitory interneurons. Single axon excitatory postsynaptic potentials were brief in time course and displayed conventional voltage relations, increasing in amplitude with membrane hyperpolarization with no change in time course. Excitatory postsynaptic potential amplitude distributions were not skewed. Paired pulse facilitation was profound at interspike intervals < 50 ms, but not altered by raising extracellular [Ca2+] from 2.5 to 5 mM, despite an apparent increase in release probability. Raising presynaptic firing frequency did however produce an increase in excitatory postsynaptic potentials elicited by first spikes that was associated with a decline in excitatory postsynaptic potentials elicited by second and third spikes in brief trains of presynaptic spikes. That this pattern of synaptic activity may result from low probabilities of transmitter release is discussed. It is proposed that while raising Ca2+ and increasing presynaptic firing both increase release probability, repetitive presynaptic firing raises probability more effectively than does raising extracellular [Ca2+]. However, concomitant exhaustion of readily releasable transmitter at higher firing rates may partially obscure this effect. It is concluded that the major differences in the firing rate- and firing pattern-dependent properties of pyramid-pyramid and pyramid-interneuron connections are due to the typically lower release probability at synapses onto interneurons. The accompanying paper describes the morphology of these connections.

Action Potentials↗
PubMed1990

Peptides in the neocortex in Alzheimer's disease and ageing.

Studies which have examined neuropeptides in Alzheimer's disease (AD) and normal ageing are reviewed. A marked specificity and selectivity is noted: most neuropeptides are normal, and the only two peptides consistently altered are somatostatin (SRIF) and corticotropin releasing hormone (CRH). Binding sites for CRH are increased in number in a reciprocal fashion to the reduction in CRH. These findings (1) provide evidence for selective vulnerability within the cortex in AD, (2) suggest that the primary site of pathology in AD may be cortical, and (3) indicate that the pathological process of AD is distinct from that of normal ageing.

Aging↗
PubMed1985

Noncollateral projections of basal forebrain neurons to frontal and parietal neocortex in primates.

To test the hypothesis that axons of the basal forebrain cholinergic system collateralize to innervate widely separated areas of cortex, two distinct, retrogradely transported fluorescent dyes were injected into discrete neocortical regions of three macaques. In two monkeys, True Blue was injected into parietal cortex and Nuclear Yellow into frontal cortex; in a third monkey, placement of the dyes was reversed. Following these large (3-10 microliters total) injections, neurons single labeled with either Nuclear Yellow or True Blue were seen throughout most of the ipsilateral nucleus basalis of Meynert and nucleus of the diagonal band of Broca. Neurons projecting to either frontal or parietal cortex were most heavily concentrated in the anteromedial aspect of the basal forebrain. A small number of labeled neurons was also seen in the contralateral basal forebrain. Cells single labeled with either True Blue or Nuclear Yellow were frequently adjacent to one another, but in no case was a neuron labeled with both dyes. Thus, individual neurons of the basal forebrain complex do not appear to innervate both frontal and parietal lobes of monkeys. This finding is consistent with recent studies in rodents which suggest that basal forebrain neurons innervate relatively small, restricted cortical fields.

Animals↗
PubMed1988

Long-term effects of basal forebrain lesions on cholinergic, noradrenergic and serotonergic markers in mouse neocortex.

Lesions of basal forebrain cholinergic neurons projecting to cerebral cortex and hippocampus have recently been exploited as animal models for some of the neurochemical and behavioral deficits of Alzheimer's disease. We have observed that electrolytic lesions of cholinergic basal forebrain nuclei can lead to morphological plasticity in adult mouse cortex. In the present study, the acute and chronic sequelae of basal forebrain electrolytic lesion on cortical synaptic chemistry have been examined. In addition to choline acetyltransferase (ChAT) activity, levels of norepinephrine and of serotonin were reduced within a week after the lesion. Recovery of ChAT activity and of serotonin levels began within a month after the lesion. Serotonin type 2 receptor binding exhibited an acute reduction after the lesion in ipsilateral cortex, followed later by a chronic bilateral decrease. No significant changes in beta-adrenergic receptors were apparent at any time after the lesion despite a permanent and bilateral reduction of norepinephrine levels after the lesion. The potential significance of these results for cortical plasticity regulation and Alzheimer's disease is discussed.

Animals↗
PubMed1992

Somatostatin release in rat neocortex during gamma-hydroxybutyrate-provoked seizures: microdialysis combined with EEG recording.

Gamma-hydroxybutyrate (GHB) was intracortically applied in two doses (first 10 and then 20 mg/ml) to awake Wistar rats using microdialysis. Simultaneously, EEG and the release of somatostatin-like immunoreactivity (SLI) were measured from the frontal cortex. Intracerebrally administered GHB induced cortical epileptogenic spikes, but not high voltage spindles (HVS) as reported after systemic administration, and seizures with myoclonic jerks and contraversive head movements. Compared to the basal level, GHB (10 mg/ml) initially increased the release of SLI (p < 0.05). However, when the frequency of spikes and seizures rose rapidly (p < 0.001), SLI release decreased significantly (p < 0.001). Minimum release of SLI occurred when seizures were most frequent (during perfusion with 20 mg/ml GHB), while after removal of the drug it rose above the basal level (p < 0.05). According to these results, intracortically applied GHB increases the release of SLI in the surrounding tissue. However, further exposure of GHB leads to a manifestation of epileptic spikes and seizures, during which the release of SLI is significantly attenuated. This suggests that release of somatostatin is affected during epileptic phenomena induced also by intracortical GHB application.

Animals↗
PubMed1993

Acute cocaine alters cerebrovascular autoregulation in the rat neocortex.

Although cocaine abuse has been associated with an increased incidence of cerebrovascular accident, the underlying mechanisms are unknown. In this study we have investigated the effects of cocaine upon the autoregulation of local cortical blood flow (lCBF) during hypertension. Hypertension was induced in conscious rats by intravenous infusion of angiotensin-II (5 micrograms/ml; 0.5-2.5 ml/h), and animals were subsequently injected IV with either cocaine-HCl (5 mg/kg) or saline, prior to the measurement of lCBF of glucose utilization (lCGU) using [14C]-iodoantipyrine or [14C]-2-deoxyglucose quantitative autoradiography, respectively. Hypertension alone (< 155 mmHg) did not significantly alter lCBF in any cortical areas examined. However, at higher mean arterial blood pressure (MABP), lCBF increased focally (+265%) in parietal cortex. Cocaine did not alter lCBF in normotensive animals, but with increasing levels of hypertension (MABP > 145 mmHg), all cocaine-treated rats showed focal increases (200-400%) in lCBF in parietal cortex. Glucose use remained relatively unaffected in all treatment groups. This hyperaemia in cocaine-treated rats at MABP below the normal upper limit of autoregulation may provide a mechanism to explain haemorrhagic stroke in cocaine abusers.

Angiotensin II↗
PubMed1994

Neural development following NMDA administration in the rat: an electron microscopic examination of the occipital neocortex layer I.

Recent research has suggested that the N-methyl-D-aspartate (NMDA) receptor plays a role in numerous activity dependent models of synaptic plasticity. The current research attempted to determine whether chronic activation of the NMDA receptor could induce alterations in synaptic development. An examination of acute NMDA toxicity indicated that rats become increasingly resistant to NMDA over development. Male rats aged 8 days were administered one, 1/10 LD50, SC injection of either NMDA or saline vehicle every 8 h until 18 days of age and were sacrificed 2 days later. Chronic administration of NMDA produced no changes in body or brain weight, the length of synaptic contacts, or the number of synapses per unit area in the neocortical molecular layer. There was a significant 10% increase in the depth of the occipital cortex molecular layer, yielding a 15% increase in the estimated total number of synapses within that area. These results suggest that activation of the NMDA receptor is capable of altering certain aspects of neural development, while other components are not affected.

Aging↗
PubMed1986

Dendritic development in the neocortex of adult rats following a maintained prenatal and/or early postnatal life undernutrition.

The Golgi-Cox method was used to study the maturation of the large pyramidal cells of the Vth cortical layer in three groups of adult rats: one subjected to undernutrition during the first month of life, another throughout the first 2 mth of life, and the last one during gestation and the suckling period. The main alterations consist of a decrease in the number and span of dendritic basilar processes of large pyramidal cells. In animals malnourished during prenatal life and the suckling period the reduction of the basal dendritic arborization was more apparent. It is postulated that the vulnerable period for the basal dendritic development occupies the period from the end of pregnancy until the first 3 wk of postnatal life in the rat (suckling period). Noxious influences acting during this phase induce sequelae that cannot be reversed by subsequent refeeding. A maintained nutritional insult during prenatal and early postnatal life induces the most severe changes in dendritic arborizations, compared to those resulting from a prolonged postnatal malnutrition.

Animals↗
PubMed1995

Retrograde axonal transport of different fluorescent tracers from the neocortex to the suprageniculate nucleus in the rat.

The retrograde fluorescent tracers in a combination of two different dyes (Fluoro gold/Nuclear yellow or Fast blue/Fluoro gold) were used for the study of the projections from the medial geniculate body to the frontal and temporal cortices in rats. There were only single-labeled cells, no double-labeled ones in the medial geniculate body (MGB). The suprageniculate nucleus (SG) was considered to be the origin of the rat direct pathway to the frontal cortex. The present results suggest that projections from the suprageniculate nucleus to the frontal cortex and the temporal cortex consist of separate neuronal groups in the rat MGB and SG. The inputs to the SG from the auditory and oculomotor system may be processed in different ways.

Amidines↗
PubMed1990

The effects of potassium-induced depolarization, glutamate receptor antagonists and N-methyl-D-aspartate on neuronal survival in cultured neocortex explants.

The effects of elevating the potassium concentration of the growth medium of neocortical explants was studied. Under control conditions, 10 mM potassium resulted in ca 20% decrease in the number of surviving neurons. The same potassium concentration, however, was clearly neurotrophic in tetrodotoxin-grown cultures: tetrodotoxin-induced neuronal death was significantly reduced. Both effects could be mimicked by the addition of 10 microM N-methyl-D-aspartate (NMDA); lower concentrations were without effect; higher concentrations were neurotoxic under both control and tetrodotoxin conditions. The neurotoxic, as well as the neurotrophic effects of 10 mM potassium appear to be mediated through depolarization-induced glutamate release since they could be influenced by the application of glutamate receptor antagonists. The addition of the NMDA receptor antagonist D-2-amino-7-phosphonoheptanoate (APH) blocked the trophic effect of 10 mM potassium in tetrodotoxin-grown cultures, resulting in low survival. On the other hand, the addition of the non-NMDA antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) resulted in neuronal survival similar to control cultures, indicating that it blocked the toxic effects of glutamate, leaving the trophic effects on the NMDA receptor untouched. Under control (non-TTX) conditions, neither DNQX nor APH showed significant effects on 10 mM potassium-induced cell death, indicating that stimulation of the non-NMDA, as well as the NMDA receptors is neurotoxic. This differential effect of NMDA receptor stimulation on neuronal survival is discussed with respect to the maturational and/or functional state of the neurons in the culture.

2-Amino-5-phosphonovalerate↗
PubMed1991

Chronic blockade of bioelectric activity in neonatal rat neocortex in vitro: physiological effects.

We have examined what effect the loss of spontaneous bioelectric activity has on neural network formation in organotypic rat neocortical explants grown under serum-free culture conditions. Explants were taken from dorsal midline (presumptive visual) and lateral (presumptive auditory) occipital cortex and chronically exposed to tetrodotoxin which blocked all measurable bioelectric activity between change of medium. Extracellular recordings revealed complex, rhythmic spontaneous and evoked multiunit discharges in all explants examined (following tetrodotoxin washout in the experimental group). Control auditory explants had significantly more sites from which electric activity could be recorded compared with control visual explants. Auditory cultures showed no effect of the tetrodotoxin treatment, whereas visual explants showed significant increases over control values, equalling the auditory values. This increased level of spontaneous bioelectric activity was maintained for at least 10 days following transfer of the cultures to control growth medium. There was no significant difference between control visual and auditory explants regarding the number of sites from which evoked activity was seen. Nor did either cortex group show an effect of tetrodotoxin on the number of sites from which evoked activity was seen. The frequency with which spontaneous bioelectric discharges occurred per site increased with age in auditory vs visual cortex. These differences, however, were abolished in the tetrodotoxin-treated groups. It was concluded that neocortical explants which have experienced chronic suppression of spontaneous electric activity did not suffer deficits in neural network formation, though there is an effect on the incidence and frequency with which such activity is given.

Action Potentials↗
PubMedDate not supplied

Dendritic development in neocortex of infants with early postnatal life undernutrition.

The structure of large pyramidal cells from layer V of the motor cortex of undernourished and well-nourished infants was studied to determine the effects of postnatal nutrition on cortical dendritic development. In undernourished infants, the arborization and span of the basilar dendrites were decreased in comparison to controls. These findings indicated that undernutrition experienced during the first months of postnatal life could affect the growth of pyramidal cells, especially the formation of basilar dendrites.

Bronchopneumonia↗
PubMed1994

Neuropeptide Y and somatostatin in the neocortex of young and aging rats: response to nucleus basalis lesions.

Lesions of the nucleus basalis of Meynert (NBM) have been used to mimic, in part, cholinergic deficits occurring in age-related neurodegenerative disorders, i.e., Alzheimer's disease. In our study, the effect of a persistent cholinergic denervation of the fronto-parietal cortex on neuropeptide Y (NPY) and somatostatin (SOM) was examined in young adult (3 months old) and aging (> 18 months old) rats, 1, 3 and 6 months after bilateral stereotaxic NBM lesions with quisqualic acid. In aging, non-lesioned rats a significant decrease in radioimmunologically and immunohistochemically detectable NPY and SOM was found with no further changes after lesions. Morphological markers for these peptidergic populations (cell size and number, NADPH-diaphorase histochemistry, electron microscopy) demonstrated no signs of alterations in both age groups after lesion. Densitometric analysis of peptide fibre networks displayed a heterogeneous response with a significant rarefication in young rats 1 month after the lesion, followed by restoration and a tendency towards increase 6 months post lesioning in individual animals. These findings were confirmed by radioimmunological measurements. Examination of synaptic and cytoskeletal markers, i.e., synaptophysin, GAP-43, MAP-2, Tau-1 and amyloid precursor protein, did not reveal any signs for neuronal reorganization or sprouting. These data are discussed in the context of plasticity and pathology in age-related neurodegenerative disorders with cholinergic impairment.

Acetylcholinesterase↗