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PubMed1991

Time-dependent recovery of taste aversion learning by fetal brain transplants in gustatory neocortex-lesioned rats.

We recently showed that fetal brain transplants produced a significant recovery in the ability of gustatory neocortex-lesioned rats to learn a conditioned taste aversion. In this report we assessed the capability of gustatory neocortex fetal brain transplants to produce behavioral recovery at different times. Four groups of male Wistar rats showing disrupted taste aversions due to gustatory neocortex lesions were studied. The lesioned animals received fetal cortical grafts, obtained from 16-day-old fetuses, and were retrained in the behavioral procedure after 15, 30, 45, or 60 days postgraft. Behavioral results showed a very good functional recuperation at 60 days, slight recovery at 45 and 30 days, and a poor recovery at 15 days postgraft. Results with HRP histochemistry revealed that at 30, 45, and 60 days postgrafting there were increased connections with the ventromedial nucleus of the thalamus and with the amygdala. At 15 days postgrafting there was an absence of HRP-labeled cells. In addition, behavioral recovery was correlated with increased acetylcholinesterase activity, detected histochemically, and with morphological neuronal maturation, revealed by Golgi staining. These results suggest that morphological maturity and reconnectivity between grafts and host tissue are important for behavioral recovery in gustatory neocortex-lesioned rats.

Acetylcholinesterase↗
PubMed1990

Gradients of neurogenesis in possum neocortex.

Gradients of neurogenesis in neocortex of the brushtailed possum were determined with [3H]thymidine autoradiography, using data taken from 16 possums injected with [3H]thymidine between postnatal (P) days 5-68, and allowed to survive until brain cytoarchitecture was mature. Gradients of neurogenesis shown in neocortex were: (a) an inside-out radial gradient within cortical areas with neurogenesis beginning around P5 in layer 6 and concluding between 1 and 2 months later in layer 2, and (b) a single, simple, regional gradient across all neocortex. On the lateral surface of the hemisphere neurogenesis runs anteroventrolateral to posterodorsomedial, and on the medial surface neurogenesis runs anteroventral to posterodorsal. When plotted for the whole neocortex, the two regional gradients from the lateral and medial surfaces of the hemisphere are seen as parts of the one simple pattern. The time duration of neurogenesis in possum cortex is 1-2 months, and is similar to that seen in monkeys.

Animals↗
PubMed1995

The topographic distribution of the efferents from neocortical neurons is not only dependent upon where in the neocortex the cells develop. A transplantation study within one single neocortical region.

It has been proposed that the distribution of efferents developed by neocortical neurons depends upon where in the neocortex the cells develop, not where they were generated. However, the capacity of diverse isocortical areas to differentiate connectional characteristics belonging to other isocortical areas has recently been questioned in several experiments using heterotopic transplantation paradigms. The present study was designed to determine whether the principle of multipotentiality is still valid within one single isocortical region. Mediolateral bands of embryonic (E16) frontal neocortex were dissected out and grafted into the left frontal cortex of neonate hosts according to either correct or inverted mediolateral orientation. Five to six months after grafting, a retrograde tracer was injected into the dorsomedial or ventrolateral left neostriatum of the host. The mediolateral distribution of the cell labeling within the transplant was then compared to that of an equivalent frontal cortical area (ECA) in control cases. The results indicate that strips of embryonic frontal neocortex transplanted according to a correct mediolateral orientation are able to develop a projection towards the host striatum whose mediolateral topographical distribution is not significantly different from that arising from the frontal neocortex of control animals. The percentages of transplant cells labeled in the medial or lateral division of the grafts were not significantly different from those found medially or laterally in the ECA in control cases. Following inversion of the mediolateral orientation of the grafts at the time of transplantation, the percentages of cells labeled in the medial or lateral division of the grafts were nearly equal whatever the site of tracer deposit within the host neostriatum. These results indicate that even within one single neocortical region the principle of areal interchangeability is not entirely validated and that the development of neocortical efferents is not only guided by extrinsic factors.

Animals↗
PubMed1981

Radial-maze performance in the rat following lesions of posterior neocortex.

The present experiment was designed t investigate the role of posterior neocortex (areas 17, 18 and 18a) in the maintenance of performance on the radial maze. Following training to criterion on the 8-arm radial maze, rats received either sham operations, bilateral eye enucleations, lesions of posterior neocortex, or combined enucleations and lesions of posterior neocortex. While the enucleated animals with intact brains showed a slight, but significant performance decrement relative to the sham-operated group, the other two groups, with lesions of areas 17, 18 and 18a, each showed a massive deficit. This large deficit was observed even in the group in which both the eyes and neocortex had been removed. These results suggest that the visual projection areas of cortex not only play an important role in the maintenance of accurate radial-maze performance in sighted animals, but that the integrity of these areas is necessary for the maintenance fo criterion performance in blind animals.

Animals↗
PubMed1994

Concurrent immediate early gene induction by epileptic seizures in heterotopic cortical grafts and neocortex.

Cortical primordia of rat fetuses (gestation day 14) were stereotactically grafted into the rostral striatum of adult recipient rats. After 8 weeks, the transplants had developed into a highly differentiated population of mature neuroectodermal cells. Host rats were then subjected to 15 min of bicuculline-induced epileptic seizures or served as controls. Seizure-elicited immediate early gene (IEG) expression was investigated after various postictal survival times (up to 24 h), using immunocytochemistry with specific antisera against seven IEG encoded proteins (c-FOS, FOS B, c-JUN, JUN B, JUN D, KROX-24, KROX-20). Constitutive IEG expression in intra striatum grafted neocortical neurons was identical to that in the corresponding host neocortex. In particular, abundant KROX-24 and lack of c-JUN expression implies the establishment of synaptic contacts within the graft or with the host circuitry. Postictal expression kinetics of individual IEG encoded proteins within the transplants were strikingly similar to those seen in the neocortex in situ. c-FOS and KROX-24 were most rapidly induced, followed by c-JUN and JUN B, and a more delayed induction of FOS B, JUN D and KROX-20. Apart from a slightly prolonged c-FOS expression in grafts, individual transcription factors remained elevated for different time periods and showed a concurrent decline in transplants and in neocortex in situ. In conclusion, IEG induction in grafts closely paralleled that in the host neocortex but differed from the adjacent striatum which exhibited no c-JUN induction at any time point investigated. These results indicate that following an appropriate differentiation period, heterotopically grafted embryonic cortical neurons respond to extracellular stimuli with changes of gene expression that closely resemble the normal host cortex. This suggests development of a similar molecular phenotype, including proper acquisition and intracellular processing of information.

Animals↗
PubMed1991

beta-Amyloid protein load is relatively uniform throughout neocortex and hippocampus in elderly Alzheimer's disease patients.

beta-Amyloid protein immunoreactivity in neocortex and hippocampus of Alzheimer's disease and control brains has been measured using an automatic image analysis system. Successive fields from the pial surface to white matter in 4 neocortical sites, parahippocampal gyrus and along the pyramidal cell layer in the hippocampus have been measured using a number of variables including: area fraction or load, counts per unit area and deposit size. In Alzheimer's disease beta-amyloid protein load in neocortex and hippocampus was significantly greater than in non-demented age-matched controls. beta-Amyloid protein load, as measured by size variables, was relatively uniform throughout the neocortex in elderly Alzheimer's disease patients. However, greater variability in deposition was measured in parahippocampal gyrus and hippocampus than in neocortex. Size and density variables used to measure beta-amyloid protein deposition were not correlated with age although there was a tendency for the cortical load to decrease with age beyond 80 years.

Aged↗
PubMed1997

Distribution of kainate receptor subunit mRNAs in human hippocampus, neocortex and cerebellum, and bilateral reduction of hippocampal GluR6 and KA2 transcripts in schizophrenia.

The mRNAs encoding kainic acid (KA) preferring glutamate receptor subunits (GluR5-7, KA1 and KA2) are differentially expressed in rat brain. We have used regional and cellular in situ hybridization histochemistry with subunit-specific 35S-labelled oligodeoxyribonucleotides to examine these mRNAs in adult human hippocampus, neocortex and cerebellum. GluR5 mRNA was detected only in Purkinje cells and a few scattered hippocampal neurons. GluR6 mRNA was relatively abundant in all areas, notably in dentate gyrus, pyramidal neurons of CA3, and cerebellar granule cells, as well as being present in superficial and deep laminae of the neocortex. Moderate signal for GluR7 mRNA was seen in deep laminae of the neocortex with a weak signal in the dentate gyrus; in dipped sections GluR7 mRNA was also apparent over some pyramidal and non-pyramidal cells in hippocampus and over putative cerebellar stellate/basket cells. KA1 mRNA was detected in the dentate gyrus but not reliably elsewhere. The expression profile and abundance of KA2 mRNA was similar to that of GluR6 mRNA. For all five transcripts, concurrent hybridization of rat brain sections produced the anticipated distribution of signal. The data indicate that the regional and cellular distribution of KA receptor subunit mRNAs in human hippocampus, neocortex and cerebellum largely parallels that in the corresponding areas of rat brain, albeit at lower levels, especially with regard to GluR5 and KA1 transcripts. In schizophrenia there is a partial loss of hippocampal non-NMDA receptors, but there are no data concerning KA receptor subunit expression. KA2 and GluR6 mRNAs were sufficiently abundant for a comparison in the left and right hippocampus between 11 schizophrenics and 13 controls. Using film autoradiography, both mRNAs were significantly reduced in the schizophrenics, having controlled for the effects of brain pH, post mortem interval and age. GluR6 mRNA was also quantitated in cerebellum, wherein no differences were found between cases and controls. In conjunction with earlier findings of reduced hippocampal GluR1 and GluR2 expression and a loss of [3H]KA binding sites, these data show that schizophrenia is associated with impaired expression of both AMPA- and KA-preferring ionotropic glutamate receptors. These deficits are likely to contribute to the glutamatergic component of the disease pathophysiology.

Aged↗
PubMed1997

Development of proenkephalin gene expression in rat neocortex: a non-radioactive in situ hybridization study.

Products of the proenkephalin gene are not only neurotransmitters but may also influence brain development. The ontogeny of the expression of the proenkephalin gene in neocortex was studied in embryonic and postnatal rats with in situ hybridization. At embryonic day 14, the proliferating cells in the ventricular zone strongly expressed the gene. Thereafter, the expression decreased and was hardly detectable up to embryonic day 21. At the day of birth and during the subsequent week, proliferating cells in the subventricular zone were labelled. The expression of the proenkephalin gene in proliferating neuronal and glial progenitors indicates that gene products may affect proliferation and/or commitment. In the neocortex, cells which strongly expressed the gene were first seen at postnatal day 7 in the outer part of the neocortex. Seven days later, a second band of positive cells had appeared in the inner part of the cortex, i.e. the adult pattern of distribution had been established. Thus, in rat neocortex the expression of the proenkephalin gene developed in an outside-first, inside-last mode.

Animals↗
PubMed1997

Colocalization of parvalbumin and calbindin D-28k in neurons including chandelier cells of the human temporal neocortex.

Chandelier cells are cortical GABAergic interneurons with a unique synaptic specificity enabling them to exert a strong inhibitory influence on pyramidal cells. By using immunocytochemistry for the calcium-binding protein calbindin D-28k in the human temporal neocortex, we have found numerous immunoreactive processes that were identified as chandelier cell axon terminals. This was a striking find since in previous immunocytochemical studies of the primate neocortex, chandelier cell axon terminals had been shown to be immunoreactive for another calcium-binding protein, parvalbumin, and colocalization studies indicate that parvalbumin and calbindin are present in almost completely separate neuronal populations. Here, we present double-label immunofluorescence experiments showing that parvalbumin and calbindin immunoreactivities are colocalized in certain neurons that include a subpopulation of chandelier cells whose cell bodies are located mainly in layers V and VI of the human temporal neocortex. The results suggest a selective laminar distribution of neurochemical subtypes of chandelier cells which is a peculiar feature of the organization of the human neocortex.

Adolescent↗
PubMed1977

Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

Rats lacking gustatory neocortex (n = 24) and normal rats (n = 24) were familiarized to either hydrochloric acid (10(-1.6) M) or quinine hydrochloride (10(-4) M) solutions during free-drinking trials. They were trained subsequently to avoid either the familiar or the novel taste stimulus, using a balanced design, by pairing the to-be-associated taste with ip injections of apomorphine hydrochloride. Balanced, nonpaired presentations of the other taste solution and water were presented also. Normal rats more efficiently learned to avoid the novel compared with the familiar taste. Rats with gustatory neocortex lesions did not differentiate novel from familiar tastes. They learned aversions to both in a manner highly similar to the aversion learning of familiar tastes by the normal group. Therefore, rats lacking gustatory neocortex displayed an associative deficiency, relative to normal, only when they were trained on novel stimuli. This observation supports an earlier suggestion that gustatory neocortex lesions disrupt the conditionability of taste stimuli by reducing or eliminating responses to taste novelty. This suggestion is supported further by the absence of a "neophobic" response in the operated rats to the first presentation of a taste stimulus.

Animals↗
PubMed1997

Threshold effects in synaptosomal and nonsynaptic mitochondria from hippocampal CA1 and paramedian neocortex brain regions.

After a brief period of global ischemia, the hippocampal CA1 region is more susceptible to irreversible damage than the paramedian neocortex. To test whether primary differences in bioenergetic parameters may be present between these regions, respiration rates and respiratory control activities were measured. In synaptosomal and nonsynaptic mitochondria isolated from the hippocampal CA1 region, state 3 respiration rates and complex IV activities were significantly lower than those present in synaptosomal and nonsynaptic mitochondria from the paramedian neocortex. These results suggest that mitochondria from the CA1 hippocampal area differ in some properties of metabolism compared with the neocortex area, which may render them more susceptible to a toxic insult such as that of ischemia. In addition, when complex I and IV activities were titrated with specific inhibitors, thresholds in ATP synthesis and oxygen respiration became apparent. Complex I and IV activities were decreased by 60% in nonsynaptic mitochondria from the hippocampal CA1 region and paramedian neocortex before oxidative phosphorylation was severely compromised; however, in synaptosomes from these regions, complex I activities had a threshold of 25%, indicating heterogenous behaviour for brain mitochondria. Reduced complex I thresholds in mitochondria, in association with other constitutive defects in energy metabolism, may induce a decreased ATP supply in the synaptic region. The implications of these findings are discussed in relation to delayed neuronal death and processes of neurodegeneration.

Animals↗
PubMed1995

Abnormal expression of microtubule-associated protein 2 (MAP-2) in neocortex in Rett syndrome.

Immunocytochemical evaluations of the neocortex of three classical Rett syndrome (RS) individuals revealed a selective abnormality in the expression of microtubule-associated protein 2 (MAP-2). MAP-2 immunoreactivity (ir) was reduced throughout the neocortex of all three RS cases with a reversal of the normal pattern of more intense staining in deep cortical layers. This anomaly was selective for MAP-2 because nonphosphorylated neurofilament (SMI-32) labeling of deep pyramidal neurons and calbindin (CaBP)-stained GABAergic cells remained unchanged. Moreover, MAP-2 ir was virtually undetected in white matter while GABAergic and, particularly, peptidergic (neuropeptide Y: NPY) profiles were easily recognized. These results demonstrate a marked disruption of a major cytoskeletal component in neocortex in RS which seems to affect, predominantly, pyramidal projection and white matter neurons. MAP-2 expression appears early in neuronal maturation of the neocortex, particularly in the subplate region, the future superficial white matter, suggesting that these reported abnormalities in RS represent a developmental disturbance. Considering that MAP-2 expression is regulated by several neurotransmitter systems in adult cerebral cortex, particularly dopaminergic and cholinergic afferents that are deficient in RS, these neurochemical alterations could be related to this anomalous MAP-2 expression.

Adult↗
PubMed1987

Effects of maternal dietary restriction in vitamin B-6 on neocortex development in rats: B-6 vitamer concentrations, volume and cell estimates.

Influence of the time of maternal restriction in dietary vitamin B-6 on vitamer concentrations and morphological development of neocortex was examined. Rats were fed ad libitum a vitamin B-6-free diet supplemented with 0.0 or 0.6 mg pyridoxine X hydrochloride (PN X HCl)/kg diet during gestation followed by a control diet (7.0 mg PN X HCl/kg) during lactation or were supplemented with 0.6 or 7.0 mg PN X HCl/kg diet throughout gestation and lactation. During postweaning offspring received the maternal diets fed during lactation. Neocortices of offspring were examined at 30 d of age by liquid chromatography and light microscopy. Vitamin restriction during gestation and 30 d postnatal was the only vitamin B-6-restricted treatment of the three administered that altered B-6 vitamer levels in neocortex; all vitamers were depressed equally. Brain weight and volume of neocortex were not changed significantly by the maternal restrictions imposed. However, each restriction adversely affected neurogenesis and neuron longevity of the neocortex and when expressed as percent reduction from control, neuron longevity was affected more severely than neurogenesis.

Animals↗
PubMed1990

Effects of maternal restriction in vitamin B-6 on neocortex development in rats: neuron differentiation and synaptogenesis.

Effects of maternal restrictions in vitamin B-6 on neuron differentiation and synaptogenesis in developing neocortex were examined. Rats were fed ad libitum a vitamin B-6-free diet supplemented with 0.0 or 0.6 mg pyridoxine hydrochloride (PN.HCl)/kg diet during gestation followed by a control level of 7.0 mg/kg diet during lactation, or they were fed the vitamin B-6-free diet supplemented with 0.6 or 7.0 mg PN.HCl/kg diet throughout gestation and lactation. Neocortices of the offspring were examined at 30 d of age by light and electron microscopy. All maternal restrictions in vitamin B-6 reduced the number of higher order dendrites on stellate neurons in layer II and on pyramidal neurons in layer V of the neocortex and decreased synaptic density in the neuropil of the neocortex. The findings indicated that vitamin B-6 restriction during gestation, either marginal or severe, was the critical treatment factor that adversely affected synaptogenesis and at least one event in neuron differentiation in the neocortex, the arborization of dendrites.

Animals↗
PubMed1996

Neocortex size and behavioural ecology in primates.

The neocortex is widely held to have been the focus of mammalian brain evolution, but what selection pressures explain the observed diversity in its size and structure? Among primates, comparative studies suggest that neocortical evolution is related to the cognitive demands of sociality, and here I confirm that neocortex size and social group size are positively correlated once phylogenetic associations and overall brain size are taken into account. This association holds within haplorhine but not strepsirhine primates. In addition, the neocortex is larger in diurnal than in nocturnal primates, and among diurnal haplorhines its size is positively correlated with the degree of frugivory. These ecological correlates reflect the diverse sensory-cognitive functions of the neocortex.

Animals↗
PubMed1992

Characterization of the 5-hydroxytryptamine receptor modulating the release of 5-[3H]hydroxytryptamine in slices of the human neocortex.

In the rat brain, the presynaptic 5-hydroxytryptamine (5-HT) autoreceptors located on 5-HT terminals correspond to the 5-HT1B subtype. The presence of a 5-HT receptor probably located on 5-HT nerve endings and modulating transmitter release in the human neocortex has been reported, but its detailed pharmacological characterization is not yet available. On the other hand, receptor binding and autoradiographic results indicate that the 5-HT1B receptor subtype is not present in the human brain. We, therefore, studied the modulation of the electrically evoked release of [3H]5-HT by various 5-HT receptor agonists and antagonists in preloaded slices of human neocortex obtained from 18 patients undergoing neurosurgery. The nonselective 5-HT1A/1B/1D receptor agonist 5-carboxamidotryptamine produced a potent inhibition (70% at 0.03 microM) of the electrically evoked release of [3H]5-HT which was blocked by 5-HT receptor antagonists with the following relative order of potency: methiothepin greater than metergoline = methysergide greater than propranolol. The selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin at 0.1 microM did not modify the electrically evoked release of [3H]5-HT. The 5-HT1A/1B receptor agonist RU 24969 was 10 times more potent at inhibiting [3H]5-HT overflow in the rat frontal cortex than in the human neocortex. The potent 5-HT1B receptor antagonist cyanopinodolol did not modify the 5-carboxamidotryptamine-induced inhibition of the electrically evoked release of [3H]5-HT in slices of the human neocortex, but produced by itself a small inhibition of [3H]5-HT overflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Effects of 5-HT receptor agonists on depolarization-induced [3H]-noradrenaline release in rabbit hippocampus and human neocortex.

1. The present study attempted to determine whether noradrenaline (NA) release in rabbit hippocampus and human neocortex is modulated by presynaptic 5-hydroxytryptamine (5-HT) receptors. 2. Slices of rabbit hippocampus and human neocortex, loaded with [3H]-noradrenaline ([3H]-NA) were superfused and the effects of 5-hydroxytryptamine (5-HT) receptor ligands on electrically evoked [3H]-NA release were investigated. 3. In rabbit hippocampus, 5-HT, 5-carboxamidotryptamine (5-CT; 32 microM) and 2-CH3-5-HT (32 microM) increased [3H]-NA release elicited with 360 pulses/3 Hz. Facilitation of transmitter release was not influenced by the 5-HT3 receptor antagonist, tropisetron but was prevented by the alpha 2-adrenoceptor antagonist, rauwolscine. When autoinhibition was avoided by stimulating the tissue with 4 pulses/100 Hz (pseudo-one pulse-(POP) stimulation), 2-CH3-5-HT decreased evoked transmitter release, whereas 5-HT and 5-CT had no effect. Inhibition caused by 2-CH3-5-HT was not affected by tropisetron but counteracted by the alpha 2-adrenoceptor ligands, clonidine and rauwolscine. Inhibition caused by clonidine was diminished in the presence of 5-CT or 2-CH3-5-HT. 4. In human neocortex, [3H]-NA release elicited with 360 pulses/3 Hz was increased by 10 microM 5-HT and 32 microM 5-CT, whereas 2-CH3-5-HT was ineffective. [3H]-NA release evoked with a modified POP stimulation (2 bursts of 4 pulses/100 Hz, 3.5 min apart) was not affected by 2-CH3-5-HT or 5-CT. 5. The present results indicate that 5-HT, 2-CH3-5-HT and 5-CT can act on presynaptic alpha 2-autoreceptors as partial agonists (2-CH3-5-HT; in rabbit hippocampal tissue) or antagonists (5-HT and 5-CT; in tissue of rabbit hippocampus and human neocortex). Furthermore the existence of autoinhibition dictates whether these drugs cause facilitation of release, inhibition or have no effect.

Age Distribution↗
PubMed1996

Long-term effect of postnatal alcohol exposure on the number of cells in the neocortex of the rat: a stereological study.

Behavioral and morphological studies suggest that exposure to alcohol during development may cause damage in the neocortex. In this study, rat pups were exposed to alcohol during the brain growth spurt and examined at adulthood to ascertain the long-term effect of alcohol exposure on the neocortex. Four-day-old rat pups were surgically implanted with an intragastric cannula while under ether anesthesia and artificially reared from postnatal day (PN) 4 through PN11. Two of the consecutive 12 daily feeds contained either alcohol (4.5 g/kg; alcohol-exposed) or an isocaloric maltose/dextrin solution (gastrostomy control) from PN4 through PN9. On PN115, animals were perfused intracardially and the brains removed. Unbiased stereological methods were used to determine the neocortical volume, the total number of neurons and glial cells in the entire neocortex and in layer V, and the mean cell volume of neurons or mean nuclear volume of glial cells in layer V. No effect of alcohol was seen in the neuronal population on either cell number or mean cell volume, nor was there any difference in the total number or mean nuclear volume of glial cells in layer V. These findings suggest that neither the entire neocortex nor layer V alone are vulnerable to permanent alcohol-induced cell death.

Animals↗