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PubMed1981

Projections from the superior colliculus and the neocortex to the pulvinar nucleus in Galago.

We have studied the projections from the superior colliculus and the neocortex to the pulvinar nucleus in Galago senegalensis by using the retrograde transport of horseradish peroxidase (HRP). Injections of various parts of the pulvinar complex, both the inferior and superior divisions, both the tectorecipient zone and the nontectorecipient zone as defined by Glendenning et. al. ('75), produce labeled cells in the lower tier of stratum griseum superficiale. The distribution of labeled cells in the superior colliculus varies with the locus of the injection, indicating a retinotopic projection system from the entire superior colliculus to all sectors of the pulvinar complex. These experiments also provide an opportunity to study the distribution and laminar origin of neurons giving rise to cortical descending projections. The entire visual cortex projects onto the pulvinar complex. The cells or origin can be divided into two populations--one located in layer V and the other in layer VI. In seven of the nine cases reported, the layer V population is restricted entirely or mainly to the striate area. In the two exceptional cases, the layer V population is located in the adjacent extrastriate cortex, areas 18 and 19. The difference in the layer of origin of the cortical descending fibers reflects a difference in the layer of termination of the reciprocal ascending projection. These findings identify the entire visual field as primary visual cortex. The importance of this conclusion is underscored by the fact that the visual field comprises as much as one-half of the whole neocortex.

Animals↗
PubMed1991

A comparative analysis of the distribution of prosomatostatin-derived peptides in human and monkey neocortex.

Comparative analyses were made of the immunohistochemical and biochemical distributions of three prosomatostatin-derived peptides (PSDP) in human, perfused monkey, and unperfused monkey neocortex. The PSDP we examined were the tetradecapeptide somatostatin 14 (SS14); the N-terminal extension of this peptide, somatostatin 28 (SS28); and somatostatin 28(1-12) (SS28(1-12)). In immunohistochemical experiments, numerous SS28-immunoreactive perikarya were located in both superficial and deep layers of perfused monkey cortex, but none were present in the cerebral cortex from unperfused monkey or autopsied human brains. In contrast, the number of SS28(1-12)-immunoreactive neurons was five times greater in the superficial cortical layers of unperfused monkey than of perfused monkey brain. Moreover, unperfused monkey and human cortex contained notably more SS14-immunoreactive processes than perfused monkey cortex. These data suggested that SS28 may have been converted into SS14 and SS28(1-12) in unperfused tissue during the post-mortem interval. This hypothesis was examined biochemically by measuring the levels of immunoreactivity of SS14, SS28, and SS28(1-12) in samples of unperfused monkey cortex frozen at different time intervals after removal from the brain. Samples frozen 10 minutes or longer after removal contained only 10-20% the level of SS28 immunoreactivity measured in samples frozen immediately or 1 minute after removal. The levels of SS14 and SS28(1-12) immunoreactivity did not demonstrate such reductions, and may instead have increased at early time points. To further characterize post-mortem effects on PSDP and to explore for species differences, we performed a detailed comparison of the regional, laminar, and cellular distribution of SS28(1-12) immunoreactivity under the three conditions. A progressive loss of immunoreactivity, particularly in radial fibers, was found at increasing post-mortem intervals in unperfused monkey neocortex, indicating that differences in density and distribution of immunoreactive fibers between human and perfused monkey may result from post-mortem peptide degradation in unperfused tissue. In contrast, the larger size of SS28(1-12)-immunoreactive white matter neurons in humans as compared to monkeys appeared partially due to a post-mortem effect but also reflected a species difference. In addition, the density of white matter neurons was found to be significantly greater in human than in perfused or unperfused monkey. These data indicate that any study of human autopsy material must be assessed in light of possible post-mortem effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Cell migration in the rat embryonic neocortex.

Three-dimensional reconstructions of the normal rat embryonic (E) neocortex on days E15, E17, E19, and E21, using Skandha (software designed by J. Prothero, University of Washington, Seattle), show that the neocortical ventricular zone shrinks rapidly in the medial direction during cortical morphogenesis. [3H]thymidine autoradiography indicates that the shrinkage of the ventricular zone occurs before neurons in lateral and ventrolateral parts of layers IV-II are generated. Consequently, most of these neurons originate 400-1000 microns medial to their settling sites in the cortical plate. Embryos killed at daily intervals up to E21 after a single injection of [3H]thymidine on either E17 or E18 revealed the presence of a prominent migratory path, the lateral cortical stream, used by neurons migrating to the lateral and ventrolateral cortical plate; neurons migrating to the dorsal cortical plate follow a direct radial path. Arrival times of neurons in the cortical plate depend on the migratory path and are proportional to the overall distance travelled. Neurons that migrate only radially arrive in the dorsal cortical plate in two days (shortest route). Neurons that migrate laterally arrive in the lateral cortical plate in 3 days (longer route) and in the ventrolateral cortical plate in 4 days (longest route). [3H]thymidine autoradiography also shows that cells generated in the neocortical ventricular zone migrate in the lateral cortical stream for 5 or more days and accumulate in a reservoir. Cells leave the reservoir to enter the piriform cortex and destinations (as yet undetermined) in the basal telencephalon. The lateral cortical stream is found wherever the neocortical primordium surrounds the basal ganglia and is absent behind the basal ganglia. A computer analysis of nuclear orientation in anterior and posterior parts of the intermediate zone in the dorsal neocortex between days E17 and E22 shows that horizontally oriented nuclei are more common anteriorly where many cells are migrating laterally than posteriorly where most cells are migrating radially.

Animals↗
PubMed1992

The selective innervation by serotoninergic axons of calbindin-containing interneurons in the neocortex and hippocampus of the marmoset.

The serotoninergic input to the mammalian cerebral cortex originates in the median and the dorsal raphe nuclei. Median raphe neurons have been previously shown to give rise to beaded varicose axons which form dense pericellular arrays (baskets) surrounding the soma and the proximal dendrites of certain cortical neurons. In the present study, we have searched for specific markers characterizing the neurons of the marmoset neocortex and hippocampus surrounded by these thick varicose serotonin-containing fibers. The non-pyramidal nature of these neurons, suggested by their dendritic arborization, was correlated, in immunocytochemical experiments with double-labelling to demonstrate their surrounding serotonin-containing basket and their content of glutamic acid decarboxylase (GAD) or of the calcium-binding protein calbindin. Another calcium-binding protein common in numerous non-pyramidal cortical neurons, parvalbumin, was never found in neurons surrounded by serotonin-containing baskets. This organization was found in all areas of the neocortex and of the hippocampus where serotonin-containing baskets were present. One of the serotoninergic cortical inputs which originates from the brainstem tegmentum, traditionally described as "diffuse," proves to be highly selective in that a subset of its axons terminates preferentially on a subpopulation of inhibitory interneurons of the cerebral cortex. It may be emphasized that this subset of cortical interneurons has now been shown to be characterized not only by its axonal and dendritic arborization and its neurotransmitter, but also by a specific type of input which can modulate cortical function in a unique manner.

Animals↗
PubMed1993

Neocortex and hippocampus contain distinct distributions of calcium-calmodulin protein kinase II and GAP43 mRNA.

Calcium-calmodulin protein kinase II and GAP43 are two molecules which have been linked to synaptic plasticity. Localization of mRNA for these molecules identifies the neuronal populations which have the potential to utilize these mechanisms. General descriptions for calcium-calmodulin protein kinase II or GAP43 mRNA have been previously reported. In light of recent evidence that suggests that at some sites these two molecules may interact, we sought to determine the cortical distribution in detail, and to examine the extent of overlap between neuronal populations containing each mRNA. To this end we have used in situ hybridization techniques to study the distribution of calcium-calmodulin protein kinase II and GAP43 mRNA in adjacent sections of adult rat forebrain. Overall, the distribution patterns were distinct but partially overlapping. For both calcium-calmodulin protein kinase II and GAP43, mRNA levels were highest in hippocampus, allo- and neocortex, compared to moderate to low levels in striatum and thalamic nuclei. Within the heavily labeled regions certain populations expressed both calcium-calmodulin protein kinase II and GAP43 mRNA at high levels, while other populations were selective for calcium-calmodulin protein kinase II. In the hippocampus, the stratum pyramidale of CA1-3 expressed high levels of both calcium-calmodulin protein kinase II and GAP43 mRNA. Granule cells of the fascia dentata and the stratum radiatum of CA3 both contained moderate to high levels of calcium-calmodulin protein kinase II mRNA, but near background levels of GAP43 mRNA label. Within the neocortex, deep layers were distinguished from superficial layers by their lack of calcium-calmodulin protein kinase II mRNA expression within the neuropil, and the presence of GAP43 mRNA in neurons located in layer V and the deepest part of layer VI. Thus, layer V and deep layer VI neurons showed high levels of label for both GAP43 and calcium-calmodulin protein kinase II mRNA, while neurons of superficial layers contained only calcium-calmodulin protein kinase II mRNA. These markers differentiate neuronal populations which can also be distinguished on the basis of their ability to undergo specific forms of synaptic plasticity. These different forms of plasticity may be due in part to the laminar-specific patterns of GAP43 and calcium-calmodulin protein kinase II mRNA that we have described.

Animals↗
PubMed1994

A study of SMI 32-stained pyramidal cells, parvalbumin-immunoreactive chandelier cells, and presumptive thalamocortical axons in the human temporal neocortex.

Immunocytochemical studies in the primate neocortex have shown that particular populations of pyramidal cells can be identified by antibody SMI 32 that recognizes a nonphosphorylated epitope of neurofilament protein, while chandelier cells (a powerful type of cortical inhibitory interneuron) and presumptive thalamocortical axons can be identified by antibodies directed against the calcium-binding protein parvalbumin (PV). We used these antibodies in correlative light and electron microscopic immunocytochemical studies to analyze certain aspects of the synaptic circuitry of human temporal neocortex. In sections cut in the tangential plane, many PV-immunoreactive chandelier cell axon terminals and apical dendrites of SMI 32-stained pyramidal cells were distributed in small clusters. Combination of immunocytochemistry for PV and SMI 32 revealed four subpopulations of pyramidal cells with regard to the immunocytochemical staining by SMI 32 and the innervation of their axon initial segments by PV-positive or -negative chandelier cell axon terminals, but there were differences in the concentration and proportion of these subpopulations by layers. Furthermore, we present electron microscopic evidence suggesting that the characteristic layer III dense band of PV-immunoreactive puncta is made up mainly of presumptive thalamocortical axon terminals. Besides, coincidence was found between the dense PV-immunoreactive band and the dendritic plexus formed by the SMI 32-stained pyramidal cells in the lower half of layer III, which leads us to think that they are probably a major target of PV-immunoreactive thalamic terminations.

Antibodies, Monoclonal↗
PubMed1994

Neocortex provides direct synaptic input to interstitial neurons of the intermediate zone of kittens and white matter of cats: a light and electron microscopic study.

The existence of direct synaptic input from the neocortex to intermediate zone and white matter interstitial neurons was examined in both neonate and adult cats. This projection was studied by injecting the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) into the neocortex and examining whether cortical efferent axons formed synapses in the intermediate zone or white matter. Anterogradely labeled boutons establishing synapses in the intermediate zone and white matter were found at the electron microscopic level after injecting PHA-L into the primary visual, somatosensory, and suprasylvian cortex. Although labeled synapses were found in the intermediate zone of kittens injected at postnatal days 2 and 6, their morphological features appeared immature compared to those found in kittens aged 3 weeks or in adults. Postsynaptic targets of efferent cortical axons were studied in serial sections and shown to be dendritic shafts and spines. This paper shows that cortical efferent axons contribute synapses to interstitial neurons located in the intermediate zone of kittens and white matter of adults. The functional role of the corticointermediate zone/white matter projection remains to be determined.

Animals↗
PubMed1995

Relationship between astrocytic processes and "perineuronal nets" in rat neocortex.

"Perineuronal nets" (PNs) ensheath a subtype of inhibitory neurons in the mammalian neocortex. In the light of the proposal that PNs consist of glial processes, we have analyzed the relationship between intracellularly injected glial cells and PNs in the rat neocortex. Glial cells were injected iontophoretically with Lucifer Yellow in lightly fixed tissue slices and PNs were visualized with the lectin from Vicia villosa. Using confocal laser scanning microscopy, glial processes and PNs were identified as distinct structures. Lectin labeling was consistently associated with the extracellular space interposed between LY-labeling was consistently associated with the extracellular space interposed between LY-labeled astrocyte processes and neurons. Of the different types of glial cells injected, only the densely-ramifying protoplasmic astrocytes extended processes which could be traced to contact PNs. These protoplasmic astrocytes also sent out processes to adjacent neurons not ensheathed by PNs, and to capillaries. The present data strongly suggests that PNs do not consist of glial processes but rather support the idea that PNs represent specialized extracellular material interposed between the surface of some inhibitory interneurons and astrocytic processes.

Animals↗
PubMed1989

Distribution of cholinergic receptors in the rat and human neocortex.

Autoradiographic labelling of muscarinic (M1, M2, NMS binding sites) and nicotinic receptors shows an inhomogeneous distribution over architectonically identified cortical areas of the rat brain with highest concentrations in the medial prefrontal and frontal areas. Beside this general trend the areal patterns of different receptors are slightly varying. The laminar distribution of these receptors in the rat and human neocortex is characterized by two different patterns, one with highest receptor densities in the supragranular layers (M1 receptors, NMS binding sites), the other with a preferential labelling of layer IV and (with a lower intensity) layer V (M2 and nicotinic receptors). M1 receptors and NMS binding sites are codistributed at the laminar level with each other and with GABAA, D1, 5-HT1 and glutamate receptors; M2 receptors are codistributed only with nicotinic receptors. Immuno-histochemical studies with antibodies against muscarinic and nicotinic receptors demonstrate that these structures occur mainly in pyramidal and spiny stellate cells and to a lesser extent (13%) in a variety of interneurons. The immunoreactivity is visible in the perikaryon, dendrites and postsynaptic membranes. Neurons are found in the human neocortex, which react exclusively with one of the two antibodies, but a fraction of the neurons (about 30%) contains antigenic sites reacting with both antibodies. This is interpreted as colocalization of nicotinic and muscarinic receptors in some cortical neurons.

Animals↗
PubMed1996

Opioid receptor-mediated control of acetylcholine release in human neocortex tissue.

The effects of various opioid receptor agonists and antagonists on evoked acetylcholine release were studied in slices of human neocortex prelabelled with [3H]-choline, superfused and depolarized electrically (2 min, 3 Hz, 2 ms, 24 mA) or by K+ (20 mM). The delta-opioid receptor agonist DPDPE and the kappa-opioid receptor agonist U50488 reduced the evoked [3H]-overflow (acetylcholine release) in a concentration-dependent fashion; the delta-opioid receptor antagonist naltrindole and the kappa-opioid receptor antagonist norbinaltorphimine, respectively, antagonized these effects. Application of the mu-opioid receptor agonist DAGO also resulted in an inhibition of acetylcholine release; however, both delta- and kappa-opioid receptor antagonists were able to block this effect. The mu-opioid receptor agonists morphine and (+)-nortilidine had no effect. These results indicate that acetylcholine release in human neocortex is inhibited through delta- and kappa-opioid receptors, but not through mu-opioid receptors. Acetylcholine release was significantly increased by the delta-opioid receptor antagonist naltrindole in the presence of a mixture of peptidase inhibitors providing evidence for a delta-opioid receptor-mediated inhibition of acetylcholine release by endogenous enkephalin. K(+)-evoked acetylcholine release in the presence of TTX was inhibited by U50488, but not by DPDPE, suggesting the presence of kappa-opioid receptors on cholinergic terminals and the localization of delta-receptors on cortical interneurons. Therefore, the potent effect of DPDPE on acetylcholine release is likely to be indirect, by modulation of intrinsic cortical neurons. These interneurons probably do not use GABA as neurotransmitter since both GABAA and GABAB receptor agonists (muscimol and baclofen, respectively) were without effect on acetylcholine release.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Origin and fate of fetuin-containing neurons in the developing neocortex of the fetal sheep.

The development of the neocortex has previously been extensively studied in carnivores (cat and ferret), rodents (rat and mouse) and primates (monkey and human). In these species, it has been shown that the initial population of cells migrating from the ventricular zone forms the primordial plexiform layer. This is subsequently split into marginal zone and subplate zone by the insertion of later-migrating cells into the primordial plexiform layer, to form the cortical plate proper. Many of the cells derived from the split primordial plexiform layer are transient. The neurons of the subplate zone are found in the deeper part of layer VI, and white matter deep to layer VI in the more mature cortex; most of these neurons disappear by adulthood. [3H]-thymidine labelling in the present study has shown a similar pattern of neocortical development in Artiodactyla (sheep). In addition it has been shown that the previously described staining of subplate and cortical plate cells for the fetal protein fetuin indicates that fetuin is a useful marker for a proportion of this transient population of neurons and defines its extent in neocortical development more clearly. Dividing cells were labelled by a single intra-amniotic injection of [3H]-thymidine at E26 to E35 (birth is at E150). The brains were subsequently examined at E40 or E80 for [3H]-thymidine labelling and fetuin staining by a combination of autoradiography and immunocytochemistry. The earliest generated neocortical cells detected in this study (E26) were found in two layers by E40, the outer marginal zone and inner subplate zone. Neurons of the marginal zone were generated up to E28; those of the early subplate zone were generated up to E31. The cortical plate proper was generated by cells "born" on E32 and later. This sequence is similar to that described in other species, especially the cat. A proportion of the early-generated neurons in the marginal zone, subplate zone and early cortical plate stained for fetuin. By E80 these earliest-generated, fetuin-positive cells were found in the white matter deep to the forming neocortical layers and in layer VI. In adult brains no fetuin-positive neurons could be identified in the neocortex, and neurons had almost entirely disappeared from the white matter. The fetal glycoprotein fetuin seems to be specifically associated with a population of cells that has the same developmental history as the transient marginal zone and subplate neurons described in other species.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Tyrosine hydroxylase immunoreactive neurons in organotypic slice cultures of the rat striatum and neocortex.

Organotypic slice cultures of striatum and neocortex were prepared from newborn to seven day old rats and cultured for three to 60 days. When processed for tyrosine hydroxylase (TH) immunocytochemistry medium-sized, aspiny TH immunoreactive (TH-i) neurons with a similar morphology were revealed in the striatum and the neocortex. The neurons had a very similar morphology in both tissues and were present both when the two tissues were grown separately as single cultures and when grown together either en bloc as part of the same tissue slices or as co-cultures. In order to examine whether innervation by dopaminergic fibers would affect the expression of TH-i neurons in the striatal slice cultures, co-cultures of ventral mesencephalon (VM) and striatum were prepared, but the ingrowth of TH-i fibers from the VM did not alter the expression of TH immunoreactivity by a subpopulation of striatal neurons.

Animals↗
PubMed1995

Chromaffin cell xenografts in the rat neocortex can produce antidepressive activity in the forced swimming test.

Adrenal medullary allografts, as well as other monoaminergic tissues, have been demonstrated in our laboratory to increase antidepressive activity when transplanted into the frontal neocortex of rats. Refinement in the optimal parameters for xenograft viability has indicated that isolated bovine chromaffin cells may be an improved source of graft donor tissue. The aim of the present study was to determine whether isolated bovine chromaffin cell grafts to the rat frontal neocortex could provide an alternative source of catecholamines for antidepressant activity. Isolated bovine chromaffin cells, isolated bovine fibroblasts, or an equal volume of vehicle were unilaterally implanted into the right or left frontal cortex or right visual cortex. All rats were assessed before and 6 weeks after transplantation using the forced swimming test, a popular measure of antidepressant activity. Bovine chromaffin cell grafts in either the right or left frontal cortex produced significant increases in antidepressant activity compared to grafts of bovine fibroblasts and sham-operated or nontransplanted rats. In contrast, bovine chromaffin cells transplanted to the visual cortex did not affect antidepressant activity. Bovine fibroblast grafts in the frontal cortex also induced slight increases in antidepressant activity, although significantly less than chromaffin cell grafts. Morphological analysis revealed robust survival of tyrosine hydroxylase-positive chromaffin cells that retained their in situ ultrastructure and occasionally formed synaptic connections with the host parenchyma. These results suggest that xenografted isolated bovine chromaffin cells can provide a viable source of catecholamines for antidepressive activity.

Adrenal Medulla↗
PubMed1989

Expression of cholinergic markers in transplants of immature mouse neocortex into adult mouse parietal cortex.

Cerebral cortex of embryonic and newborn mouse was removed and transplanted into adult mouse neocortex to investigate whether the development of cholinergic markers would proceed normally after transplantation. It is shown that both AChE and muscarinic receptors developed in transplanted mouse neocortex. However, while muscarinic receptor binding increased to adult levels in transplants from both pre- and postnatal donors AChE staining intensity only achieved adult levels in tissue from postnatal donors. These results are in accordance with the normal developmental time course of the two different cholinergic markers, since muscarinic receptors appear prenatally in cortex while AChE becomes histochemically detectable after birth. These data suggest that the prenatal donor tissue, unlike the postnatal transplants, lacks an environmental signal for the appearance of AChE stained elements, that is, presumably host AChE fiber ingrowth. Transplantation of immature donor CNS tissue into adult host thus appears to be a useful paradigm to study the regulation of differentiation processes.

Animals↗
PubMed1989

Senile plaque neurites fail to demonstrate anti-paired helical filament and anti-microtubule-associated protein-tau immunoreactive proteins in the absence of neurofibrillary tangles in the neocortex.

Although much work has been directed recently towards unravelling the protein chemistry of neurofibrillary tangle (NFT) and senile plaque (SP) components in Alzheimer's disease, the pathogeneses of these lesions remains largely unknown and the problem of their relationship is unresolved. In particular, although paired helical filaments (PHF) have long been documented in SP neurites, we do not know if they are of pathogenetic relevance for the formation of the SP. To investigate the relationship between NFT and SP, we examined antigenic properties of proteins in SP neurites in neocortical tissues of patients with senile dementia of Alzheimer type, in the presence or absence of NFT in the same cortical area. We used two polyclonal antibodies directed against PHF and microtubule-associated protein (MAP)-tau and three monoclonal antibodies (MAbs) (RT97, BF10, 147) to phosphorylated epitopes of human neurofilament polypeptides, as well as the Gallyas silver impregnation method which specifically stains PHF in NFT and neurites. The main finding of our investigations consists in a differential pattern of immunoreactivity of SP neurites depending on the presence or absence of NFT in the neocortex. In the presence of NFT, there were numerous neuropil threads and SP neurites containing Gallyas-positive, as well as anti-PHF- and anti-tau-labelled material. In the absence of NFT in the neocortex there was a striking absence of any Gallyas-positive or PHF- and tau-immunoreactive structure in the cortical neuropil and in SP neurites, irrespective of the maturation stage of the SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Interaction of penicillin and pentobarbital with inhibitory synaptic mechanisms in neocortex.

In this study we characterized the responses of neocortical neurons to iontophoretically applied gamma-aminobutyric acid (GABA) and examined how these GABA responses as well as the inhibitory postsynaptic potentials (IPSPs) were affected by the presence of penicillin or pentobarbital. Intracellular recordings were obtained from slices of rat neocortex maintained in vitro; injection of the dye Lucifer yellow indicated that recordings were primarily from pyramidal neurons. Orthodromically evoked responses were always depolarizing at the cell's resting membrane potential. Such depolarizing responses could easily be reversed in polarity by depolarizing the cell 10-15 mV, suggesting that the response consisted partly of an IPSP. In some cases, depolarization unmasked a small, short-latency excitatory postsynaptic potential (EPSP). Responses to iontophoretically applied GABA were also depolarizing at rest. Biphasic hyperpolarizing-depolarizing responses were occasionally observed upon depolarization of the neuron. Bath application of penicillin (1.7-3.4 mM) decreased the amplitude of the IPSPs and increased their time to peak, an effect associated with the development of epileptiform activity. Penicillin also reduced the maximum response to iontophoretically applied GABA without affecting the dose required to obtain a half-maximal response, suggesting a noncompetitive antagonism. Pentobarbital (100-200 microM) prolonged the time course and increased the amplitude of the IPSPs while producing a leftward shift in the GABA charge-response relation. These results suggest that the convulsant penicillin and the anticonvulsant pentobarbital have opposing actions on GABAergic inhibition in the neocortex.

Animals↗
PubMed1991

Expression of highly polysialylated NCAM in the neocortex and piriform cortex of the developing and the adult rat.

The expression of a highly polysialylated form of the neural cell adhesion molecule (NCAM-H) has been investigated in the neocortex and piriform cortex of the developing and the adult rat by using a monoclonal antibody 12E3, which has been found to recognize the polysialic acid portion of NCAM-H. Immunoblot analysis of the cortical homogenates showed that NCAM-H was temporarily expressed during the late embryonic and early postnatal stages. Further, immunohistochemical observations revealed that NCAM-H appeared at embryonic day 13 (E13) in the plexiform primordium in horizontally-oriented cells, probably Cajal-Retzius cells, which are the first neurons to differentiate. During the late embryonic stage, the marginal zone, subplate, and intermediate zone strongly stained, whereas the ventricular zone stained weakly. After birth, the NCAM-H expression was progressively attenuated from a week onwards, and almost vanished in the adult neocortex. In the primordium of the piriform cortex, NCAM-H immunoreactivity also became positive at E13. The time sequences of the NCAM-H expression in these neurons were similar to those of the neurons in the neocortical area. In the piriform cortex, however, the expression remained in a number of neurons in the layer II, which receives a large number of olfactory fibers from the olfactory bulb, where prolonged neurogenesis and construction of neural circuits take place in adulthood. These results suggest that NCAM-H not only plays an important role in the developing rat cortex, but also may be involved in some functions related to reorganization in the adult piriform cortex.

Animals↗
PubMed1993

Independent effects of cholinergic and serotonergic lesions on acetylcholine and serotonin release in the neocortex of the rat.

Rats received a unilateral lesion of the nucleus basalis magnocellularis (NBM) by infusion of ibotenic acid. In addition, the dorsal raphe nucleus was lesioned by infusion of 5,7-dihydroxytryptamine (5,7-DHT). The release of acetylcholine (ACh), choline, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) was measured in the frontal neocortex by means of microdialysis. Lesions of the NBM, but not the raphe nucleus, reduced the release of ACh significantly (-47%). The release of 5-HT and 5-HIAA was reduced by raphe lesions (-44% and -79%+), but not by NBM lesions. In no case did the combined lesion affect neurotransmitter release more than a single lesion. These results suggest that serotonergic projections from the dorsal raphe nucleus are not involved in tonic inhibition of ACh release in the neocortex.

5,7-Dihydroxytryptamine↗