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At least 1,747 records · Page 97Linked to original sources
PubMed2003

A morphogenetic role for acetylcholine in mouse cerebral neocortex.

Recently, cholinergic afferents to cerebral cortex have met renewed attention regarding the regulation of plasticity as well as cognitive processing. My laboratory has developed a mouse neonatal basal forebrain lesion paradigm that has contributed considerably to the understanding of cholinergic mechanisms in cortical development. We have shown that transient cholinergic deafferentation, beginning at birth, precipitates alterations in neuronal differentiation and synaptic connectivity that persist into maturity, and contribute to altered cognitive behavior. These data are in general agreement with studies in rats in which the cholinergic basal forebrain is lesioned very early in development but contrast with effects of later developmental lesions. Moreover, in mouse, both morphological and behavioral consequences of the lesion are sex dependent. Studies of receptors and secondary messengers that are instrumental in morphogenesis and plasticity suggest that sex dependent molecular alterations occur within days if not hours following cortical cholinergic deafferentation.

Acetylcholine↗
PubMed1996

The neurochemistry of morphine addiction in the neocortex.

Different strategies have been used in an attempt to understand the neurobiology of opioid addiction. Here, Michéle Simonato initially discusses the identification of key anatomical areas involved in the phenomenon and purposes an explanation of opioid addiction based on the theory of complexity. The variable importance of direct and indirect effects in phenotypically different neuronal populations can imply differences in the adaptive changes that occur with chronic morphine exposure. Opioid addiction is therefore proposed as a complex multicellular event, where individual neurones differentially adapt both on the basis of the signals they receive and of their second messengers and genetic programmes.

Animals↗
PubMed1997

Decreased expression of nuclear and mitochondrial DNA-encoded genes of oxidative phosphorylation in association neocortex in Alzheimer disease.

We recently reported 50% decreases in mRNA levels of mitochondrial DNA (mtDNA)-encoded cytochrome oxidase (COX) subunits I and III in Alzheimer disease (AD) brains. The decreases were observed in an association neocortical region (midtemporal cortex) affected in AD, but not in the primary motor cortex unaffected in AD. To investigate whether the decreases are specific to mtDNA-encoded mRNA, we extended this analysis to nuclear DNA (nDNA)-encoded subunits of mitochondrial enzymes of oxidative phosphorylation (OXPHOS). Brains from five AD patients showed 50-60% decreases in mRNA levels of nDNA-encoded subunit IV of COX and the beta-subunit of the F0F1-ATP synthase in midtemporal cortex compared with mRNA levels from midtemporal cortex of control brains. In contrast, these mRNAs were not reduced in primary motor cortices of the AD brains. The amount of nDNA-encoded beta-actin mRNA and the amount of 28S rRNA were not altered in either region of the AD brain. The results suggest that coordinated decreases in expression of mitochondrial and nuclear genes occur in association cortex of AD brains and are a consequence of reduced neuronal activity and downregulation of OXPHOS machinery.

Aged↗
PubMed1986

Survival of adrenal gland implants in the neocortex of the rat: a morphological study.

The survival of adrenal gland implantation in the cerebral cortex of the rat was studied. In the present study, mature adrenal gland had survived after six months of implantation. No scar tissue was observed between the adrenal gland cortex and the host cerebral cortex. The implanted tissue showed some reorganization in its cortex and medulla. In the adrenal cortex there was an observable increase in connective tissue fibers and some degeneration of cells. In the medulla, again, both surviving and degenerating cells were observed. This study shows that mature adrenal gland has the capacity to survive after implantation in the cerebral cortex of the rats. Further studies are being carried out on fetal and mature tissue implantation and the ability of the adrenal medulla to secrete catecholamines.

Adrenal Glands↗
PubMed2002

Morphological alterations in neurons forming corticocortical projections in the neocortex of aged Patas monkeys.

Recent studies indicate that the cognitive processes mediated by the prefrontal cortex, such as working memory, are impaired during normal aging. These disturbances in cortical function may be a consequence of abnormalities in neocortical circuits, even though the numbers of cortical neurons are preserved in normal aging. We performed retrograde tract-tracing of cortical projections connecting the temporal cortex to the prefrontal cortex in combination with dye-filling and three-dimensional neuronal reconstructions in aged patas monkeys. Age-related changes affected the apparent complexity of the apical dendrites of projection neurons and caused a significant loss of dendritic spines at all levels of their dendritic trees. These results indicate that normal aging is accompanied by neuronal changes that are quite subtle, and possibly involves discrete cellular components of certain cortical neurons selectively rather than inducing major alterations such as cell death.

Aging↗
PubMed1985

Comparative localization of Cajal-Retzius cells in the neocortex of normal and reeler mutant mice fetuses.

The Cajal-Retzius cells (CRc) appear as an histochemically advanced subpopulation, since they are the only neocortical neurons able to express an acetylcholinesterase activity at an early stage of corticogenesis. Thus a comparative study of the CRc population was carried out on normal and reeler mice fetuses. The use of an appropriate cytochemical technique to reveal this endogenous cell marker, in conjunction with coronal and tangential sections show that: the Cajal-Retzius cells form a sheet in the more superficial layer of the embryonic cortex, with a relative cell density giving the same value in both phenotypes; a difference is observed in the relative depth position of these cells with regard to the pial basal lamina and in the pattern of cell grouping between the heterozygous and homozygous mutant littermates. This technique appears of great interest for a further analysis of the CRc population during cortical ontogenesis.

Acetylcholinesterase↗
PubMed2001

A major role for thalamocortical afferents in serotonergic hallucinogen receptor function in the rat neocortex.

Activation of 5-hydroxytryptamine(2A) (5-HT(2A)) receptors by hallucinogenic drugs is thought to mediate many psychotomimetic effects including changes in affect, cognition and perception. Conversely, blockade of 5-HT(2A) receptors may mediate therapeutic effects of many atypical antidepressant and antipsychotic drugs. The purpose of the present study was to determine the source of subcortical glutamatergic afferents, which would project widely throughout the anterior-posterior axis of the rat brain to the apical dendrites of layer V pyramidal cells of the medial prefrontal cortex, from which serotonin induces transmitter release via activation of 5-HT(2A) receptors. Fiber-sparing chemical lesions of the medial thalamus selectively decreased the frequency of serotonin-induced excitatory postsynaptic currents recorded from layer V pyramidal cells in the prelimbic region of the medial prefrontal cortex by 60%. In contrast, large bilateral lesions of the amygdala did not alter the serotonin response. These thalamic lesions significantly decreased the amount of binding to either mu-opioid or metabotropic glutamate 2/3 receptors in the prelimbic region of the medial prefrontal cortex as expected from previous evidence that these agonists for these receptors suppress serotonin-induced excitatory postsynaptic currents by a presynaptic mechanism. Surprisingly, the amount of specific binding to cortical 5-HT(2A) receptors was significantly increased by the medial thalamic lesions. Thus, these experiments demonstrate that activation of cortical 5-HT(2A) receptors modulates transmitter release from thalamocortical terminals. Unexpectedly, lesioning the thalamocortical terminals also alters 5-HT(2A) receptor binding in the prefrontal cortex. These findings are of interest with respect to understanding therapeutic effects of antidepressant/antipsychotic drugs and the known behavioral effects of thalamic lesions in humans.

Amygdala↗
PubMed1997

Plastic changes in the cholinergic innervation of the rat cerebral cortex after unilateral lesion of the nucleus basalis with alpha-amino-3-OH-4-isoxozole propionic acid (AMPA): effects of basal forebrain transplants into neocortex.

Unilateral AMPA lesions of the nucleus basalis magnocellularis (nbm) produced a nearly complete loss of cholinergic markers in the ipsilateral frontal and parietal cortices with no recovery at 6 months. The loss was associated with compensatory increases in AChE-positive fibre density in the contralateral cortex, in ipsilateral cortical regions not receiving their cholinergic innervation from the nbm and in the size of cholinergic magnocellular neurones in the contralateral nbm. The hypertrophy and increase in AChE-positive fibre density were apparent at 4-6 weeks after lesion and increased with time. Cholinergic transplants to cholinergically deafferented cortex prevented development of the compensatory increases in AChE-positive fibre density and restored AChE-positive fibre density and ChAT activity to control levels in ipsilateral cholinergically deafferented regions, partially after 6-8 weeks and completely after 6 months. In contrast, when cholinergic grafts were placed into unlesioned cortex, axonal outgrowth was localized to the vicinity of the transplant and did not develop with time. These results support the concept that vacant synapses promote and direct axonal outgrowth from transplanted neurones and that grafted cholinergic neurones integrate into the lesioned forebrain cholinergic projections system and prevent the lesion-induced changes in AChE-positive fibre density and ChAT activity.

Animals↗