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At least 1,153 records · Page 64Linked to original sources
PubMed2006

Long-term potentiation is associated with changes in synaptic ultrastructure in the rat neocortex.

Long-term potentiation (LTP) in the sensorimotor cortex of freely moving rats has been associated with changes in dendritic morphology and dendritic spine density. The current research examined changes in synaptic number and ultrastructure associated with LTP in this cortical region. LTP was induced over a 1 h period and the animals were sacrificed 2 h after the initial stimulation of the LTP group. Synapses within the terminal area of the apical dendrites from layer III pyramidal neurons were quantified by determining the total number of synapses per neuron, the number of excitatory and inhibitory contacts, number of synapses with different curvature subtypes, number of perforated synapses, and synaptic length. Several changes in synaptic morphology of excitatory synapses were revealed but no overall increase in the number of synapses per neuron was evident. Specifically, the induction of LTP was associated with an increased number of excitatory perforated and concave shaped synapses. Increased numbers of perforated concave synapses were also found to be significantly correlated with the degree of potentiation in the LTP animals. These and previous results suggest similar synaptic changes in both the cortex and hippocampus during the early phases of LTP maintenance and distinct synaptic changes during later phases of LTP maintenance.

Analysis of Variance↗
PubMed2001

Attraction exerted in vivo by grafts of embryonic neocortex on developing thalamic axons.

In a previous study we provided evidence that embryonic (E) day 16 frontal cortical cells grafted into the occipital cortex of newborn rats receive inputs from the ventrolateral (VL) and ventromedial (VM) thalamic nuclei which, normally, project to the frontal cortex (25). The present study was designed to examine further the conditions of development of the thalamic innervation of heterotopic neocortical grafts. We demonstrate that VL/VM axons do not provide transitory aberrant input to the occipital cortex either in intact newborn animals or in rats having received neonatal occipital lesion and subsequent graft of E16 occipital cells. These findings indicate, therefore, that the VL/VM projection to the graft does not result from the stabilization of an initial widespread cortical projection from these thalamic nuclei occurring either spontaneously or in response to the lesion and homotopic transplantation procedures. We also show that the VL/VM projection to frontal-to-occipital grafts develops within a few days posttransplantation and is maintained in adulthood. Finally, this study establishes that most VL/VM axons which enter the grafts are not collaterals of thalamofrontal axons. After having reached the cortex, they proceed caudally primarily within the infragranular layers. The findings of this and previous (25) in vivo studies for the first time provide evidence that developing thalamic axons have the capacity to respond to signals from grafts of E16 cortical cells and are capable of deviating their trajectory to establish contact with the grafts. Only those axons arising from thalamic nuclei appropriate for the cortical locus of origin of the grafted cells respond to the guidance signals. The mechanisms by which the thalamic axons find their way to the graft probably rely on cell-contact signaling and/or long-range attraction exerted by diffusible molecules.

Animals↗
PubMed1999

Intrinsic physiological and morphological properties of principal cells of the hippocampus and neocortex in hamsters infected with scrapie.

Scrapie is a transmissible spongiform encephalopathy, or "prion disease." We investigated the effects of intracerebral Sc237 scrapie inoculation in hamsters on the physiology and morphology of principal cells from neocortical and hippocampal slices. Scrapie inoculation resulted in increased branching of basal dendrites of hippocampal CA1 pyramidal cells (Sholl analysis), reduced amplitudes of medium and late afterhyperpolarizations (AHPs) in CA1 pyramidal cells and layer V neocortical cells, loss of frequency potentiation of depolarizing afterpotentials (DAPs), and double action potentials in synaptically evoked CA1 pyramidal cell responses. Postsynaptic double action potentials could also be evoked in normal hamster CA1 pyramidal cells by acute pharmacological block of AHPs, suggesting that the depressed AHPs in scrapie-infected hamsters caused the action potential doublets. Both the AHP and the DAP potentiations depend on increased intracellular calcium, which suggests that the underlying deficit, in hamsters infected with Sc237 scrapie, may lie in calcium entry and/or homeostasis. Fast IPSPs, passive membrane properties, and density of dendritic spines remained unchanged. These last two results differ markedly from recent studies on mice infected with ME7 scrapie, indicating diversity of pathophysiology in this group of diseases, perhaps associated with the progressive and substantial neuronal loss found in the ME7, and not the Sc237, model.

Action Potentials↗
PubMedDate not supplied

Effect of stimulation of the lateral hypothalamus on the correlation of neuron spike activity in the rabbit neocortex.

Cross-correlation and autocorrelation histograms were constructed with the aim of studying correlated spike activity of neurons in the visual and sensorimotor regions of both hemispheres of the rabbit brain before and after stimulation of the right and left lateral hypothalamic regions, which generates food-motivated responses. Stimulation of the left hypothalamus produced larger rearrangements in correlated neuron firing than stimulation of the right hypothalamus. Stimulation of the left hypothalamus, unlike that of the right hypothalamus, was followed by significant increases in the numbers of pairs of left hemisphere neocortical neurons with linked activity, and also induced the sequential firing of neurons in a particular defined order: sensorimotor cortex cells fired first, followed by visual cortex neurons after delays of up to 120 msec. It is concluded that cortical interhemisphere asymmetry in conditions of hunger is associated with nonuniform functioning of the right and left lateral hypothalamic regions.

Animals↗
PubMed1997

Immunoblotting patterns of cytoskeletal dendritic protein expression in human neocortex.

Qualitative and quantitative evaluations of cytoskeletal proteins are critical for understanding physiological and pathological processes affecting the nervous system. Most of such studies on human samples have only used immunohistochemical techniques. We describe a complementary immunoblotting approach, for the assessment of neuronal cytoskeletal proteins, which employs fresh frozen postmortem tissues. We found that cytosolic fractions are suitable for qualitative and quantitative evaluations of four major dendritic cytoskeletal proteins: microtubule-associated protein (MAP)-2, MAP-5, and high- and medium-molecular-weight nonphosphorylated neurofilaments. The enhanced chemiluminescence (ECL) technique revealed consistent and distinctive immunoblotting patterns for all four proteins in both monkey (no postmortem delay) and human (17-34 h postmortem interval) samples, some of which differed from those found in rodents. Quantitations of blots, by tissue protein-optical density curves that demonstrated linearity of the measurements in the 0- to 100-microgram range, support the feasibility of these immunoassays for the study of neurologic disorders.

Animals↗
PubMed1998

Changes by short-term hypoxia in the membrane properties of pyramidal cells and the levels of purine and pyrimidine nucleotides in slices of rat neocortex; effects of agonists and antagonists of ATP-dependent potassium channels.

In a first series of experiments, intracellular recordings were made from pyramidal cells in layers II-III of the rat primary somatosensory cortex. Superfusion of the brain slice preparations with hypoxic medium (replacement of 95%O2-5%CO2 with 95%N2-5%CO2) for up to 30 min led to a time-dependent depolarization (HD) without a major change in input resistance. Short periods of hypoxia (5 min) induced reproducible depolarizations which were concentration-dependently depressed by an agonist of ATP-dependent potassium (K(ATP)) channels, diazoxide (3-300 microM). The effect of 30 but not 300 microM diazoxide was reversed by washout. Tolbutamide (300 microM), an antagonist of K(ATP) channels, did not alter the HD when given alone. It did, however, abolish the inhibitory effect of diazoxide (30 microM) on the HD. Neither diazoxide (3-300 microM) nor tolbutamide (300 microM) influenced the membrane potential or the apparent input resistance of the neocortical pyramidal cells. Current-voltage (I-V) curves constructed at a membrane potential of -90 mV by injecting both de- and hyperpolarizing current pulses were not altered by diazoxide (30 microM) or tolbutamide (300 microM). Moreover, normoxic and hypoxic I-V curves did not cross each other, excluding a reversal of the HD at any membrane potential between -130 and -50 mV. The hypoxia-induced change of the I-V relation was the same both in the absence and presence of tolbutamide (300 microM). In a second series of experiments, nucleoside di- and triphosphates separated with anion exchange HPLC were measured in the neocortical slices. After 5 min of hypoxia, levels of nucleoside triphosphates declined by 29% (GTP), 34% (ATP), 44% (UTP) and 58% (CTP). By contrast, the levels of nucleoside diphosphates either did not change (UDP) or increased by 13% (GDP) and 40% (ADP). In slices subjected to 30 min of hypoxia the triphosphate levels continued to decrease, while the levels of GDP and ADP returned to control values. The tri- to diphosphate ratios progressively declined for ATP/ADP and GTP/GDP, but not for UTP/UDP when the duration of hypoxia was increased from 5 to 30 min. Hence, the rapid fall in the ratios of nucleoside tri- to diphosphates without the induction of a potassium current failed to indicate an allosteric regulation of a plasmalemmal K(ATP) channel by purine and pyrimidine nucleotides. Diazoxide had no effect on neocortical pyramidal neurons and was effective only in combination with a hypoxic stimulus; it is suggested that both plasmalemmal and mitochondrial K(ATP) channels are involved under these conditions. The hypoxic depolarization may be due to blockade of K+,Na+-ATPase by limitation of energy supplying substrate.

Adenosine Triphosphate↗
PubMed2003

Ih channels as modulators of presynaptic terminal function: ZD7288 increases NMDA-evoked [3H]-noradrenaline release in rat neocortex slices.

Recent observations indicate the presence of hyperpolarization-activated cation channels (I(h) channels) in presynaptic terminals of central neurons, but their functional impact is still unclear. To investigate whether there are operative I(h) channels on presynaptic terminals of noradrenergic neurons, the effect of the I(h) channel blocker ZD7288 on the N-methyl-D-aspartate (NMDA)-evoked [3H]-noradrenaline release ([3H]-NA release) was tested. Neocortical slices of the rat, preloaded with [(3)H]-NA, were superfused in the presence of TTX (0.32 microM) and stimulated twice by addition of 300 microM NMDA. Application of 1 and 10 microM ZD7288 increased the NMDA-evoked [(3)H]-NA release by 29 and 44%, respectively, in the presence of 3 mM external K+. Elevation of external K+ to 6 mM significantly reduced the increasing effect of 10 microM ZD7288 to 15% only. Our results indicate the presence of I(h) channels on presynaptic terminals of noradrenergic neurons and suggest that presynaptic I(h) channels may attenuate transmitter release, at least under the present test conditions.

Animals↗
PubMed2003

Role of the neocortex in consolidation of fear conditioning memories in rats.

The aim of the present work was to investigate, by means of the reversible inactivation technique, the distinct roles of three neocortical sites, the Prefrontal (PFC), Frontal (FC) and Parietal (PAC) cortices, during memory consolidation of conditioned freezing to a tone, a defined conditioned stimulus (CS), and to the training context. Reversible tetrodotoxin inactivations were performed at increasing post-acquisition delays (0.25, 24 or 96 h). Retention testing was always performed 72 h after the inactivation procedure in order to avoid any possible influence on the retrieval phase. It was found that none of the three sites are involved in context freezing consolidation, but that FC and PAC are differentially involved in the consolidation of memory to the CS. FC inactivation was followed by retention impairment only when performed immediately after acquisition while PAC inactivation was followed by amnesia when performed both immediately after acquisition and 24 h later, but not when performed 96 h later. PFC inactivation was not followed by retention impairment at any of the employed delays. These findings show that some neocortical structures are involved in auditory-cued fear conditioning during the initial phases of the consolidation process.

Acoustic Stimulation↗
PubMed2000

Heterotopia in microcephaly induced by cytosine arabinoside: hippocampus in the neocortex.

Pregnant mice were injected intraperitoneally with cytosine arabinoside (Ara-C) on days 13.5 and 14.5 of pregnancy. The brains of their offspring were studied histologically and histochemically. In addition to dysgenic microcephaly, nodular structures consisting of cells with a relatively homogeneous morphology were observed in the depths of the cerebral cortex. The cell clusters were first seen around postnatal day 4, and had a cellular continuity with the disarrayed pyramidal cell layer in the CA 1 region of the hippocampus. Golgi-Cox staining showed a number of pyramidal-shaped cells in the clusters. Morphologically, they resembled the pyramidal neurons of the hippocampus. Immunohistochemical examination, using anti-serotonin or anti-tyrosine hydroxylase antibodies, also indicated similarities between the cell clusters and the pyramidal cell layer. It is, therefore, proposed that the cell clusters consisted of heterotopic pyramidal cells of the hippocampus. A few synaptic structures could already be detected in the heterotopic cell clusters on postnatal day 3 by electron microscopy. This early establishment of synaptic contact with related neurons may have caused the heterotopic localization of the pyramidal cells.

Abnormalities, Drug-Induced↗
PubMed2003

[3H]GR113808 binding to serotonin 5-HT(4) receptors in the postmortem neocortex of Alzheimer disease: a clinicopathological study.

Abnormalities in neural transmission of serotonin (5-HT) may play a role in both cognitive and neuropsychiatric features of Alzheimer disease (AD). We measured 5-HT(4) receptors in the postmortem frontal and temporal cortex of 34 AD subjects and 15 controls by radioligand binding with [3H]GR113808. Receptor binding data was then correlated with prospectively assessed cognitive (Mini-Mental State Examination, MMSE) and behavioral (Present Behavioural Examination, PBE) data. [3H]GR113808 binding affinity (K(D)) and density (B(max)) in AD were unchanged compared to controls in both cortical regions, and did not correlate with MMSE or PBE data. The binding parameters were also not related to disease duration, senile plaque and neurofibrillary tangle counts, and neuroleptic medication. We conclude that unlike other 5-HT receptors, 5-HT(4) receptor binding affinity and density do not seem to be affected in the frontal and temporal cortex in AD and may not have a direct role in the clinical features of the disease.

Aged↗
PubMed2004

Transgenic activation of Ras in neurons increases synapse formation in mouse neocortex.

The small G protein Ras, which is a molecular switch in neurotrophic signal transduction, is implicated in synaptic plasticity and synapse development during ontogeny and in the adult nervous system. To characterise the involvement of Ras-dependent signaling in synaptogenesis, the cortical synapse-to-neuron ratio was investigated in synRas mice overexpressing Val12-Ha-Ras in postmitotic neurons (introduced by Heumann, 2000). The number of synapses per neuron was analysed in cortical layers II/III of the somatosensory cortex at different stages of postnatal development by stereological methods. The synapse-to-neuron ratio was still identical in wild-type and synRas mice at postnatal day 4 before the onset of transgene expression. At P12, P47 and in the adult, analyses revealed a significant increase in the synapse-to-neuron ratio in synRas mice which correlated with the strength of transgene expression. The data presented here provide evidence that Ras activity might be profoundly involved in synaptogenesis by reinforcing the formation or maintenance of synapses during the development and in the adult.

Animals↗