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A Lou

Publications and source records attributed to A Lou.

5 recordsLinked to original sources
PubMed2001

Attenuation of neurotoxicity in cortical cultures and hippocampal slices from E2F1 knockout mice.

The E2F1 transcription factor modulates neuronal apoptosis induced by staurosporine, DNA damage and beta-amyloid. We demonstrate E2F1 involvement in neuronal death induced by the more physiological oxygen-glucose deprivation (OGD) in mouse cortical cultures and by anoxia in mouse hippocampal slices. E2F1(+/+) and (-/-) cultures were comparable, in that they contained similar neuronal densities, responded with similar increases in intracellular calcium concentration ([Ca(2+)]i) to glutamate receptor agonists, and showed similar NMDA receptor subunit mRNA expression levels for NR1, NR2A and NR2B. Despite these similarities, E2F1(-/-) cultures were significantly less susceptible to neuronal death than E2F1(+/+) cultures 24 and 48 h following 120-180 min of OGD. Furthermore, the absence of E2F1 significantly improved the ability of CA1 neurons in hippocampal slices to recover synaptic transmission following a transient anoxic insult in vitro. These results, along with our finding that E2F1 mRNA levels are significantly increased following OGD, support a role for E2F1 in the modulation of OGD- and anoxia-induced neuronal death. These findings are consistent with studies showing that overexpression of E2F1 in postmitotic neurons causes neuronal degeneration and the absence of E2F1 decreases infarct volume following cerebral ischemia.

Animals↗
PubMed2000

Antagonism of a PCP drug discrimination by hallucinogens and related drugs.

Drugs such as PCP and MK-801 can cause psychotic reactions in humans by antagonizing NMDA receptors. This action is ultimately toxic to certain cortical neurons and may be one mechanism underlying neurodegenerative diseases, including schizophrenia. It has been reported that hallucinogens such as LSD, DOM, and DOI can block the neurotoxic effects of NMDA antagonists, possibly by activating inhibitory 5-HT2A receptors on GABAergic interneurons that normally inhibit glutamatergic projections to the retrosplenial and cingulate cortexes. The purpose of this experiment was to determine the extent to which similar drugs might also alter the behavioral effects of one NMDA antagonist, PCP. Rats were trained to discriminate this compound (2.5 mg/kg) from saline and were then given a series of antagonist tests. It was found that LSD (0.32 mg/kg) and DOM (4.0 mg/kg) blocked the PCP cue completely; DMT (8.0 mg/kg) and a structural congener of LSD, lisuride (LHM; 0.4 mg/kg), blocked the effects of PCP partially. The 5-HT/DA antagonists spiperone and ritanserin had no effect on the PCP cue. These data suggest that LSD, DOM, and, less effectively, DMT and LHM can block the behavioral as well as the neurotoxic effects of NMDA antagonists most likely through agonist actions at 5-HT2 receptors.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1997

Systematic and random errors in compression testing of trabecular bone.

We sought to quantify the systematic and random errors associated with end-artifacts in the platens compression test for trabecular bone. Our hypothesis was that while errors may depend on anatomic site, they do not depend on apparent density and therefore have substantial random components. Trabecular bone specimens were first tested nondestructively using newly developed accurate protocols and then were tested again using the platens compression test. Percentage differences in modulus between the techniques (bovine proximal tibia [n = 18] and humerus [n = 17] and human lumbar spine, [n = 9]) were in the range of 4-86%. These differences did not depend on anatomic site (p = 0.21) and were only weakly dependent on apparent density and specimen aspect ratio (r2 < 0.10). The mean percentage difference in modulus was 32.6%, representing the systematic component of the end-artifact error. Neglecting the minor variations explained by density and specimen size (approximately 10%), an upper bound on the random error from end-artifacts in this experiment was taken as the SD of the modulus difference (+/-18.2%). Based on a synthesis of data taken from this study and from the literature, we concluded that the systematic underestimation error in the platens compression test can be only approximated and is in the range of 20-40%; the substantial random error (+/-12.5%) confounds correction, particularly when the sample size is small. These errors should be considered when interpreting results from the platens test, and more accurate testing techniques should be used when such errors are not acceptable.

Animals↗
PubMed1997

[Effect of ginsenosides on nucleolar organizer region of neuron and sprouting of mossy fibre terminals of hippocampus in rats].

During the production of long-term potentiation (LTP) of the granular cell layer in hippocampal dentate gyrus (DG) and the enhancement of the ability of the memory retention in rats induced by ginsenosides (GSS), the effects of GSS on the number of silver-nucleolar organizer region (Ag-NOR) of neuron and the sprouting of mossy fiber (MF) terminals in hippocampus were studied. Giving GSS for 7 days, the amplitude of population spike (PS) increased by 87.71 +/- 1.91% and the onset and peak latency of PS decreased by 16.60 +/- 1.53%, and 13.5 +/- 0.87% respectively. Meanwhile, GSS could markedly promote the ability of memory retention in rats. In CA3 and DG area, the average number of Ag-NOR of single pyramidal and granular cell in the three GSS groups increased by 66.17 +/- 2.32% and 72.07 +/- 0.93% respectively (P < 0.01). Moreover in CA3, the average of rating scales of MF terminals sprouting in three GSS groups increased 1-3 times as compared with saline groups (P < 0.01). It is suggested that GSS could enhance the transcriptional activity of rDNA and the synthetic ability of protein in hippocampal neuron, as well as promote the sprouting of MF terminals in hippocampus for increasing the efficiency of transmission by hippocampal synapses.

Animals↗