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Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons.
Akaike A, Tamura Y, Sato Y, Yokota T. Akaike A, et al. Eur J Pharmacol. 1993 Sep 7;241(1):1-6. doi: 10.1016/0014-2999(93)90925-8. Eur J Pharmacol. 1993. PMID: 7901032
The effects of methylcobalamin, a vitamin B12 analog, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h …
The effects of methylcobalamin, a vitamin B12 analog, on glutamate-induced neurotoxicity were examined using cultured rat cortical ne …
Mechanisms of cholecystokinin-induced protection of cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.
Tamura Y, Sato Y, Akaike A, Shiomi H. Tamura Y, et al. Brain Res. 1992 Oct 2;592(1-2):317-25. doi: 10.1016/0006-8993(92)91691-7. Brain Res. 1992. PMID: 1360313
Glutamate- and NMDA-induced cytotoxicity was also reduced by N omega-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor. ...Moreover, CCK did not affect NMDA-induced Ca2+ influx measured with rhod-2, a fluorescent Ca2+ indicator. Therefore, release of a
Glutamate- and NMDA-induced cytotoxicity was also reduced by N omega-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor. ...Mor …
Ionic mechanisms involved in muscarinic regulation of neuronal and paraneuronal activity.
Akaike A. Akaike A. Jpn J Pharmacol. 1992 Feb;58(2):83-93. doi: 10.1254/jjp.58.83. Jpn J Pharmacol. 1992. PMID: 1380572 Review.
During voltage clamp recording at the RMP, ACh induced a transient inward current (fast response) followed by a long-lasting current (slow response). ...These results indicate that the muscarinic excitation of adrenal chromaffin cells was triggered by a reduc …
During voltage clamp recording at the RMP, ACh induced a transient inward current (fast response) followed by a long-lasting c …
Cholecystokinin-induced protection of cultured cortical neurons against glutamate neurotoxicity.
Akaike A, Tamura Y, Sato Y, Ozaki K, Matsuoka R, Miura S, Yoshinaga T. Akaike A, et al. Brain Res. 1991 Aug 23;557(1-2):303-7. doi: 10.1016/0006-8993(91)90149-p. Brain Res. 1991. PMID: 1684128
A desulfated analog CCK-8NS, which acts selectively as an antagonist of CCKB receptors, also reduced glutamate neurotoxicity. The neuroprotective effects of CCK were antagonized by L-365260, a CCKB receptor antagonist, but not by L-364718, a CCKA receptor ant
A desulfated analog CCK-8NS, which acts selectively as an antagonist of CCKB receptors, also reduced glutamate neurotoxicity. The neu
Voltage and current clamp studies of muscarinic and nicotinic excitation of the rat adrenal chromaffin cells.
Akaike A, Mine Y, Sasa M, Takaori S. Akaike A, et al. J Pharmacol Exp Ther. 1990 Oct;255(1):333-9. J Pharmacol Exp Ther. 1990. PMID: 2213564
A dose-dependent increase in the extracellularly recorded firing of cells was observed when 10(-6) to 10(-4) M acetylcholine (ACh) were locally applied to the cells in the vicinity of the target cell being recorded using a microinflow method. During voltage clamp re
A dose-dependent increase in the extracellularly recorded firing of cells was observed when 10(-6) to 10(-4) M acetylcholine (ACh) we
A patch clamp study of muscarinic excitation of the rat adrenal chromaffin cells.
Akaike A, Mine Y, Sasa M, Takaori S. Akaike A, et al. J Pharmacol Exp Ther. 1990 Oct;255(1):340-5. J Pharmacol Exp Ther. 1990. PMID: 2213565
A patch clamp study was performed to determine the ionic mechanisms underlying the muscarinic excitation of rat adrenal chromaffin cells. ...These results indicate that muscarinic-induced suppression of K+ currents is caused by a decrease in the number of active K+
A patch clamp study was performed to determine the ionic mechanisms underlying the muscarinic excitation of rat adrenal chromaffin ce
Muscarinic inhibition as a dominant role in cholinergic regulation of transmission in the caudate nucleus.
Akaike A, Sasa M, Takaori S. Akaike A, et al. J Pharmacol Exp Ther. 1988 Sep;246(3):1129-36. J Pharmacol Exp Ther. 1988. PMID: 2843628
A combination of acetylcholine (10(-6) to 10(-4) M) with physostigmine (10(-6) M) also inhibited the orthodromic response of CN neuron, but nicotine (10(-6) to 10(-3) M) had no effects on the neuronal activity. ...When carbachol (10(-5) M) was added to the bath, the number
A combination of acetylcholine (10(-6) to 10(-4) M) with physostigmine (10(-6) M) also inhibited the orthodromic response of CN neuro
Excitatory and inhibitory effects of dopamine on neuronal activity of the caudate nucleus neurons in vitro.
Akaike A, Ohno Y, Sasa M, Takaori S. Akaike A, et al. Brain Res. 1987 Aug 25;418(2):262-72. doi: 10.1016/0006-8993(87)90094-1. Brain Res. 1987. PMID: 2890403
In addition, during application of a high concentration (100 microM) of dopamine there was a marked elevation of the threshold potential of the action potential elicited by a higher depolarizing current. ...In addition, the excitatory effect induced by a
In addition, during application of a high concentration (100 microM) of dopamine there was a marked elevation of the threshold …
Inhibitory effects of thyrotropin-releasing hormone on neuronal activity in the nucleus accumbens.
Takatani T, Sasa M, Akaike A, Takaori S. Takatani T, et al. Neuropharmacology. 1987 Sep;26(9):1389-94. doi: 10.1016/0028-3908(87)90104-3. Neuropharmacology. 1987. PMID: 3118234
The effects of thyrotropin-releasing hormone (TRH) were examined on neuronal activity in the nucleus accumbens, receiving an input from the parafascicular nucleus of the thalamus or the hippocampus, in chloral hydrate-anesthetized rats, using a microiontophoretic technique …
The effects of thyrotropin-releasing hormone (TRH) were examined on neuronal activity in the nucleus accumbens, receiving an input from the …
Nicotine-induced protection of cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.
Akaike A, Tamura Y, Yokota T, Shimohama S, Kimura J. Akaike A, et al. Brain Res. 1994 May 2;644(2):181-7. doi: 10.1016/0006-8993(94)91678-0. Brain Res. 1994. PMID: 7519524
A 1-h exposure of the cultures to kainate or alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) reduced cell viability. ...Maximum protection against glutamate cytotoxicity was induced with a 2-h nicotine incubation. Exposure to nicotine for up to 2 h
A 1-h exposure of the cultures to kainate or alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) reduced cell viability.
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