Acute & Chronic Barbiturates: in Vitro Biochemistry

McCaslin, Patrick P.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute on Drug Abuse (NIDA)
• Type: First Independent Research Support & Transition (FIRST) Awards (R29)
• Project #: 7R29DA005737-05
• Application #: 3461180
• Study Section: Drug Abuse Biomedical Research Review Committee (DABR)
• Project Start: 1990-07-01
• Project End: 1995-06-30
• Budget Start: 1994-04-01
• Budget End: 1994-06-30
• Support Year: 5
• Fiscal Year: 1993

Institution

• Name: Ochsner Clinic Foundation
• City: New Orleans
• State: LA
• Country: United States
• Zip Code: 70121

Publications

Oh, S; McCaslin, P P (1995) The iron component of sodium nitroprusside blocks NMDA-induced glutamate accumulation and intracellular Ca2+ elevation. Neurochem Res 20:779-84

Cai, Z; McCaslin, P P (1993) Acute, chronic and differential effects of several anesthetic barbiturates on glutamate receptor activation in neuronal culture. Brain Res 611:181-6

Cai, Z; McCaslin, P P (1992) Amitriptyline, desipramine, cyproheptadine and carbamazepine, in concentrations used therapeutically, reduce kainate- and N-methyl-D-aspartate-induced intracellular Ca2+ levels in neuronal culture. Eur J Pharmacol 219:53-7

McCaslin, P P; Yu, X Z (1992) Cyanide selectively augments kainate- but not NMDA-induced release of glutamate and taurine. Eur J Pharmacol 228:73-5

Cai, Z; McCaslin, P P (1992) Selective effects of cyanide (100 microM) on the excitatory amino acid-induced elevation of intracellular calcium levels in neuronal culture. Neurochem Res 17:803-8

McCaslin, P P; Yu, X Z; Ho, I K et al. (1992) Amitriptyline prevents N-methyl-D-aspartate (NMDA)-induced toxicity, does not prevent NMDA-induced elevations of extracellular glutamate, but augments kainate-induced elevations of glutamate. J Neurochem 59:401-5