Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro
Abstract
The radioprotectant, dithiothreitol (DTT) has been shown to increase excitability in the hippocampal slice preparation. In the present study, intracellular recording techniques were used to further examine the actions of DTT. Electrophysiological recordings from CA1 pyramidal cells were examined prior to, during and after DTT exposure. DTT caused a small depolarization without altering membrane resistance. DTT-induced spontaneous firing and occasional burst firing in normally silent neurons. These effects were accompanied by a reduction in spike frequency adaptation but no change in the after hyperpolarization following a train of action potentials. Following DTT exposure, orthodromic stimulation produced multiple firing. subthreshold excitatory postsynaptic potentials (EPSPs) were significantly prolonged. Isolating the CA1 subfield, attenuated the prolongation of the EPSP by DTT. Recurrent inhibitory postsynaptic potentials were unaffected by DTT. The actions of DTT are likely to result from DTT-induced reduction of disulfide bonds since the reduced form of DTT does not cause a similar hyperexcitability.
- Authors:
- Publication Date:
- Research Org.:
- Armed Forces Radiobiology Research Inst., Bethesda, MD (USA)
- OSTI Identifier:
- 6275944
- Report Number(s):
- AD-A-203084/9/XAB; AFRRI-SR-88-28
- Resource Type:
- Technical Report
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; HIPPOCAMPUS; NERVE CELLS; BIOLOGICAL RADIATION EFFECTS; RADIOPROTECTIVE SUBSTANCES; ELECTROPHYSIOLOGY; CHEMICAL BONDS; DEPOLARIZATION; EXCITATION; RECORDING SYSTEMS; SULFIDES; ANIMAL CELLS; BIOLOGICAL EFFECTS; BODY; BRAIN; CENTRAL NERVOUS SYSTEM; CHALCOGENIDES; DRUGS; ENERGY-LEVEL TRANSITIONS; NERVOUS SYSTEM; ORGANS; PHYSIOLOGY; RADIATION EFFECTS; SOMATIC CELLS; SULFUR COMPOUNDS; 560152* - Radiation Effects on Animals- Animals
Citation Formats
Tolliver, J M, and Pellmar, T C. Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro. United States: N. p., 1988.
Web.
Tolliver, J M, & Pellmar, T C. Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro. United States.
Tolliver, J M, and Pellmar, T C. Fri .
"Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro". United States.
@article{osti_6275944,
title = {Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro},
author = {Tolliver, J M and Pellmar, T C},
abstractNote = {The radioprotectant, dithiothreitol (DTT) has been shown to increase excitability in the hippocampal slice preparation. In the present study, intracellular recording techniques were used to further examine the actions of DTT. Electrophysiological recordings from CA1 pyramidal cells were examined prior to, during and after DTT exposure. DTT caused a small depolarization without altering membrane resistance. DTT-induced spontaneous firing and occasional burst firing in normally silent neurons. These effects were accompanied by a reduction in spike frequency adaptation but no change in the after hyperpolarization following a train of action potentials. Following DTT exposure, orthodromic stimulation produced multiple firing. subthreshold excitatory postsynaptic potentials (EPSPs) were significantly prolonged. Isolating the CA1 subfield, attenuated the prolongation of the EPSP by DTT. Recurrent inhibitory postsynaptic potentials were unaffected by DTT. The actions of DTT are likely to result from DTT-induced reduction of disulfide bonds since the reduced form of DTT does not cause a similar hyperexcitability.},
doi = {},
url = {https://www.osti.gov/biblio/6275944},
journal = {},
number = ,
volume = ,
place = {United States},
year = {1988},
month = {1}
}