6-cyano-7-nitroquinoxaline-2-3-dione and Protein-Energy-Malnutrition

There is growing evidence for an effect of prenatal protein malnutrition on the GABAergic neurotransmitter system in the rat hippocampus and associated structures. In the present study, we examined the functional electrophysiological consequences of observed alterations in GABA(A) and benzodiazepine receptor systems. Whole-cell patch clamp recordings of spontaneous and of miniature inhibitory postsynaptic currents (mIPSCs) generated by CA1 pyramidal cells were performed in in vitro hippocampal slices prepared from control and prenatally protein malnourished adult male rats. The characteristics of spontaneous synaptic currents were unaltered by the prenatal insult, as were the amplitudes and kinetics of GABA(A) receptor-mediated mIPSCs. The frequency of mIPSCs, however, was significantly increased in CA1 pyramidal cells in slices prepared from prenatally malnourished vs. control rats. The effect of the benzodiazepine receptor agonist chlordiazepoxide on the characteristics of mIPSCs was also examined and found to be the same in cells from both nutritional groups. The increased frequency of mIPSCs together with the lack of a change in amplitude, kinetics, or modulation by benzodiazepines of mIPSCs in response to prenatal protein malnutrition indicate a presynaptic locus of effect of this insult.

Topics: 2-Amino-5-phosphonovalerate; 6-Cyano-7-nitroquinoxaline-2,3-dione; Animal Nutritional Physiological Phenomena; Animals; Chlordiazepoxide; Energy Intake; Excitatory Amino Acid Antagonists; Female; GABA Modulators; gamma-Aminobutyric Acid; Hippocampus; In Vitro Techniques; Male; Membrane Potentials; Neural Inhibition; Patch-Clamp Techniques; Pregnancy; Prenatal Exposure Delayed Effects; Protein-Energy Malnutrition; Pyramidal Cells; Rats; Rats, Sprague-Dawley; Synapses; Tetrodotoxin