Depletion of glucose causes presynaptic inhibition of neuronal transmission in the rat dorsolateral septal nucleus
✍ Scribed by Takashi Akasu; Masashi Tsurusaki; Shingo Shoji
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 859 KB
- Volume
- 24
- Category
- Article
- ISSN
- 0887-4476
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✦ Synopsis
The role of glucose in synaptic transmission was examined in the rat dorsolateral septal nucleus (DLSN) with single-microelectrode voltage-clamp and slicepatch techniques. Removal of glucose from the oxygenated Krebs solution caused a n outward current associated with an increased membrane conductance. The currentvoltage relationship (I-V curve) showed that the hypoglycemia-induced outward current was reversed in polarity a t the equilibrium potential for K'. Exposure of DLSN neurons to the glucose-free solution for 5-20 min depressed the excitatory postsynaptic current (EPSC), the inhibitory postsynaptic current (IPSC), and the late hyperpolarizing current (LHC). Replacement of glucose with 2-deoxy-D-glucose (2DG), an antimetabolic substrate, mimicked the deprivation of glucose. Mannoheptulose (10 mM) and dinitrophenol, inhibitors of glucose metabolism, also depressed the PSCs, even in the presence of 10 mM glucose. Glucose-free perfusion did not significantly depress the glutamate-induced inward current, indicating that the inhibition of the EPSC by the glucose-free perfusion was presynaptic. y-aminobutyric acid (GABA)-induced outward currents were depressed by the glucose-free solution. Intracellular dialysis of DLSN neurons with a patch-pipette solution containing 5 mM ATP attenuated the hypoglycemia-induced outward current.
Glucose-free superfusion consistently inhibited the IPSC and the LHC without changing the GAl3A-induced outward current in ATP-treated DLSN neurons. It is suggested that glucose metabolism directly regulates the release of both excitatory amino acids and GABA from the presynaptic nerve terminals. o 1996 Wiley-Liss, Inc.