Glucose regulation of synaptic transmission in the dorsolateral septal nucleus of the rat

• Published in: Synapse (New York, N.Y.) Vol. 12; no. 4; p. 322
• Main Author: Shoji, S
• Format: Journal Article
• Language: English
• Published: United States 01.12.1992
• Subjects: Action Potentials; Animals; Deoxyglucose - pharmacology; Electrophysiology; Glucose - antagonists & inhibitors; Glucose - metabolism; Glucose - physiology; Hypoglycemia - physiopathology; Male; Neural Inhibition; Rats; Rats, Inbred WKY; Receptors, Amino Acid - physiology; Receptors, GABA-A - physiology; Septal Nuclei - physiology; Synapses - physiology; Synaptic Transmission - physiology
• ISSN: 0887-4476
• DOI: 10.1002/syn.890120409

Intracellular recordings were made from neurons in the dorsolateral septal nucleus (DLSN) of rat brain slices. Lowering the concentration of extracellular glucose resulted in a concentration-dependent membrane hyperpolarization associated with a cessation of spontaneous firing. The amplitude of the excitatory postsynaptic potential (EPSP), inhibitory postsynaptic potential (IPSP), and late hyperpolarizing potential (LHP) evoked by a single stimulus applied to the fimbrial/fornix pathway was decreased when the concentration of glucose was reduced to 0-2 mM. Substitution of glucose with 2-deoxy-D-glucose (11 mM), an antimetabolite of glucose substrate, mimicked the effects of glucose depletion. Mannoheptulose (10-20 mM), a potent hexokinase blocker, and dinitrophenol (50 microM), a potent inhibitor of oxidative phosphorylation, produced both the hyperpolarization and inhibition of postsynaptic potentials, even in the presence of 11 mM glucose. The sulphonylureas, glibenclamide (10 microM) and tolbutamide (1 mM), did not antagonize the hyperpolarization and the inhibition of the postsynaptic potentials produced by glucose depletion. The amplitude of membrane depolarizations produced by pressure application of glutamate (10 mM) and the membrane hyperpolarizations produced by pressure application of either muscimol (1 mM) or baclofen (1 mM) were almost unchanged, even when glucose was reduced to 1-2 mM. These results indicate that intracellular glucose metabolism regulates the function of septal neurons, not only by changing the resting membrane potential, but also by presynaptically affecting neurotransmission between the hippocampal formation and the lateral septum.