Glucose-depletion suppresses synaptic transmissions in rat dorsolateral septal nucleus.
Removal of extracellular glucose hyperpolarized the post-synaptic membrane of dorsolateral septal nucleus (DLSN) neurons. Glucose-depletion suppressed the excitatory postsynaptic potential (EPSP) and the late hyperpolarizing potential (LHP) without affecting the responses induced by glutamate or baclofen. Glibenclamide did not antagonize the effects produced by glucose-depletion. These results suggest that glucose is necessary to maintain the membrane excitability and transmitter-release in rat DLSN.
Shoji
S
S
Department of Endocrinology and Metabolism, Kurume University School of Medicine, Japan.
Akasu
T
T
Hasuo
H
H
Nonaka
K
K
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism* / Q000502:physiology; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D008297:Male; D008564:Membrane Potentials; D051381:Rats; D011919:Rats, Inbred Strains; D017981:Receptors, Neurotransmitter / Q000502:physiology*; D012686:Septal Nuclei / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
D005971:Glutamates; D017981:Receptors, Neurotransmitter; D018698:Glutamic Acid; D001418:Baclofen; D005947:Glucose