Hippocampal inputs to the lateral septal nucleus: patterns of facilitation and inhibition

DeFrance, Jon F.; Shimono, T.; Kitai, S.T.

doi:10.1016/0006-8993(72)90681-6

Cited by 37 publications

(8 citation statements)

References 17 publications

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“…This indicates that lowering glucose decreases the transmitter release from presynaptic nerve terminals. DLSN neurons receive excitatory synaptic inputs from the hippocampal formation via the fimbrid fornix pathway (DeFrance et al, 1972;McLennan and Miller, 1974). The majority of the hippocampal neurons that provide the dorsolateral septal input originate in the hippocampal CA3 area and are branches that form the Schaffer collateral pathway (Andersen et al, 1966;Lorente de NO, 1934;Swanson et al, 1980).…”

Section: Hyperpolarization Induced By Glucose Depletionmentioning

confidence: 99%

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

Shoji

1992

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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.

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Section: Hyperpolarization Induced By Glucose Depletionmentioning

confidence: 99%

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

Shoji

1992

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“…The dorsolateral septal nucleus (DLSN) receives major nerve input from neurons in the hippocampal CA3 area through the fimbridfornix pathway (Andersen et al, 1966;DeFrance et al, 1972;McLennan and Miller, , and GABA receptor antagonists (C) on the EPSC, IPSC, and LHC evoked by stimulation of the fimbridfornix pathway. These PSCs were recorded by single-electrode voltage-clamp methods from three different cells.…”

Section: Introductionmentioning

confidence: 99%

Depletion of glucose causes presynaptic inhibition of neuronal transmission in the rat dorsolateral septal nucleus

Akasu

Tsurusaki

Shoji

1996

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The role of glucose in synaptic transmission was examined in the rat dorsolateral septal nucleus (DLSN) with single-microelectrode voltage-clamp and slice-patch technique. Removal of glucose from the oxygenated Krebs solution caused an outward current associated with an increased membrane conductance. The current-voltage relationship (I-V curve) showed that the hypoglycemia-induced outward current was reversed in polarity at 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. gamma-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 GABA-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.

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“…The NMDA receptor-channel complex, especially, has been demonstrated to have several unique characteristics (for reviews see Ascher & Nowak, 1987;Collingridge & Bliss, 1987). Dorsolateral septal nucleus (DLSN) neurones receive excitatory input from the hippocampus (DeFrance, Shimono & Kitai, 1972;McLennan & Miller, 1974) and this input is mediated by an excitatory amino acid neurotransmitter (KStorm-Mathisen, 1978). The majority of the hippocampal neurones which provide the dorsolateral septal input originate in hippocampal area CA3 and are branches of axons which form the well-known Schaffer collateral pathway (Lorente de No.…”

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confidence: 99%

Excitatory amino acid‐receptor‐mediated EPSPs in rat dorsolateral septal nucleus neurones in vitro.

Gallagher

Hasuo

1989

The Journal of Physiology

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SUMMARY1. Intracellular recordings were made from rat dorsolateral septal nucleus (DLSN) neurones in vitro. We investigated depolarizations resulting from pressure application of excitatory amino acids and compared these to synaptically evoked excitatory postsynaptic potentials (EPSPs).2. EPSPs evoked by focal fimbrial afferent stimulation in saline with 30-50 /tMbicuculline and 1-2 mM-Mg2+ yielded a linear amplitude-voltage relationship; their reversal potential was -3 mV. These EPSPs exhibited little sensitivity to 2-amino-5-phosphonopentanoate (APV), an N-methyl-D-aspartate(NMDA)-receptor-specific antagonist, but were markedly depressed by kynurenic acid, a broad-spectrum excitatory amino acid antagonist.3. In Mg2+-free solution, the amplitude and the duration of EPSPs were increased markedly masking the following inhibitory postsynaptic potential (IPSP) and the late hyperpolarizing potential (LHP). These facilitated and broadened EPSPs were sensitive to APV or Mg2+. The 5. Our data demonstrate the existence of NMDA-receptor-mediated synaptic potentials in the rat DLSN, the characteristics of which are similar to those in other central nervous system regions.

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Hippocampal inputs to the lateral septal nucleus: patterns of facilitation and inhibition

Cited by 37 publications

References 17 publications

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

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

Depletion of glucose causes presynaptic inhibition of neuronal transmission in the rat dorsolateral septal nucleus

Excitatory amino acid‐receptor‐mediated EPSPs in rat dorsolateral septal nucleus neurones in vitro.

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