An ATP-driven Cl− pump regulates Cl− concentrations in rat hippocampal neurons

Inoue, Masafumi; Hara, Mitsuyoshi; Zeng, Xun-Ting; Hirose, Takuji; Ohnishi, Shiho; Yasukura, Tohru; Uriu, Toshiko; Omori, Kyoko; Minato, Akio; Inagaki, Chiyoko

doi:10.1016/0304-3940(91)90512-r

Cited by 96 publications

(27 citation statements)

References 15 publications

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“…Because of the difficulty of studying propagation with experimental techniques, we have chosen to address these issues by modelling action potentials in the posterior pituitary nerve terminal. The results of this theoretical study lend additional support to the importance of depolarization block in the inhibition of neurosecretion (Inoue et al 1991). However, a value similar to ours was obtained with liquid anion-exchanger microelectrodes in frog dorsal root ganglion cells (Alvarez-Leefmans et al 1990), where GABA-activated Cl-channels depolarize the membrane (Davidoff & Hackman, 1985).…”

Section: Discussionsupporting

confidence: 51%

GABAA receptor activation and the excitability of nerve terminals in the rat posterior pituitary.

Zhang

Jackson

1995

The Journal of Physiology

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1. The activation of GABAA receptors in nerve terminal membranes gates a Cl-channel.Experiments were conducted to determine how the activation of this receptor influences membrane potentials, action potentials and voltage-activated Na+ and K+ channels.2. When activation of the GABAA receptor produced only conductance changes and no voltage changes, action potentials changed only slightly. The threshold for action potential generation increased by 15%. GABA reduced the broadening of action potentials caused by high frequency stimulation by only 7%. These results indicate that membrane shunting by GABA-gated Cl-channels plays a relatively minor role.3. By recording changes in the current through K+ channels in cell-attached patches, the activation of GABAA receptors was shown to depolarize the nerve terminal membrane from rest by 14 mV. The GABAB receptor agonist baclofen produced no change in resting membrane potential as measured by this same technique. 4. In whole-terminal recordings under current clamp, with pipettes containing various Clconcentrations, the GABA-induced depolarization increased with Ec.. 90 % of the Na+ channels and activated a small amount of K+ current. This suggests that inactivation of Na+ channels makes a major contribution to the inhibition of action potentials by GABA. 8. These results are consistent with the hypothesis that GABA inhibits neurosecretion by retarding impulse propagation into the terminal arborization. These results support a depolarization block mechanism for the inhibition of secretion, in which depolarization inactivates Na+ channels sufficiently to block action potentials.

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Section: Discussionsupporting

confidence: 51%

GABAA receptor activation and the excitability of nerve terminals in the rat posterior pituitary.

Zhang

Jackson

1995

The Journal of Physiology

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“…A number of studies have demonstrated that the Cl Ϫ concentration in mature neurons is actually below electrochemical equilibrium, suggesting the presence of an "active" Cl Ϫ efflux mechanism (Inoue et al, 1991, Thompson et al, 1988. In situ hybridization experiments suggest that the expression of the KCC2 isoform of the K-Cl cotransporter is confined to neurons (Payne et al, 1996).…”

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confidence: 98%

Developmental regulation of the neuronal-specific isoform of K-CL cotransporter KCC2 in postnatal rat brains

1999

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“…Consequently, synaptic GABA-A-receptor-mediated currents can trigger action potentials in neonatal neurons. The excitatory effect of GABA is due to elevated intracellular concentration of chloride in immature neurons and therefore depolarized reversal potential of the GABA-A-receptor-mediated responses [Hara et al, 1992;Inoue et al, 1991;Luhmann and Prince, 1991;Rohrbough and Spitzer, 1996;Serafini et al, 1995;Zhang et al, 1991]. In addition to this direct excitatory action, GABA also activates voltage-gated calcium channels [Chen et al, 1996;Connor et al, 1987;Hales et al, 1994;Leinekugel et al, 1995;LoTurco et al, 1995;Obrietan and van den Pol, 1995;Reichling et al, 1994;Yuste and Katz, 1991] and potentiates the activity of NMDA receptors via attenuation of the voltage-dependent magnesium block Leinekugel et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

Dual Role of GABA in the Neonatal Rat Hippocampus

et al. 1999

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The effects of modulators of GABA-A receptors on neuronal network activity were studied in the neonatal (postnatal days 0–5) rat hippocampus in vitro. Under control conditions, the physiological pattern of activity of the neonatal hippocampal network was characterized by spontaneous network-driven giant depolarizing potentials (GDPs). The GABA-A receptor agonist isoguvacine (1–2 μM) and the allosteric modulator diazepam (2 μM) induced biphasic responses: initially the frequency of GDPs increased 3 to 4 fold followed by blockade of GDPs and desynchronization of the network activity. The GABA-A receptor antagonists bicuculline (10 μM) and picrotoxin (100 μM) blocked GDPs and induced glutamate (AMPA and NMDA)-receptor-mediated interictal- and ictal-like activities in the hippocampal slices and the intact hippocampus. These data suggest that at early postnatal ages GABA can exert a dual – both excitatory and inhibitory – action on the network activity.

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An ATP-driven Cl− pump regulates Cl− concentrations in rat hippocampal neurons

Cited by 96 publications

References 15 publications

GABAA receptor activation and the excitability of nerve terminals in the rat posterior pituitary.

GABAA receptor activation and the excitability of nerve terminals in the rat posterior pituitary.

Developmental regulation of the neuronal-specific isoform of K-CL cotransporter KCC2 in postnatal rat brains

Dual Role of GABA in the Neonatal Rat Hippocampus

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