Arachidonic acid inhibits sodium currents and synaptic transmission in cultured striatal neurons

Fraser, Douglas D.; Hoehn, Katja; Weiss, Samuel; MacVicar, Brian A.

doi:10.1016/0896-6273(93)90075-3

Cited by 96 publications

(56 citation statements)

References 61 publications

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“…In striatal neurons, the block of voltage-dependent Na ϩ currents by A A is associated with a slowing of the rate of recovery from inactivation (Fraser et al, 1993). In the present experiments A A also delayed the rate of recovery of the transient current from inactivation (n ϭ 5).…”

Section: A a Decreases The Rate Of Recovery From Inactivationsupporting

confidence: 53%

“…This effect on spike frequency is unlikely to result from a blockade of the transient current, because any reduction of the transient current would be expected to increase the spike discharge frequency. These latter effects and the effects on spike threshold are more probably attributable to an effect of A A on voltage-dependent Na ϩ channels, similar to that described for striatal neurons (Fraser et al, 1993), or alternatively by activation of the M current (Schweitzer et al, 1990).…”

Section: A a Does Not Alter The Time Course Of Single Action Potentialsmentioning

confidence: 78%

“…In the present experiments, however, the continued presence of A A led to the cessation of all electrographic activity and the termination of action potential firing, suggesting that prolonged A A exposure ultimately prevents action potential activity presumably by altering the activity of a variety of ion channels in hippocampal neurons. These effects may arise in part from the action of A A on both voltage-dependent Na ϩ channels (Fraser et al, 1993) and /or activation of the M current (Schweitzer et al, 1990). An understanding of the modulation of the currents responsible for these combined cellular mechanisms, together with the action of A A on the transient current, will ultimately provide insight into the total functional significance of A A modulation of hippocampal neurons.…”

Section: Discussionmentioning

confidence: 99%

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Arachidonic Acid Inhibits Transient Potassium Currents and Broadens Action Potentials during Electrographic Seizures in Hippocampal Pyramidal and Inhibitory Interneurons

Keros

McBain

1997

J. Neurosci.

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The transient outward potassium current was studied in outside-out macropatches excised from the soma of CA1 pyramidal neurons and stratum (st.) oriens-alveus inhibitory interneurons in rat hippocampal slices. Arachidonic acid dose dependently decreased the charge transfer associated with the transient current, concomitant with an increase in the rate of current inactivation. Arachidonic acid (A A) did not affect the voltage dependence of steady state inactivation but did prolong the period required for complete recovery from inactivation. The effects of A A were mimicked by the nonmetabolizable analog of A A, 5,8,11,14-eicosatetraynoic acid, suggesting that metabolic products of A A were not responsible for the observed blocking action. In addition, A A blocked st. oriensalveus-lacunosum-moleculare interneuron transient currents but not currents recorded from basket cell interneurons. In current clamp experiments, A A was without effect on the action potential waveform of CA1 pyramidal neurons under control recording conditions. In voltage-clamp experiments, the use of a test pulse paradigm, designed to mimic the action potential voltage trajectory, revealed that the transient current normally associated with a single spike deactivates too rapidly for A A to have an effect. Transient currents activated by longer duration "action potential" waveforms, however, were attenuated by A A. Consistent with this finding was the observation that A A broadened interictal spikes recorded in the elevated [K ϩ ] o model of epilepsy. These data suggest that A A liberated from hippocampal neurons may act to block the transient current selectively in both CA1 pyramidal neurons and inhibitory interneurons and to broaden action potentials selectively under pathological conditions.

show abstract

Section: A a Decreases The Rate Of Recovery From Inactivationsupporting

confidence: 53%

Section: A a Does Not Alter The Time Course Of Single Action Potentialsmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Arachidonic Acid Inhibits Transient Potassium Currents and Broadens Action Potentials during Electrographic Seizures in Hippocampal Pyramidal and Inhibitory Interneurons

Keros

McBain

1997

J. Neurosci.

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“…Glutamate, which causes excitotoxic neuronal damage, increases calcium influx through N-methyl-Daspartate receptors in postsynaptic neurones, leading to phospholipase A2 mediated arachidonic acid release (7). The increase in arachidonic acid in brain may mediate neuronal injury by inhibiting the sodium ion channels (8). Earlier work showed that GDH activity in the adult rat brain was increased during diabetes (9).…”

Section: Vol 44 No 1 1998 Biochemistryand Molecular Biology Intermentioning

confidence: 99%

Brain glutamate dehydrogenase changes in streptozotocin diabetic rats as a function of age

Biju

Paulose

1998

IUBMB Life

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SUMMARYKinetic parameters of brain glutamate dehydrogenase (GDH) were compared in the brain stem, cerebellum and cerebral cortex of three weeks and one year old streptozotocin (STZ) induced four day diabetic rats with respective controls. A single intrafemoral dose of STZ (60mg/Kg body weight) was administered to induce diabetes in both age groups. After four days the blood glucose levels showed a significant increase in the diabetic animals of both age groups compared with the respective controls. The increase in blood glucose was significant in one year old compared to the three weeks old diabetic rats. The Vm~, of the enzyme was decreased in all the brain regions studied, of the three weeks old diabetic rats without any significant change in the Kin. In the adult the Vm~x of GDH was increased in cerebellum and brain stem but was unchanged in the cerebral cortex. The K~ was unchanged in cerebellum and cerebral cortex but was increased in the brain stem. These results suggest there may be an important regulatory role of the glutamate pathway in brain neural network disturbances and neuronal degeneration in diabetes as a function of age.

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“…n-3 PUFAs reduces heart hyperexcitability (Billman et al, 1994;Kang and Leaf, 1994;Xiao et al, 1995). It has therefore been postulated that they might be anticonvulsant as both the brain and the heart are excitable tissues (Climax and Sewell, 1981;Fraser et al, 1993;Yehuda et al, 1994).…”

Section: Omega-3 Supplementation -A Novel Therapy For Epilepsymentioning

confidence: 99%

1. The anticonvulsant effects of docosahexaenoic acid in rodents

Trépanier

Burnham

2013

Clinical Neurophysiology

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Arachidonic acid inhibits sodium currents and synaptic transmission in cultured striatal neurons

Cited by 96 publications

References 61 publications

Arachidonic Acid Inhibits Transient Potassium Currents and Broadens Action Potentials during Electrographic Seizures in Hippocampal Pyramidal and Inhibitory Interneurons

Arachidonic Acid Inhibits Transient Potassium Currents and Broadens Action Potentials during Electrographic Seizures in Hippocampal Pyramidal and Inhibitory Interneurons

Brain glutamate dehydrogenase changes in streptozotocin diabetic rats as a function of age

1. The anticonvulsant effects of docosahexaenoic acid in rodents

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