Inhibition by l-3,4-dihydroxyphenylalanine of hippocampal CA1 neurons with facilitation of noradrenaline and γ-aminobutyric acid release

Akbar, Muhammad; Ishihara, Kumatoshi; Sasa, Masashi; Misu, Yoshimi

doi:10.1016/s0014-2999(01)00793-2

Cited by 15 publications

(4 citation statements)

References 24 publications

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“…Electrophysiological studies have underlined the existence of a direct effect of L-DOPA on L-DOPA recognition sites in the CA1 region of the rat hippocampus. This phenomenon induces the release of NA (Akbar et al, 2001). In light of this evidence, similar mechanisms can underlie the involvement of the β-adrenoreceptors in the restoration of DG LTD by L-DOPA treatment.…”

Section: Discussionmentioning

confidence: 64%

l-DOPA reverses the impairment of Dentate Gyrus LTD in experimental parkinsonism via β-adrenergic receptors

Pendolino

Bagetta

Ghiglieri

et al. 2014

Experimental Neurology

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Section: Discussionmentioning

confidence: 64%

l-DOPA reverses the impairment of Dentate Gyrus LTD in experimental parkinsonism via β-adrenergic receptors

Pendolino

Bagetta

Ghiglieri

et al. 2014

Experimental Neurology

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“…Indeed, we have observed the intracellular Ca 2þ raising response upon DOPA stimulation in primary cultured mice hippocampal neurons (manuscript in preparation). However, it has been shown that DOPA suppressed the CA3-CA1 excitatory synaptic transmission in hippocampal slices via the indirect effect of DOPA, which activates the noradrenergic and/or GABAergic interneurons (Akbar et al, 2001). Faint immunostaining signal in radial and molecular layers in CA1 may represent the OA1 expression in such interneurons.…”

Section: Oa1 Expression In the Central Nervous Systemmentioning

confidence: 99%

Expression of ocular albinism 1 (OA1), 3, 4- dihydroxy- L-phenylalanine (DOPA) receptor, in both neuronal and non-neuronal organs

et al. 2015

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“…At 24 h, 5 and 10 days after the final injection of drugs, hippocampal slices were prepared as described previously 7. Briefly, after decapitation of rats under ether anesthesia, the brain was removed and placed in ice‐cold Ca 2+ ‐free artificial cerebrospinal fluid (ACSF).…”

Section: Methodsmentioning

confidence: 99%

“…At 24 h, 5 and 10 days after the final injection of drugs, hippocampal slices were prepared as described previously. 7 Briefly, after decapitation of rats under ether anesthesia, the brain was removed and placed in ice-cold Ca 2+ -free artificial cerebrospinal fluid (ACSF). Hippocampal slices (450 µm in thickness) cut with a microslicer (DTK-1000, Dosaka EM, Kyoto, Japan) were incubated in ACSF for 1 h at 34°C, and preserved at room temperature until recording.…”

Section: Methodsmentioning

confidence: 99%

Augmentation of Serotonin‐Induced Inhibition of Neuronal Activity in the Hippocampus Following Repeated Treatment with Methamphetamine

Kimura

Ishihara

Ozawa

et al. 2004

Annals of the New York Academy of Sciences

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Electrophysiological studies were performed to determine whether or not hippocampal serotonergic modulation was affected following repeated administration of methamphetamine (MAP). Rats were i.p. administered with MAP (5 mg/kg) or saline once a day for 5 days. Hippocampal slices were prepared at 24 h, 5 and 10 days after the final MAP or saline injection. The population spikes (PS) induced by stimulation of Schaffer collateral/commissural fibers were recorded in the hippocampal CA1 region. Application of serotonin (5-HT) via a bath perfusion system inhibited the PS in a concentration-dependent manner. At 24 h after the final injection, 10-microM 5-HT-induced inhibition of PS was not affected by MAP treatment. However, 5 days after the final injection, the inhibition by 5-HT (10 microM) of PS was significantly augmented in the MAP-treated group. Ten days after the final injection, this augmentation was not statistically significant compared with that of control group. 8-OH-DPAT, a 5-HT1A receptor agonist, inhibited PS, but the inhibition was not enhanced or reduced 5 days after the final MAP treatment. However, the enhancement of PS by RS 67333, a 5-HT4 receptor agonist, was attenuated 5 days after the MAP treatment. It was found that 5-HT-induced inhibition of PS in the hippocampal CA1 region was potentiated 5 days after cessation of MAP, and this effect was suggested to be due to reduction of excitatory 5-HT4 receptor functions.

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Inhibition by l-3,4-dihydroxyphenylalanine of hippocampal CA1 neurons with facilitation of noradrenaline and γ-aminobutyric acid release

Cited by 15 publications

References 24 publications

l-DOPA reverses the impairment of Dentate Gyrus LTD in experimental parkinsonism via β-adrenergic receptors

l-DOPA reverses the impairment of Dentate Gyrus LTD in experimental parkinsonism via β-adrenergic receptors

Expression of ocular albinism 1 (OA1), 3, 4- dihydroxy- L-phenylalanine (DOPA) receptor, in both neuronal and non-neuronal organs

Augmentation of Serotonin‐Induced Inhibition of Neuronal Activity in the Hippocampus Following Repeated Treatment with Methamphetamine

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