PubMed Health⌕ Search

Biomedical subjects

Y Edagawa

Publications and source records attributed to Y Edagawa.

7 recordsLinked to original sources

Systemic administration of lentinan, a branched beta-glucan, enhances long-term potentiation in the rat dentate gyrus in vivo.

We investigated the effects of oral and intravenous application of lentinan, a branched beta-glucan, on the induction of long-term potentiation (LTP) in the rat dentate gyrus in vivo. Oral administration of lentinan (200 mg/kg) enhanced the induction of LTP evoked by sub-threshold tetanic stimulation (20 pulses at 60 Hz) of the perforant pathway without affecting normal synaptic potentials. Intravenous injection of the compound (0.2-10.0 mg/kg) also enhanced the induction of LTP in a bell-shaped manner, whereas it had no effect on LTP evoked by supra-threshold tetanic stimulation (100 pulses at 100 Hz). Structurally related beta-glucans did not mimic the lentinan-triggered enhancement of LTP. These results suggest that peripherally applied lentinan facilitates the synaptic efficacy of the dentate gyrus neurons in vivo.

Adjuvants, Immunologic↗

Endogenous serotonin contributes to a developmental decrease in long-term potentiation in the rat visual cortex.

The primary visual cortex shows synaptic plasticity during a postnatal "critical period," and its plasticity declines with development. Indeed, we found a developmental decrease in the induction of long-term potentiation (LTP) in the rat visual cortex. In visual cortex slices obtained from 2- to 3-week-old rats, tetanic stimulation (100 Hz for 1 sec, twice at an interval of 30 sec) of the white matter reproducibly induced LTP of field potentials in layer II/III. However, in slices from 5-week-old rats, the same tetanic stimulation failed to induce LTP. We hypothesized that endogenous serotonin (5-HT) is responsible for the developmental decrease in visual cortex LTP, because the induction of visual cortex LTP was suppressed by the addition of exogenous 5-HT (10 microm) and because the amount of 5-HT in the visual cortex increased during development. To test this hypothesis, we investigated the effect of methysergide, a 5-HT receptor antagonist, on the induction of visual cortex LTP. When visual cortex slices from 5-week-old rats were perfused with 50 microm methysergide, tetanic stimulation of the white matter induced robust LTP in layer II/III. Furthermore, serotonergic neurons were lesioned by intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT). LTP was induced in visual cortex slices from 5,7-DHT-treated, 5-week-old rats. These results suggest that the induction of visual cortex LTP in 5-week-old rats is suppressed by endogenous 5-HT. 5-HT may be a factor that determines a critical period for synaptic plasticity in the rat visual cortex.

5,7-Dihydroxytryptamine↗

The serotonin 5-HT2 receptor-phospholipase C system inhibits the induction of long-term potentiation in the rat visual cortex.

The effect of serotonin 5-HT2 receptor stimulation on long-term potentiation (LTP) in the primary visual cortex was investigated by using rat brain slices in vitro. Field potentials evoked by stimulation of layer IV were recorded in layer II/III. The 5-HT2 receptor agonist 1-(2,5-dimethyl-4-iodophenyl)-2-aminopropane (DOI) did not affect baseline synaptic potentials evoked by single-pulse test stimulation, but significantly inhibited the induction of LTP in a concentration-dependent manner (0.1-10 microM). The LTP-inhibiting effect of DOI (10 microM) was blocked by the 5-HT2,7 receptor antagonist ritanserin (10 microM), but not by the 5-HT1A receptor antagonist NAN-190 (10 microM) nor by the 5-HT3,4 receptor antagonist MDL72222 (10 microM). The inhibitory effect of DOI was also blocked by the phospholipase C inhibitor U73122, but not by its inactive analogue U73343. These results suggest that visual cortex LTP is inhibited by activation of the 5-HT2 receptor-phospholipase C system. In addition, the LTP-inhibiting effect of DOI was abolished by the presence of the GABAA receptor antagonist bicuculline (10 microM), suggesting that 5-HT2 receptor-mediated inhibition of visual cortex LTP is dependent on GABAergic inhibition.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex.

We have previously found that stimulation of serotonin 5-HT1A receptors inhibits the induction of long-term potentiation (LTP) in the rat visual cortex. In the present study, the selective 5-HT1A receptor agonist 8-hydroxy-2-(N,N-dipropylamino)tetralin (8-OH-DPAT) significantly reduced N-methyl-d-aspartate (NMDA) receptor-mediated synaptic responses recorded in Mg2+-free medium in rat visual cortical slices. In addition, there was good correlation between the inhibitory effects of 8-OH-DPAT on NMDA responses and LTP. These results suggest that 5-HT1A receptor stimulation inhibits the induction of LTP by suppressing NMDA receptor-mediated synaptic excitation in the rat visual cortex.

2-Amino-5-phosphonovalerate↗

5-HT1A receptor-mediated inhibition of long-term potentiation in rat visual cortex.

We investigated the effect of 8-hydroxy-2-(N,N-dipropylamino)tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, on the induction of long-term potentiation in rat visual cortex slices. Perfusion of 8-OH-DPAT (0.1-10 microM) did not affect layer II/III field potentials evoked by test stimulation of layer IV, but significantly reduced long-term potentiation induced by tetanic stimulation. The inhibitory effect of 8-OH-DPAT was blocked by the 5-HT1A receptor antagonist, pindolol (10 microM), but not by the 5-HT2,7 receptor antagonist, ritanserin (100 microM), nor by the 5-HT3,4 receptor antagonist, MDL72222 (100 microM). These results suggest that the rat visual cortex long-term potentiation is inhibited by 5-HT1A receptor stimulation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Serotonin inhibits the induction of long-term potentiation in rat primary visual cortex.

1. The effect of serotonin (5-hydroxytryptamine; 5-HT) on the induction of long-term potentiation (LTP) in rat visual cortex was investigated by using slice preparations in vitro. 2. Bath application of 5-HT (0.1-10 microM) did not affect the baseline synaptic potentials evoked by single-pulse test stimulation, but inhibited the induction of LTP in a concentration-dependent manner. 3. The effect of 5-HT was blocked by the 5-HT1 receptor antagonist pindolol or the 5-HT2,7 receptor antagonist ritanserin, but not by the 5-HT3,4 receptor antagonist MDL72222. 4. These results suggest that 5-HT plays a role in suppressing the induction of LTP in the rat visual cortex.

Animals↗