Background: Novel therapeutic approaches against influenza are required. Bakuchiol is a phenolic isoprenoid found in Babchi seeds.Results: Bakuchiol enantiomer-selectively inhibited influenza A viral infection and growth and activated the Nrf2 pathway.Conclusion: Bakuchiol showed novel enantiomer-selective anti-influenza viral activity.Significance: The study of bakuchiol will contribute to the development of novel approaches to influenza therapy.

In the nucleus accumbens (NAc), a medium spiny (MS) neuron receives GABAergic inputs from two major sources: fast-spiking (FS) neurons and other, adjacent MS neurons. These two types of inhibitory synapses are considered to play different roles in output activities, i.e., FS→MS connections suppress output from the NAc whereas MS→MS connections contribute to lateral inhibition. In the present study, we focused on the electrophysiological properties of unitary inhibitory postsynaptic currents (uIPSCs) obtained from MS→MS connections and FS→MS connections and examined the effects of quinpirole, a dopamine D(2)-like receptor agonist, on uIPSCs with multiple whole cell patch-clamp recording. Application of quinpirole (1 μM) reliably suppressed the amplitude of uIPSCs by 29.6% in MS→MS connections, with increases in paired-pulse ratio and failure rate. The suppressive effects of quinpirole on uIPSCs were mimicked by 1 μM PD128907, a D(2/3) receptor agonist, whereas quinpirole-induced suppression of uISPCs was blocked by preapplication of 1 μM sulpiride or 10 μM nafadotride, both D(2/3) receptor antagonists. On the other hand, quinpirole (1 μM) had divergent effects on FS→MS connections, i.e., quinpirole increased uIPSC amplitude in 38.1% of FS→MS connections and 23.8% of FS→MS connections were suppressed by quinpirole. Analysis of coefficient of variation in uIPSC amplitude implied the involvement of presynaptic mechanisms in quinpirole-induced effects on uIPSCs. These results suggest that activation of D(2)-like receptors facilitates outputs from MS neurons in the NAc by reducing lateral inhibition during a dormant period of FS neuron activities.

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Abstract. Aripiprazole, an atypical antipsychotic drug, is a D 2 dopamine-receptor partial agonist, but also has affinity to several serotonin receptors (5-HT 1A,2A,2C,7 ). However, little is known about the contribution of serotonin receptors in the action of aripiprazole. The present study investigated the effects of aripiprazole on 5-HT 2A receptor-mediated behaviors and compared them with the effects on dopamine receptor-mediated behavior in rats. Aripiprazole (10, 30 mg/ kg, p.o.) inhibited the stereotyped behavior induced by apomorphine (1 mg / kg, s.c.), a dopamine-receptor agonist, and the wet-dog shake responses induced by DOI (2,5-dimethoxy-4-iodoamphetamine, 2 mg / kg, s.c.), a 5-HT 2A -receptor agonist. Moreover, aripiprazole improved the disruption of prepulse inhibition induced by both apomorphine and DOI significantly. These data suggest that not only the dopaminergic system, but also the serotonergic system are involved in the antipsychotic effect of aripiprazole.

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The rate of smoking in patients with schizophrenia is higher than that in the general population. Nicotinic acetylcholine receptors (nAChR) are involved in the sensorimotor gating deˆcits in schizophrenia. We have revealed that nicotine ameliorates the disruption of the PPI, a model of sensorimotor gating, which is induced by apomorphine, a dopamine receptor agonist, but is not eŠective for the disruption of the PPI induced by phencyclidine, a glutamine NMDA receptor antagonist, in rats. Furthermore, the ameliorating eŠect of nicotine is antagonized by methyllycaconitine, a selective a 7 nAChR antagonist. The eŠect of nocitine was also investigated in the stereotyped behavior induced by apomorphine, however, nicotine was found to have no signiˆcant eŠect. Considering these results, the ameliorating eŠect of the disruption of the PPI via a 7 nAChR is therefore thought to be involved in dopaminergic systems. The dopaminergic systems involved in a 7 nAChR may be diŠerent from the systems involved in stereotypy. In addition, this review describes the eŠects of the a 7 nicotinic receptor agonists.