Disinhibitory circuit mediated by connections from vasoactive intestinal polypeptide to somatostatin interneurons underlies the paradoxical decrease in spike synchrony with increased border ownership selective neuron firing rate.

The activity of border ownership selective (BOS) neurons in intermediate-level visual areas indicates which side of a contour owns a border relative to its classical receptive field and provides a fundamental component of figure-ground segregation. A physiological study reported that selective attention facilitates the activity of BOS neurons with a consistent border ownership preference, defined as two neurons tuned to respond to the same visual object. However, spike synchrony between this pair is significantly suppressed by selective attention. These neurophysiological findings are derived from a biologically-plausible microcircuit model consisting of spiking neurons including two subtypes of inhibitory interneurons, somatostatin (SOM) and vasoactive intestinal polypeptide (VIP) interneurons, and excitatory BOS model neurons. In our proposed model, BOS neurons and SOM interneurons cooperate and interact with each other. VIP interneurons not only suppress SOM interneuron responses but also are activated by feedback signals mediating selective attention, which leads to disinhibition of BOS neurons when they are directing selective attention toward an object. Our results suggest that disinhibition arising from the synaptic connections from VIP to SOM interneurons plays a critical role in attentional modulation of neurons in intermediate-level visual areas.

Extended action of MKC-242, a selective 5-HT(1A) receptor agonist, on light-induced Per gene expression in the suprachiasmatic nucleus in mice.

We reported previously that (S)-5-[3-[(1,4-benzodioxan-2-ylmethyl)amino]propoxy]-1,3-benzodioxole hydrochloride (MKC-242) (3 mg kg(-1), i.p.), a selective 5-HT(1A) receptor agonist, accelerated the re-entrainment of hamster wheel-running rhythms to a new 8 hr delayed or advanced light-dark cycle, and also potentiated the phase advance of the wheel-running rhythm produced by light pulses. The molecular mechanism underlying MKC-242-induced potentiation of this phase shift, however, has not yet been elucidated. We examined the effects of MKC-242 on light-induced mPer1 and mPer2 mRNA expression in the suprachiasmatic nucleus (SCN) of mice. MKC-242 (5 mg kg(-1), i.p.) potentiated light-induced mPer1 and mPer2 expression in the SCN of mice housed in constant darkness for 2 days, when mRNA levels were observed 3 hr after light-exposure. More potentiating action of MKC-242 on mPer2 expression in the SCN was observed in mice housed in constant darkness for 9-10 days. This facilitatory action of MKC-242 on mPer1 expression was antagonized by WAY100635, a selective 5-HT(1A) receptor blocker, indicating that MKC-242 activated 5-HT(1A) receptors. Other drugs such as 8-hydroxy-dipropylaminotetralin (10 mg kg(-1), i.p.), paroxetine (10 mg kg(-1), i.p.), buspirone (10 mg kg(-1), i.p.), and diazepam (10 mg kg(-1), i.p.) did not display a potentiating action on light-induced mPer1 and mPer2 expression in the SCN. In the behavioral experiments, we found that MKC-242 (5 mg kg(-1), i.p.) potentiated light-induced phase delays of free-running rhythm in mice. The present results suggest that prolonged increase of mPer1 or mPer2 expression in the SCN by MKC-242 may be involved in the potentiation of photic entrainment by MKC-242 in mice.