Pupil constriction via the parasympathetic pathway precedes perceptual switch of ambiguous stimuli.

Perceptual rivalry of ambiguous stimuli reflects the interaction of neural activity among multiple cortical regions. However, it remains unclear what drives a spontaneous perceptual alteration. We hypothesized that increased fluctuations in spontaneous neural activity due to arousal reduction drive the perceptual switch. Here, we show that the pupils shrank a few seconds prior to the onset of the spontaneous perceptual switch. Such pupil constriction was not observed before the exogenous perceptual switch. Pharmacological experiments confirmed that the pupil constriction disappeared when the peripheral parasympathetic pathway (pupil sphincter muscle) was blocked, but it remained intact when the peripheral sympathetic pathway (pupil dilator muscle) was manipulated. Furthermore, rapid pupil dilations with behavioral response are also mediated by the peripheral parasympathetic pathway. The present findings suggested that transient arousal drops, as denoted by the autonomic nervous modulation of pupil size, are involved in inducing the spontaneous perceptual switch of bistable stimuli.

G Protein-Coupled Glutamate and GABA Receptors Form Complexes and Mutually Modulate Their Signals.

Molecular networks containing various proteins mediate many types of cellular processes. Elucidation of how the proteins interact will improve our understanding of the molecular integration and physiological and pharmacological propensities of the network. One of the most complicated and unexplained interactions between proteins is the inter-G protein-coupled receptor (GPCR) interaction. Recently, many studies have suggested that an interaction between neurotransmitter GPCRs may mediate diverse modalities of neural responses. The B-type gamma-aminobutyric acid (GABA) receptor (GBR) and type-1 metabotropic glutamate receptor (mGluR1) are GPCRs for GABA and glutamate, respectively, and each plays distinct roles in controlling neurotransmission. We have previously reported the possibility of their functional interaction in central neurons. Here, we examined the interaction of these GPCRs using stable cell lines and rat cerebella. Cell-surface imaging and coimmunoprecipitation analysis revealed that these GPCRs interact on the cell surface. Furthermore, fluorometry revealed that these GPCRs mutually modulate signal transduction. These findings provide solid evidence that mGluR1 and GBR have intrinsic abilities to form complexes and to mutually modulate signaling. These findings indicate that synaptic plasticity relies on a network of proteins far more complex than previously assumed.