It is well known that nitric oxide (NO) functions as a neurotransmitter: NO is produced by NO synthase (NOS) in postsynaptic nerves and diffuses through membranes into presynaptic ones to activate soluble guanylyl cyclase (sGC). This causes the production of cGMP, resulting in the feedback control of presynaptic nerve activity. In taste sensory systems, however, the NO-cGMP cascade might act differently. In vertebrate taste receptors, evidence for NOS expression, function of cGMP as a second messenger and regulation of the cGMP level by NO has been reported. These reports suggest that NO could participate in the signal transduction in the taste receptor cells. In gustatory receptor neurons of the blowfly, Phormia regina, the importance of cGMP in the sugar taste transduction has also been suggested. If cGMP is a second messenger of the sugar taste transduction, cGMP may be produced by NO-sensitive sGC in the sugar receptor neurons. In this paper, we review recent progresses in our study on the signal transduction including NO-cGMP cascade in the sugar receptor neurons of P. regina. Our study covers the analyses by electrophysiological recording as well as Ca²⁺/NO- imaging.

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Insects have ability to discriminate a wide diversity of odorants in the natural environment as well as to detect species-specific pheromones with high sensitivity and specificity. Olfactory signals are mediated by odorant or pheromone receptors expressed in olfactory receptor neurons in the olfactory sensilla of antennae. The signals are transmitted to the first olfactory processing center, the antennal lobe (AL), then, further processed at higher centers (mushroom body and lateral protocerebrum) to elicit specific behavior in animals. In recent years, remarkable progress has been made in our knowledge of molecular mechanisms underlying odor discrimination and pheromone perception, mainly due to the identification of odorant and sex pheromone receptor genes in insects. At the same time, extensive studies in the AL have provided many insights into neural basis of odor discrimination in the insect brain. Understanding how insects detect and discriminate the olfactory information will tell us how nervous systems process the complicated environmental information, and ultimately translate it into meaningful behaviors.

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In this review, I aim to introduce recent progress towards understanding the evolution of auditory organs in animals. Despite of 600 million years of separation of protostomia and deuterostomia, key genes needed for the development, the nature of mechanoreceptive channels, and the amplification mechanism in sensory neurons are shared between vertebrate ears and insect ears. These findings argue against the previously prevailing view that vertebrate and invertebrate ears have separate evolutionary origins. Anatomical, developmental, and molecular genetic studies consistently show that the auditory organs in insects are derived from unspecialized, low-vibration-sensitive chordotonal organs. Thus, any chordotonal organs in body appendages could evolve into auditory organs. Convergent evolution of auditory organs, therefore, is based on the specialization of the sound transmission apparatus (e.g. tympanum, tracheal expansion) rather than on the sensory neurons.

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Part 5. Actual measurement of the rate of information transmitted along cricket wind sensory neurons is shown. Input-output coherence is measured for the practical calculation of neuronal information, instead of signal-to-noise ratio. The measurement reveals that the sensory neuron can transmit information at the rate of 400 bit per second at its maximum. Energy threshold of the sensory neuron is determined to be at the order of k_BT. Based on these measurements, entropy cost of information in living neuron is also estimated to be very close to the thermo dynamic limit of 0.7k_B per bit of information.

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