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Kazushige Sasamoto

Publications and source records attributed to Kazushige Sasamoto.

3 recordsLinked to original sources

Recovery of amiloride-sensitive neural coding during regeneration of the gustatory nerve: behavioral-neural correlation of salt taste discrimination.

The chorda tympani (CT) nerve innervating the anterior tongue contains two types of NaCl-responsive fibers: one, the N-type, receives input from receptor cells, the NaCl responses of which are strongly inhibited by amiloride, whereas the other, the E-type, receives input from cells poorly sensitive or insensitive to amiloride. To investigate the formation of this differentially responsive neural system, we crushed the mouse CT nerve and examined the subsequent recovery of NaCl responses and amiloride sensitivity of the regenerated nerve and behavioral discrimination between NaCl and KCl. At 2 weeks after the nerve crush, no significant response of the nerve to chemical stimuli was observed. At 3 weeks, responses to salts gradually reappeared. In this period, almost all single fibers responding to NaCl were insensitive to amiloride (E-type). At 4 weeks, some of the single fibers showed amiloride sensitivity (N-type) and behavioral discrimination between NaCl and KCl reappeared. After >or=5 weeks, the number of N-type fibers had reached the control level and became approximately equal to that of E-type fibers. During the course of recovery, N-type and E-type fibers were clearly distinguishable on the basis of their amiloride sensitivities, their KCl/NaCl response ratios, and their concentration-response relationships to NaCl. These results suggest that two salt-responsive systems are independently reformed after the nerve crush. The selective synapse reformation may account for recovery of behavioral discrimination between NaCl and KCl after taste nerve crush and regeneration. It may also explain stable sensory coding for taste quality during the continuous turnover of receptor cells in the healthy animal.

Amiloride↗

Conditioned taste aversion learning in leptin-receptor-deficient db/db mice.

The db/db mouse has defective leptin receptors. The defects lead to impairments of leptin regulation of food intake and body weight, and result in the expression of diabetic symptoms such as hyperinsulinemia, hyperglicemia, and extreme obesity. Recent studies have proposed that leptin may also affect memory and learning processes. To examine this possibility, we compared the ability of leptin-receptor-deficient db/db mice and their normal lean litter mates to form and extinguish a conditioned taste aversion (CTA) for saccharin. We used a short-term (10 s) lick test and a long-term (48 h) two bottle preference test for measurement of consumption of test solutions. On the first day after conditioning to avoid saccharin, the db/db mice showed preference scores for saccharin as low, and aversion thresholds for sucrose lower than that of the lean mice. During the extinction test trials beginning from the second up to the 30th day after conditioning, numbers of licks and preference scores for aversive saccharin and sucrose appeared to be larger, and recovered faster to the control levels in db/db mice. These results indicate that db/db mice with leptin-receptor-deficiency may show equal capacity to form CTAs for saccharin, greater generalization from saccharin to sucrose, and a faster rate of extinction. This suggests that disruption of leptin signalling does not inhibit acquisition of CTA learning, but impairs its extinction. This differential contribution of the leptin system on CTA processes may be due to differential distribution of leptin receptors in the CTA-related brain areas.

Animals↗

Gurmarin suppression of licking responses to sweetener-quinine mixtures in C57BL mice.

Gurmarin (Gur) is a peptide that selectively suppresses responses of the chorda tympani nerve to sweet substances in rats and mice. In the present study, we examined the effect of Gur on behavioral responses to sweet substances in C57BL mice. To accomplish this, we developed a new short-term lick test and measured numbers of licks for 10 s for sweet substances mixed with quinine hydrochloride (QHCl) in water-deprived mice. Numbers of licks for sucrose mixed with 1 or 3 mM QHCl increased with increasing concentration of sucrose from 0.01 to 1.0 M. Oral infusion with 30 micro g/ml Gur produced significant decreases in responses to concentration series for sucrose mixed with 3 mM QHCl, whereas no such effect by Gur was observed in responses to QHCl alone or QHCl-mixed HCl, NaCl or monosodium glutamate. The Gur suppression of QHCl-mixed sucrose responses, which otherwise lasted for 2-3 h, rapidly returned to approximately 80% of control levels after oral infusion with beta-cyclodextrin. These results are comparable to neural data previously found in chorda tympani responses, and thereby provide further evidence for Gur as a sweet response inhibitor in C57BL mice. In the other aspect, our newly developed short-term test can also provide a tool for measurements of taste-guided behavioral responses to sweeteners.

Animals↗