Tasting the bitter and the sweet, honeybee memories, and visualizing calcium throughout entire astrocytes

This month's installment of Generally Physiological concerns identification of a channel crucial for the perception of sweet, bitter, and umami tastes; a role for caffeine in honeybee asso­ ciative olfactory memory; and meth­ ods for imaging calcium throughout entire astrocytes. A taste for CALHM1 Sweet, bitter, and umami (the savory taste elicited by glutamate) substan­ c es bind to G protein–coupled taste receptors on type II taste bud cells, ac­ tivating a signaling pathway in which Ca 2+ release leads to the Ca 2+ ­depen­ dent activation of TRPM5 channels and thereby membrane depolariza­ tion. This elicits action potentials, triggering the nonvesicular release of ATP and thereby the activation of nearby afferent gustatory neurons. Taruno et al. (2013) explored the mechanism underlying ATP release and identified the voltage­gated non­ selective ion channel calcium ho­ meo stasis modulator 1 (CALHM1) as a critical component of this process. A combination of coexpression stud­ ies, RT­PCR analysis, and analyses of mice lacking type II cells revealed that mRNA encoding CALHM1 was present in sweet, bitter, and umami type II cells, but not other taste bud cells. Moreover, whole­cell recordings of single isolated taste bud cells from wild­type and Cahlm1 / mice indi­ cated that CALHM1 mediated a slowly activating nonselective outward cur­ rent in type II cells. Although mice lacking CALHM1 had morphologi­ cally normal taste buds, they showed little if any preference for sweet or umami tastes or avoidance of bitter tastes. Consistent with these behav­ ioral data, gustatory nerve recordings revealed markedly reduced re spon­ s es to stimulation with sweet, bitter, or umami compounds in Calhm1 / mice, but not to sour compounds or salt (NaCl). CALHM1 can be ac­ tivated by decreasing extracellular calcium con centration (as well as by membrane depolarization), and its heterologous expression in various cell types promoted the release of ATP in response to depolarization or exposure to low extracellular cal­ cium concentration. Although basal [Ca 2+ ] i , taste­evoked [Ca 2+ ] i , TRPM5 expression, and voltage­gated Na + currents were comparable in wild­ type and Cahlm1 / type II cells, as was taste bud ATP content, CALHM1 knockout led to the loss of taste­ evoked ATP release. The authors thus propose that CALHM1 medi­ ates the release of ATP from type II cells, in a mechanism crucial to the perception of sweet, bitter, and umami tastes. Rewarding memories of caffeine? Bitter …