Histochemical Investigation of the Modal Specificity of Taste

Abstract

The taste mechanism was investigated in a primate (Macaca mulatta). Based on the hypothesis that intracellular enzymes contribute to the transduction of tastes to electric impulses by taste cells, a histochemical survey of the activity of several enzymes was made on taste buds from regions of the mouth associated with sweet, salt, sour, and bitter tastes. Considerable differences were noted among the modalities, which confirmed the hypothesis. An exclusively bitter enzyme was identified.

Histochemical staining of cells containing flavoenzyme D-amino acid oxidase based on its enzymatic activity: Application of a coupled peroxidation method.

“…Consequently the method was applicable to observations by both light and electron microscopy. This visible product showed high contrast in comparison with other histochemical methods including the tetrazolium method (12,16,27,38,40,46,47) and the previous coupled-peroxidation method (16) . The cerium method (3,37,41,42) is useful for electron microscopic demonstration of the oxidase activity, but is inapplicable to light microscopy because of the nonvisible product.…”

“…20) . They are based on three general means of detection : the reduction of tetrazolium (12,16,27,38,40,46,47) or ferricyanide (37) during oxidation of the substrate; the coupled peroxidation methods for hydrogen peroxide detection (14,16,(42)(43)(44) or the direct detection of hydrogen peroxide with cerous chloride (3,37,41,42) ; and immunocytochemical methods (39,43). However, it seems that they are not practical as to sensitivity or simplicity.…”

The effects of feeding a zinc‐deficient diet on taste acuity and tongue epithelium in rats

“…The etiology of zinc-deficiency induced hypoguesia is not clearly understood, Mc-Connel & Henkin (1974) discussed various factors including diminished protein synthesis (Gray & Dreosti 1972), which could adversely affect taste bud cells which have a high turnover rate (Beidler & Smallman, 1965), Other potential causes could include altered alkaline phosphatase activity (Leuke et al, 1968), an enzyme found in high concentration in the taste hud membrane (Trefz 1972, Lum & Henkin 1976); alteration of a zinc-containing salivary protein which may be responsible for the development and nutrition of human taste buds (Henkin et al 1975); and po.ssible central nervous system dysfunction related to depletion of the high zinc content in the brain (Crawford & Connor 1972). Catalanotto & Lacy (1977) proposed that the hypoguesia they observed in rats fed a zinc-deficient diet may be related to blockage or coverage of the taste pore region.…”

A histochemical study of APUD ability in the taste buds of experimentally induced zinc‐deficient mice

“…Hetikiti & Aamodt (20) reported that in patients with dysfunetion of taste and smell alkaline phosphatase aetivity of letieoeytes deereased in proportion to the lowering of the serum zine eoneentration levels. Theie arc reports in which researchers observed high alkaline phosphatase aetivity in the superficial layers of the epithelium eovering the gutters of cireumvallate papilla (21) and plasma membranes of taste bud eells (22,23). This observation suggests that in a state of zine delicieney some changes tnay occur in the alkaline phosphatase activity of taste btid cells.…”