Taurine Deficiency in the Rat and Cat: Effects on Neurotoxic and Biochemical Actions of Kainate

Abstract

Taurine occurs at high concentration in the brain and has been suspected to be a major inhibitory transmitter. However, only a compound that fulfils all the criteria for transmitter identification can be considered to play this role. One important criterion is that the pharmacological actions of the proposed transmitter be mimicked by the endogenous substance. This, in fact, has been demonstrated for taurine only in the cerebellar cortex (16). Thus, the present state of knowledge does not support a general transmitter role for taurine. Since taurine affects so many different processes in the brain, a “neuromodulator” function has been proposed. The fact that an exogenously added agent influences a process is not necessarily relevant for its normal function. A better understanding of the physiological role for a substance may come from studies where the endogenous level of that compound has been lowered, and physiological perturbations are observed. One of the chief reasons why so little is known about taurine function is that this experimental approach is difficult. There are presently two ways to deplete endogenous taurine selectively. One is to administer the taurine uptake blocker 2-guanidinoethane sulfonate (GES) to rodents (5), and the other is to feed cats a taurine-deficient diet (21,23). The first approach is inexpensive and comparatively rapid, but involves introduction of a neuroactive agent (15) which accumulates in the brain (5,11,12) and may have side-effects. The second approach leads to a more severe taurine depletion, but it is expensive and time-consuming. In both cases the treatment has to be carried out chronically. Adaptive changes may be induced and might indeed be anticipated if taurine has an important function. One such possibly homeostatic alteration is the claimed enhancement of Na⁺-independent binding of taurine after GES treatment (11).