Mechanisms of the blocking action of GABA were analyzed in isolated stretch receptor cells of crayfish and lobster. A striking parallelism between the effects of GABA and of neural inhibition has been found. GABA in concentrations near 10-5 M blocks afferent discharges caused by stretch deformation in slowly adapting receptor cells in the crayfish. Lobster cells as a rule require higher concentrations. It is proposed that the following general mechanisms bring about the blocking action of GABA and of the inhibitory neural transmitter when the dendrites and cell body are depolarized by stretch, an impulse is set up in the axon near the cell body. GABA and the neural transmitter increase the conductance within the cell, thereby reducing the stretch depolarization reaching the site of impulse origin. Thus the excitatory "drive" (or "generator potential") which leads to the setting up of conducted impulses is effectively reduced or removed, although the excitatory stimulus persists. If the cell is at rest, application of GABA or inhibitory impulses need not change the membrane potential, although the inhibitory process is fully active. In increasing concentrations GABA reduces and eventually abolishes the inhibitory synaptic potentials. This effect is brought about by the progressively increasing hyperpolarizing action of GABA which drives the cell membrane to an equilibrium level which is usually 10-15 times threshold for block GABA has a dual action; it first hyperpolarizes and then depolarizes the receptor cell. At near threshold concentrations GABA not only reduces the inhibitory synaptic potential peak but also accelerates its falling phase. GABA has the same effect on the after-positivities of antidromic impulses. Their hyperpolarization peaks are reduced and the recovery phases are shortened. The acceleration of the time course of these potentials is interpreted as an increased conductance to specific ions in the dendrites and cell body. Concentrations even 1000 times threshold for block do not affect axon conduction or change appreciably the axon time constants. If K+ in the extracellular solution is reduced or absent, the hyperpolarizing action of GABA and of the neural inhibitory transmitter is increased. This parallel effect suggests a common GABA solution still surrounds the cells. Such a recovery is prevented if the fluid around the cell is kept stirred or is periodically replaced by a fresh solution of the same concentration. These results indicate that GABA is inactivated by the tissue. Gamma guanidinobutyric acid which also blocks discharges by a similar mechanism as GABA is not inactivated in a similar manner. GABA blocks in the lobster the 7th median thoracic receptor which histologically has no inhibitory synapses. Its action, therefore, is not confined to subsynaptic inhibitory areas. It is suggested that part at least of the GABA action takes place in the large portion of dendrites and in the cell body. Although GABA is found in the nervous system, the role of an inhibitory transmitter cannot be assigned to it on the basis of available evidence.