Sigma agonist 1, 3 di-o-tolyl-guanidine (DTG) on Schizophrenia and Immobility responses

Recently in our laboratory we found that DTG (sigma receptor agonist 1,3-di-o-tolyl-guanidine) sub-chronic administration reduced the hyperlocomotor activity and reversed the neuronal hypotrophy in the prefrontal cortex, amygdala and nucleus accumbens, generated in rats with neonatal ventral hippocampus lesion (nVHL). We also observed that DTG reversed some of the behavioral and neuromorphological effects of nVHL rats, which supports the possibility that DTG has beneficial effects in the management of symptoms of schizophrenia. We also found that DTG had effects on immobility responses, in the unlesioned rats increased the duration of the dorsal immobility but it did not have effect on the duration of immobility elicited by clamping. However, the nVHL increased the duration of immobility elicited by clamping, but did not have effect on the duration of the dorsal immobility. It should be noted that DTG counteracted the increase in the duration of the immobility by clamping produced by nVHL. The increase in the duration of the dorsal immobility produced by DTG was counteracted by nVHL. We suggested that the differential effect on these two immobility responses, is due to they are different varieties of immobility mediated by different mechanisms. Therefore, we believe that this evidence could help us to connect, schizophrenia with immobility reaction, which may be associated or somehow present in catatonic schizophrenia