Genetic vasopressin deficiency facilitates performance of a lateralized reaction-time task: altered attention and motor processes.

Brattleboro rats are a variety of the outbred Long-Evans strain that possess a single nucleotide deletion in the second exon of the arginine vasopressin gene, resulting in the synthesis of an altered protein that does not enter the normal secretory pathway. Rats heterozygous (di/+) for the deletion have a partial vasopressin deficiency and exhibit a variety of behavioral and neurochemical alterations compared with normal wild-type Long-Evans rats, which provide evidence for a CNS function for vasopressin. Here, we examined the acquisition and performance of a test of visuospatial attention by di/+ Brattleboro rats and their wild-type Long-Evans control counterparts. Surprisingly, di/+ rats exhibited superior performance of the task compared with wild-type controls; performance differences included greater accuracy of detection of visual target stimuli, faster overall reaction times, and fewer trial omissions. Di/+ rats also exhibited more approaches to the reinforcer receptacle at nonreinforcement times. These results indicate that alterations of vasopressin signaling result in a clear cognitive phenotype, including faster motor initiations and superior choice accuracy in a test of visual attention.