Vasopressin (AVP)-deficient Brattleboro rats develop a specific behavioral profile,
which-among other things-include altered cognitive performance. This profile is markedly
affected by alterations in neuroendocrine state of the animal such as during lactation.
Given the links between AVP and cognition we hypothesized that AVP deficiency may
lead to changes in impulsivity that is under cognitive control and the changes might
be altered by lactation. Comparing virgin and lactating AVP-deficient female Brattleboro
rats to their respective controls, we assessed the putative lactation-dependent effects
of AVP deficiency on impulsivity in the delay discounting paradigm. Furthermore, to
investigate the basis of such effects, we assessed possible interactions of AVP deficiency
with GABAergic and serotonergic signaling and stress axis activity, systems playing
important roles in impulse control. Our results showed that impulsivity was unaltered
by AVP deficiency in virgin rats. In contrast a lactation-induced increase in impulsivity
was abolished by AVP deficiency in lactating females. We also found that chlordiazepoxide-induced
facilitation of GABAergic and imipramine-induced enhancement of serotonergic activity
in virgins led to increased and decreased impulsivity, respectively. In contrast,
during lactation these effects were visible only in AVP-deficient rats. These rats
also exhibited increased stress axis activity compared to virgin animals, an effect
that was abolished by AVP deficiency. Taken together, AVP appears to play a role in
the regulation of impulsivity exclusively during lactation: it has an impulsivity
increasing effect which is potentially mediated via stress axis-dependent mechanisms
and fine-tuning of GABAergic and serotonergic function.
