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Updated: Jul 6, 2026

A Mouse Model of Subchronic and Mild Social Defeat Stress for Understanding Stress-induced Behavioral and Physiological Deficits
Published on: November 24, 2015
Individual differences in schedule-induced polydipsia and the role of gabaergic and dopaminergic systems
M López-Grancha1, G Lopez-Crespo, M C Sanchez-Amate
1Departmento de Neurociencia y Ciencias de la Salud, Universidad de Almería, La Cañada, Almería, Spain.
Rationale:
The research of individual differences has opened new possibilities for better exploring the neurobiological basis of vulnerability to psychopathological disorders.
Objective:
We extended this approach by using schedule-induced polydipsia (SIP).
Methods:
Outbred male Wistar rats were characterized as either high (HD) or low (LD) drinker according to their behavior in SIP. Subsequently, their performance in the elevated plus maze (EPM) was studied for possible differences in anxiety-like behaviors. Finally, the effects of pentylenetetrazol (PTZ), diazepam, d-amphetamine, and cocaine on individual differences in SIP were investigated.
Results:
HD rats acquired SIP faster and reached higher asymptotic levels than LD. Nose pokes, however, were greater in LD. In the EPM, there were no differences between HD and LD animals. Gabaergic drug effects on SIP did not differ between HD and LD rats. Compared to saline, PTZ reduced and diazepam increased water SIP drinking. On the other hand, amphetamine dose-dependently reduced SIP in HD, whereas the highest dose was required to reduce SIP in LD. HD rats also showed reductions in SIP drinking after cocaine administration. However, the effects of these drugs on nose pokes did not differ between HD and LD.
Conclusion:
These data provide novel evidence that individual differences in SIP are not predictive of behavioral reactivity in animal models of anxiety and suggest an important role for the dopaminergic system in such individual differences. These findings point to SIP as a useful animal model for investigating the neurobiological basis of vulnerability to several psychopathologies in which the dopaminergic system is involved.
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