Stressor induced variations of intracranial self-stimulation from the mesocortex in several strains of mice.

Intracranial self-stimulation (ICSS) from the mesocortex was assessed in BALB/cByJ, C57BL/6J and DBA/2J mice immediately, 24 h and again 168 h following stressor application. Stressor exposure failed to influence ICSS performance in C57BL/6J mice, while self-stimulation performance was reduced among BALB/cByJ mice only in the immediate post-stressor interval. In contrast, DBA/2J mice exhibited reduced rates of responding for brain stimulation at each of the post-stressor intervals. The potential contribution of DA alterations to the strain-dependent variations of ICSS performance induced by uncontrollable footshock are discussed.

Stressor-induced behavioral alterations in intracranial self-stimulation from the ventral tegmental area: evidence for regional variations.

Exposure to uncontrollable footshock reduced responding for electrical brain stimulation (ICSS) from the ventral tegmental area (VTA) of the CD-1 mouse. Such an effect, however, varied with electrode position in the tegmental field. In both a rate-dependent and a current intensity paradigm, ICSS from the dorsal VTA was reduced immediately, 24 hr and 168 hr following exposure to acute uncontrollable footshock. In contrast, ICSS from the ventral VTA was unaffected by the stressor regimen. These data are consistent with the suggestion that a stressor may reduce the rewarding value ordinarily derived from ICSS. Inasmuch as the stressor differentially affected ICSS from the dorsal and ventral tegmentum, these data provide evidence for a functional differentiation within the midbrain tegmental area.

Behavioral characterization of intracranial self-stimulation from mesolimbic, mesocortical, nigrostriatal, hypothalamic and extra-hypothalamic sites in the non-inbred CD-1 mouse strain.

A behavioral analysis of intracranial self-stimulation (ICSS) was provided for mesolimbic/mesocortical, nigrostriatal, hypothalamic and extrahypothalamic sites in the CD-1 mouse. Robust responding and rapid acquisition of mesocortical ICSS appeared dorsally along notably fluorescent sites in rostral and caudal planes. ICSS was diminished demonstrably in medial and ventral positions in posterior planes. Mesolimbic ICSS from the medial and ventral nucleus accumbens (Nas), was accompanied by significant elevations in locomotor activity, corresponding to regions of dopamine (DA) and cholecystokinin co-localization. Stimulation-induced seizures appeared from both the Nas as well as the mesocortex. ICSS from the ventral tegmental field (VTA) was evident along its medial, lateral and dorsal borders with longer pulse durations more likely to elicit responding. Seizure activity was absent from the VTA. Striatal ICSS was conspicuously poor in dorsal and medial locations; regions presumably devoid of tegmental innervation. ICSS emerged from both the ventrocaudal and anteromedial striatum; regions linked to innervation by the dorsolateral and ventromedial VTA. The red nucleus, a previously neglected self-stimulation site supported marked responding for ICSS. Regions supporting rubral ICSS were correlated with thalamic innervation sites; notably the ventrolateral thalamic nucleus and the parafascicular nucleus, regions found to support ICSS. The substantia nigra supported high rates of responding for ICSS when electrode placement was restricted to the dorsomedial portion of the pars compacta. Electrode deviations lateral and dorsal to the substantia nigra pars medialis induced a progressive decline in responding. Hypothalamic sites were found to support significant responding for ICSS, although such performance was frequently associated with seizure induction. Taken together these data (1) provide the first behavioral analysis of ICSS in mice responding from previously unexamined DA sites in the mesolimbic (e.g. VTA, Nas) and nigrostriatal systems (e.g. caudate, red nucleus) (2) suggest an anatomical reconsideration of the assumptions underlying the elicitation of ICSS from the frontal cortex (3) suggest that the neural circuitry underlying thalamic, caudate, rubral and frontal cortical ICSS are interrelated and (4) suggest that the Nas and the frontal cortex, like the hypothalamus, in the mouse appear to be particularly sensitive to stimulation-induced seizures.

Strain-specific effects of inescapable shock on intracranial self-stimulation from the nucleus accumbens.

Responding for electrical stimulation from the nucleus accumbens was assessed in 3 inbred strains of mice (DBA/2J, C57BL/6J and BALB/cByJ) following exposure to uncontrollable footshock. While the operant response was most readily acquired in the DBA/2J strain, exposure to inescapable shock in this strain induced a marked deterioration of self-stimulation responding, which tended to dissipate over a 168-h period. In contrast to these mice, the stressor did not affect self-stimulation responding in the C57BL/6J strain, and produced a transient enhancement of responding in BALB/cByJ mice. It appears that although uncontrollable aversive events may engender an anhedonic effect, such an outcome is strain-dependent. These data suggest the importance of considering individual and genetic differences in the development of animal models of depression.