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Second-generation antipsychotics are frequently prescribed to adolescents, but the long-term consequences of their use remain understudied. These medications work via monoamine neurotransmitter systems, especially dopamine and serotonin, which undergo considerable development and pruning during adolescence. Dopamine and serotonin are linked to a wide host of behaviors, including impulsive choice and behavioral plasticity. In a murine model of adolescent antipsychotic use, male C57BL/6 mice were exposed to either 2.5 mg/kg/day risperidone or 5 mg/kg/day olanzapine via drinking water from postnatal days 22-60. To determine whether the adolescent period was uniquely sensitive to antipsychotic exposure, long-term effects on behavior were compared to an equivalently exposed group of adults where mice were exposed to 2.5 mg/kg risperidone from postnatal days 101-138. Motor activity and body weight in adolescent animals were assessed. Thirty days after exposure terminated animal's behavioral flexibility and impulsive choice were assessed using spatial discrimination reversal and delay discounting. Antipsychotic exposure produced a modest change in behavior flexibility during the second reversal. There was a robust and reproducible difference in impulsive choice: exposed animals devalued the delayed alternative reward substantially more than controls. This effect was observed both following adolescent and adult exposure, indicating that an irreversible change in impulsive choice occurs regardless of the age of exposure., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Extended pausing during discriminable transitions from rich-to-lean conditions can be viewed as escape (i.e., rich-to-lean transitions function aversively). Thus, an anxiolytic drug would be predicted to mitigate the aversiveness and decrease pausing. In the current experiment, pigeons' key pecking was maintained by a multiple fixed-ratio fixed-ratio schedule of rich (i.e., larger) or lean (i.e., smaller) reinforcers. Intermediate doses (3.0-10.0 mg/kg) of chlordiazepoxide differentially decreased median pauses during rich-to-lean transitions. Relatively small decreases in pauses occurred during lean-to-lean and rich-to-rich transitions. Effects of chlordiazepoxide on pausing occurred without appreciable effects on run rates. These findings suggest that signaled rich-to-lean transitions function aversively., (© 2021 Society for the Experimental Analysis of Behavior.)

Corticocortical fiber projections of the striate and occipital cortex of the rabbit, as degined by Rose ("31), have been determined by fiber degeneration methods following the production of cortical lesions within each of 24 rabbits. We have assumed that the striate and occipital cortices correspond respectively to the visual cortical areas 1 and 2 (VI and V2) which have been demarcated electrophysiologically by Thompson et al. ("50). A study of the ipsilateral fiber projections of the striate and occipital cortex of the rabbit reveals three distinct sets of associational corticocortical connections. (1) Neurons located in layers I-III of all regions of the striate cortex and the occipital cortex send fibers to terminate prodominantly in layer V, but also in layers IV and VI, immediately beneath the cells of origin; however, the cells in the supragranular layers have not been found to send fibers to any other region of cerebral cortex. (2) The binocular portions of VI and V2 appear to be interconnected ipsilaterally since cells in layers IV-VI of the lateral striate cortex have been shown to project to all layers of a restricted, adjacent portion of the medial occipital cortex; and the cells in layers IV-VI of medial occipital cortex send a similar, restricted projection to the adjacent lateral striate cortex. (3) Nerve cells in layers IV-VI of the lateral striate cortex (binocular VI) send a restricted projection to the lateral portion of the occipital cortex. (4) After all lesions of the striate and/or occipital cortices, degenerating fibers are seen radiating away from the lesion in layer I; the origin of these degenerating fibers could not be determined. The following observations have been made concerning the origins and terminations of commissural corticortical fibers. (1) after ablation of most of the visual cortex of one side, commissural fibers are seen to terminate in all cortical layers in two narrow bands of visual cortex: one band occupies both sides of the striate-occipital boundary; the second band is found in the lateral portion of occipital cortex. (2) More punctate lesions reveal that commissural fibers arise from layers IV-VI of the lateral striate cortex and medial occipital cortex (binocular portions of V1 and V2 respectively) and end in homotopic areas of the contralateral cortex.