Contexts exert bi-directional control over relapse to drug seeking. Contexts associated with drug self-administration promote relapse, whereas contexts associated with the absence of self-administration protect against relapse. The nucleus accumbens shell (AcbSh) is a key brain region determining these roles of context. However, the specific cell types, and projections, by which AcbSh serves these dual roles are unknown. Here, we show that contextual control over relapse and abstinence is embedded within distinct output circuits of dopamine 1 receptor (Drd1) expressing AcbSh neurons. We report anatomical and functional segregation of Drd1 AcbSh output pathways during context-induced reinstatement and extinction of alcohol seeking. The AcbSh→ventral tegmental area (VTA) pathway promotes relapse via projections to VTA Gad1 neurons. The AcbSh→lateral hypothalamus (LH) pathway promotes extinction via projections to LH Gad1 neurons. Targeting these opposing AcbSh circuit contributions may reduce propensity to relapse to, and promote abstinence from, drug use.

Introduction Professional identity development is a central aim of medical education, which has been disrupted during COVID-19. Yet, no research has qualitatively explored COVID-19’s impact across institutions or countries on medical students’ identities. Kegan proposes a cognitive model of identity development, where ‘disorientating dilemmas’ prompt student development. Given the potential of COVID-related disruption to generate disorientating dilemmas, the authors investigated the ways in which COVID-19 influenced students’ identity development. Methods The authors conducted an international qualitative study with second year medical students from Imperial College London, and third year students from Melbourne Medical School. Six focus groups occurred 2020–2021, with three to six students per group. Authors analysed data using reflexive thematic analysis, applying Kegan’s model as a sensitising theoretical lens. Results COVID-19 has resulted in a loss of clinical exposure, loss of professional relationships, and a shift in public perception of physicians. Loss of exposure to clinical practice removed the external validation from patients and seniors many students depended on for identity development. Students’ experiences encouraged them to assume the responsibilities of the profession and the communities they served, in the face of conflicting demands and risk. Acknowledging and actioning this responsibility facilitated identity development as a socially responsible advocate. Conclusions Educators should consider adapting medical education to support students through Kegan’s stages of development. Measures to foster relationships between students, patients, and staff are likely necessary. Formal curricula provisions, such as spaces for reflection and opportunities for social responsibility, may aid students in resolving the conflict many have recently experienced.

Olanzapine is a commonly used and effective second-generation antipsychotic agent used for the control of paranoia and agitation in schizophrenia and bipolar disorder as well as in the behavioural and psychological symptoms of dementia. Serious side effects of treatment are uncommon but spontaneous rhabdomyolysis represents a rare complication. We describe here a patient treated with a stable dose of olanzapine for more than 8 years who developed acute severe rhabdomyolysis without an identifiable trigger and without features suggestive of neuroleptic malignant syndrome. The rhabdomyolysis was atypical in its delayed onset and severity with a creatine kinase level of 345 125 U/L, the highest level reported in the available literature. We also describe the clinical manifestations of delayed-onset olanzapine-induced rhabdomyolysis and its differentiation from neuroleptic malignancy syndrome, and we highlight key aspects of management to prevent or minimise further complications such as acute kidney injury.

Foraging, pursuit, and predation rapidly transition into behavioral quiescence during reward capture and consumption. While appetitive-consummatory dissociations are embedded at both psychological and neural levels, the mechanisms controlling switches or transitions between appetitive seeking and consummatory behaviors remain poorly understood. Here we identify the BLA→AcbSh pathway as critical to these transitions by showing that this pathway inhibits the appetitive seeking response in the presence of consummatory demands. Using an appetitive cue-discrimination task in male rats, we show that reward delivery is a significant driver of seeking inhibition and that a BLA→AcbSh pathway mediates this inhibition. This role in suppressing seeking responses during periods of consumption was not due to a general suppression of behavior because responding to other cues during the same test was unaffected. Moreover, it was specific to the BLA→AcbSh pathway, because the contribution of the BLA→AcbC pathway to appetitive switching was distinct and modest. State-dependent silencing of BLA→AcbSh revealed that the modulation of seeking before and after reward delivery are co-dependent. Finally, we found that BLA terminals in AcbSh have functional connectivity to LH-projecting AcbSh neurons, thereby identifying a BLA→AcbSh→LH pathway as a putative route for the rapid regulation of appetitive behaviors. Taken together, these findings suggest that the BLA→AcbSh pathway is a core component of an appetitive switching system, recruited under conditions requiring rapid or dynamic shifts in appetitive behavior, and that this pathway enables these shifts by actively inhibiting seeking.