Analysis of the health economics portfolio funded by the National Institutes of Health in response to published guidance.

Health services, economics, and outcomes research (referred to as health economics research hereinafter) is one of the interdisciplinary sciences that the National Institutes of Health (NIH) supports in order to pursue its overall mission to improve health. In 2015, NIH guidance was published to clarify the type of health economics research that NIH would continue to fund. This analysis aimed to determine if there were changes in the number of health economics applications received and funded by NIH after the release of the guidance.

NIH Music-Based Intervention Toolkit: Music-Based Interventions for Brain Disorders of Aging.

Music-based interventions (MBIs) show promise for managing symptoms of various brain disorders. To fully realize the potential of MBIs and dispel the outdated misconception that MBIs are rooted in soft science, the NIH is promoting rigorously designed, well-powered MBI clinical trials. The pressing need of guidelines for scientifically rigorous studies with enhanced data collection brought together the Renée Fleming Foundation, the Foundation for the NIH, the Trans-NIH Music and Health Working Group, and an interdisciplinary scientific expert panel to create the NIH MBI Toolkit for research on music and health across the lifespan.

Building and Sustaining Community Partnerships: An Organizational Network Analysis in a Low-resource Neighborhood.

Background: Launched in 2012, the Claremont Healthy Village Initiative (CHVI) is a partnership focused on fostering community collaboration, addressing the social determinants of health, and reducing health disparities. Partners include local community centers, schools, after-school programs, health care providers, a health insurer, city agencies, tenant associations, resident leaders, elected officials, and other stakeholders.

Objectives: To understand the development and value of collaboration within the CHVI from the perspective of multiple partners.

Emerging research areas and contributions of NIH in violence research across the lifespan and throughout different settings.

This commentary provides background for NIH's interest in research designed to better understand the causes and consequences of violence and the development, evaluation, and implementation of preventive and treatment interventions to address the resulting trauma, injuries, and mortality from violence. The manuscript describes the context that contributed to a range of initiatives from the NIH focused on violence research, with a particular emphasis on firearms violence prevention research, and opportunities and gaps for future research.

Endocannabinoid genetic variation enhances vulnerability to THC reward in adolescent female mice.

Adolescence represents a developmental period with the highest risk for initiating cannabis use. Little is known about whether genetic variation in the endocannabinoid system alters mesolimbic reward circuitry to produce vulnerability to the rewarding properties of the exogenous cannabinoid Δ-tetrahydrocannabinol (THC). Using a genetic knock-in mouse model (FAAH) that biologically recapitulates the human polymorphism associated with problematic drug use, we find that in adolescent female mice, but not male mice, this FAAH polymorphism enhances the mesolimbic dopamine circuitry projecting from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and alters cannabinoid receptor 1 (CBR) levels at inhibitory and excitatory terminals in the VTA.

Correction: Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca channels.

A correction to this paper has been published and can be accessed via a link at the top of the paper.

Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca channels.

Cocaine-associated memories are critical drivers of relapse in cocaine-dependent individuals that can be evoked by exposure to cocaine or stress. Whether these environmental stimuli recruit similar molecular and circuit-level mechanisms to promote relapse remains largely unknown. Here, using cocaine- and stress-primed reinstatement of cocaine conditioned place preference to model drug-associated memories, we find that cocaine drives reinstatement by increasing the duration that mice spend in the previously cocaine-paired context whereas stress increases the number of entries into this context.

Extinction of Contextual Cocaine Memories Requires Ca1.2 within D1R-Expressing Cells and Recruits Hippocampal Ca1.2-Dependent Signaling Mechanisms.

Exposure to cocaine-associated contextual cues contributes significantly to relapse. Extinction of these contextual associations, which involves a new form of learning, reduces cocaine-seeking behavior; however, the molecular mechanisms underlying this process remain largely unknown. We report that extinction, but not acquisition, of cocaine conditioned place preference (CPP) in male mice increased Ca1.

Cacna1c in the Prefrontal Cortex Regulates Depression-Related Behaviors via REDD1.

The CACNA1C gene that encodes the L-type Ca channel (LTCC) Ca1.2 subunit has emerged as a candidate risk gene for multiple neuropsychiatric disorders including bipolar disorder, major depressive disorder, and schizophrenia, all marked with depression-related symptoms. Although cacna1c heterozygous (HET) mice have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit-level dysfunction remains unknown.

The Neuropsychiatric Disease-Associated Gene cacna1c Mediates Survival of Young Hippocampal Neurons.

Genetic variations in CACNA1C, which encodes the Cav1.2 subunit of L-type calcium channels (LTCCs), are associated with multiple forms of neuropsychiatric disease that manifest high anxiety in patients. In parallel, mice harboring forebrain-specific conditional knockout of cacna1c (forebrain-Cav1.