We investigated the association between a U.S. National Institutes of Health (NIH) R01 applicant’s self-identified race or ethnicity and the probability of receiving an award by using data from the NIH IMPAC II grant database, the Thomson Reuters Web of Science, and other sources. Although proposals with strong priority scores were equally likely to be funded regardless of race, we find that Asians are 4 percentage points and black or African-American applicants are 13 percentage points less likely to receive NIH investigator-initiated research funding compared with whites. After controlling for the applicant’s educational background, country of origin, training, previous research awards, publication record, and employer characteristics, we find that black or African-American applicants remain 10 percentage points less likely than whites to be awarded NIH research funding. Our results suggest some leverage points for policy intervention.

The voltage‐dependent potassium channel subunit Kv2.1 is widely expressed throughout the mammalian CNS and is clustered primarily on the somata and proximal dendrites, but not axons, of both principal neurones and inhibitory interneurones of the cortex and hippocampus. This expression pattern suggests that Kv2.1‐containing channels may play a role in the regulation of pyramidal neurone excitability. To test this hypothesis and to determine the functional role of Kv2.1‐containing channels, cultured hippocampal slices were incubated with antisense oligonucleotides directed against Kv2.1 mRNA. Western blot analysis demonstrated that Kv2.1 protein content of cultured slices decreased > 90 % following 2 weeks of treatment with antisense oligonucleotides, when compared with either control missense‐treated or untreated cultures. Similarly, Kv2.1 immunostaining was selectively decreased in antisense‐treated cultures. Sustained outward potassium currents, recorded in both whole‐cell and outside‐out patch configurations, demonstrated a selective reduction of amplitude only in antisense‐treated CA1 pyramidal neurones. Under current‐clamp conditions, action potential durations were identical in antisense‐treated, control missense‐treated and untreated slices when initiated by low frequency stimulation (0.2 Hz). In contrast, spike repolarization was progressively prolonged during higher frequencies of stimulation (1 Hz) only in cells from antisense‐treated slices. Similarly, action potentials recorded during electrographic interictal activity in the ‘high [K+]o’ model of epilepsy demonstrated pronounced broadening of their late phase only in cells from antisense‐treated slices. Consistent with the frequency‐dependent spike broadening, calcium imaging experiments from single CA1 pyramidal neurones revealed that high frequency Schaffer collateral stimulation resulted in a prolonged elevation of dendritic [Ca2+]i transients only in antisense‐treated neurones. These studies demonstrate that channels containing Kv2.1 play a role in regulating pyramidal neurone somato‐dendritic excitability primarily during episodes of high frequency synaptic transmission.

Neuronal activity influences myelination of the brain, but the molecular mechanisms involved are largely unknown. Here, we report that oligodendrocyte progenitor cells (OPCs) express functional adenosine receptors, which are activated in response to action potential firing. Adenosine acts as a potent neuron-glial transmitter to inhibit OPC proliferation, stimulate differentiation, and promote the formation of myelin. This neuron-glial signal provides a molecular mechanism for promoting oligodendrocyte development and myelination in response to impulse activity and may help resolve controversy on the opposite effects of impulse activity on myelination in the central and peripheral nervous systems.

The Open Researcher & Contributor ID (ORCID) registry presents a unique opportunity to solve the problem of author name ambiguity. At its core the value of the ORCID registry is that it crosses disciplines, organizations, and countries, linking ORCID with both existing identifier schemes as well as publications and other research activities. By supporting linkages across multiple datasets – clinical trials, publications, patents, datasets – such a registry becomes a switchboard for researchers and publishers alike in managing the dissemination of research findings. We describe use cases for embedding ORCID identifiers in manuscript submission workflows, prior work searches, manuscript citations, and repository deposition. We make recommendations for storing and displaying ORCID identifiers in publication metadata to include ORCID identifiers, with CrossRef integration as a specific example. Finally, we provide an overview of ORCID membership and integration tools and resources.