After weeks of worrying about how the mandatory across-the-board 2013 budget cuts known as the sequester would play out at the National Institutes of Health (NIH), the biomedical research community now has final figures. The bottom line is as grim as expected: The agency’s overall budget will fall by $1.55 billion compared to 2012, to $29.15 billion, a cut of about 5%, according to an NIH notice today. That is essentially what NIH predicted as part of the 5.1% sequestration.

As a result, NIH expects to fund 8283 new and competing research grants this year, a drop of 703, according to this table. That number firms up the “hundreds fewer” awards that NIH officials warned of earlier this year. Including ongoing (already awarded) grants that are ending, the total number of research grants will drop by 1357 to 34,902 awards. The decline “reflects the fact that NIH’s budget is being shrunk due to the new budget and political reality, which is bad news for researchers and the patients they are trying to help,” says Tony Mazzaschi of the Association of American Medical Colleges in Washington, D.C.

NIH will try to keep the size of the average award consistent with 2012; it will not award inflationary increases for future years. The agency also expects to trim continuing grants. Grants that were cut up to 10% earlier this year because of budget uncertainty “may be partially restored,” but probably not to the original commitment level, NIH’s notice says.

To be honest, when I read this article my heart dropped a little because it highlights one of the harsh realities that people in science would rather not think/talk about. I’ve always felt it was a privilege to be able to do science with federal funds but this is still disappointing. I can’t help but think how much harder getting a PhD and a postdoc is going to be :( However, I understand that sometimes you just gotta do what you gotta do and cut corners when and where you have to.

Science is not for the faint of heart. You’ve been warned. 

The day has finally come- I’m finally published and second author on a publication! Most of this work was done as part of my rotation project during my first year in graduate school. These findings (particularly the social behavior data) were my intellectual and technical contribution to the project and they laid the foundation for the NSF GRFP that I wrote in 2010 and was awarded in 2011. I’m extremely happy and proud to be able to share my personal line of research with all of you and I’d love to hear your questions/comments. Thanks for following and go click on the link above to read the full article!

Effects of Early-Life Abuse Differ across Development: Infant Social Behavior Deficits Are Followed by Adolescent Depressive-Like Behaviors Mediated by the Amygdala.

Raineki C, Cortés MR, Belnoue L, Sullivan RM.

Emotional Brain Institute, Nathan Kline Institute, Child Study Center, Child and Adolescent Psychiatry, New York University School of Medicine, Orangeburg, New York 10962.

Abuse during early life, especially from the caregiver, increases vulnerability to develop later-life psychopathologies such as depression. Although signs of depression are typically not expressed until later life, signs of dysfunctional social behavior have been found earlier. How infant abuse alters the trajectory of brain development to produce pathways to pathology is not completely understood. Here we address this question using two different but complementary rat models of early-life abuse from postnatal day 8 (P8) to P12: a naturalistic paradigm, where the mother is provided with insufficient bedding for nest building; and a more controlled paradigm, where infants undergo olfactory classical conditioning. Amygdala neural assessment (c-Fos), as well as social behavior and forced swim tests were performed at preweaning (P20) and adolescence (P45). Our results show that both models of early-life abuse induce deficits in social behavior, even during the preweaning period; however, depressive-like behaviors were observed only during adolescence. Adolescent depressive-like behavior corresponds with an increase in amygdala neural activity in response to forced swim test. A causal relationship between the amygdala and depressive-like behavior was suggested through amygdala temporary deactivation (muscimol infusions), which rescued the depressive-like behavior in the forced swim test. Our results indicate that social behavior deficits in infancy could serve as an early marker for later psychopathology. Moreover, the implication of the amygdala in the ontogeny of depressive-like behaviors in infant abused animals is an important step toward understanding the underlying mechanisms of later-life mental disease associated with early-life abuse.