Featured Research Papers - The Intramural Research Program of the National Institute on Drug Abuse

Skip Navigation

Featured Research Papers

A figure from this month's paper.
A figure from this month's paper.

Featured Paper Archives
Featured paper of the Month!

May's Featured Paper!

Central role for the insular cortex in mediating conditioned responses to anticipatory cues

PNAS January 27, 2015 vol. 112 no. 4 1190-1195

Ikue Kusumoto-Yoshida, Haixin Liu, Billy T. Chea, Alfredo Fontanini, and Antonello Bonci

Reward-related circuits are fundamental for initiating feeding on the basis of food-predicting cues, whereas gustatory circuits are believed to be involved in the evaluation of food during consumption. However, accumulating evidence challenges such a rigid separation. The insular cortex (IC), an area largely studied in rodents for its role in taste processing, is involved in representing anticipatory cues. Although IC responses to anticipatory cues are well established, the role of IC cue-related activity in mediating feeding behaviors is poorly understood. Here, we examined the involvement of the IC in the expression of cue-triggered food approach in mice trained with a Pavlovian conditioning paradigm. We observed a significant change in neuronal firing during presentation of the cue. Pharmacological silencing of the IC inhibited food port approach. Such a behavior could be recapitulated by temporally selective inactivation during the cue. These findings represent the first evidence, to our knowledge, that cue-evoked neuronal activity in the mouse IC modulates behavioral output, and demonstrate a causal link between cue responses and feeding behaviors.

You can read more about this paper at the website for PNAS.

April's Featured Paper!

An in vitro model of human neocortical development using pluripotent stem cells: cocaine-induced cytoarchitectural alterations

DMM 2014 vol. 7 no. 12 1397-1405

Abigail A. Kindberg, Raphael M. Bendriem, Charles E. Spivak, Jia Chen, Annelie Handreck, Carl R. Lupica, Jinny Liu, William J. Freed, and Chun-Ting Lee

You can read more about this paper at the website for Disease Models & Mechanisms.

March's Featured Paper!

Functional selectivity of allosteric interactions within G protein-coupled receptor oligomers: the dopamine D1-D3 receptor heterotetramer.

Mol Pharmacol. 2014 Oct;86(4):417-29.

Xavier Guitart, Gemma Navarro, Estefania Moreno, Hideaki Yano, Ning-Sheng Cai, Marta Sánchez-Soto, Sandeep Kumar-Barodia, Yamini T. Naidu, Josefa Mallol, Antoni Cortés, Carme Lluís, Enric I. Canela, Vicent Casadó, Peter J. McCormick, and Sergi Ferré

You can read more about this paper at the website for PubMed.

Related Information...

IRP Training Opportunities...


2009 Postbacs
Postdoc, Predoc, Postbac and Summer Student training opportunities available!


2009 Summer Students
Research & Training Program for Under-represented Populations

A figure from this paper.
A figure from this paper.

Hot off the Press Archives
Featured paper of the Month!

Sigma-1 receptor regulates Tau phosphorylation and axon extension by shaping p35 turnover via myristic acid

PNAS May 11, 2015, doi: 10.1073/pnas.1422001112

Shang-Yi A. Tsai, Michael J. Pokrass, Neal R. Klauer, Hiroshi Nohara, and Tsung-Ping Su

Dysregulation of cyclin-dependent kinase 5 (cdk5) per relative concentrations of its activators p35 and p25 is implicated in neurodegenerative diseases. P35 has a short t½ and undergoes rapid proteasomal degradation in its membrane-bound myristoylated form. P35 is converted by calpain to p25, which, along with an extended t½, promotes aberrant activation of cdk5 and causes abnormal hyperphosphorylation of tau, thus leading to the formation of neurofibrillary tangles. The sigma-1 receptor (Sig-1R) is an endoplasmic reticulum chaperone that is implicated in neuronal survival. However, the specific role of the Sig-1R in neurodegeneration is unclear. Here we found that Sig-1Rs regulate proper tau phosphorylation and axon extension by promoting p35 turnover through the receptor’s interaction with myristic acid. In Sig-1R–KO neurons, a greater accumulation of p35 is seen, which results from neither elevated transcription of p35 nor disrupted calpain activity, but rather to the slower degradation of p35. In contrast, Sig-1R overexpression causes a decrease of p35. Sig-1R–KO neurons exhibit shorter axons with lower densities. Myristic acid is found here to bind Sig-1R as an agonist that causes the dissociation of Sig-1R from its cognate partner binding immunoglobulin protein. Remarkably, treatment of Sig-1R–KO neurons with exogenous myristic acid mitigates p35 accumulation, diminishes tau phosphorylation, and restores axon elongation. Our results define the involvement of Sig-1Rs in neurodegeneration and provide a mechanistic explanation that Sig-1Rs help maintain proper tau phosphorylation by potentially carrying and providing myristic acid to p35 for enhanced p35 degradation to circumvent the formation of overreactive cdk5/p25.

More about this paper

Mesopontine median raphe regulates hippocampal ripple oscillation and memory consolidation

Nat Neurosci. 2015 Apr 13. doi: 10.1038/nn.3998. [Epub ahead of print]

Dong V Wang, Hau-Jie Yau, Carl J Broker, Jen-Hui Tsou, Antonello Bonci, and Satoshi Ikemoto

More about this paper

Clonidine Maintenance Prolongs Opioid Abstinence and Decouples Stress From Craving in Daily Life: A Randomized Controlled Trial With Ecological Momentary Assessment

Am J Psychiatry. 2015 Mar 17:appiajp201414081014. [Epub ahead of print]

Kowalczyk WJ, Phillips KA, Jobes ML, Kennedy AP, Ghitza UE, Agage DA, Schmittner JP, Epstein DH, Preston KL.

More about this paper

Health and Human Services Logo National Institute on Drug Abuse Logo


The National Institute on Drug Abuse (NIDA), is part of the National Institutes of Health (NIH), the principal biomedical and behavioral research agency of the United States Government. NIH is a component of the U.S. Department of Health and Human Services.

PDF documents require the free Adobe Reader. Microsoft Word documents require the free Microsoft Word viewer. Microsoft PowerPoint documents require the free Microsoft PowerPoint viewer. Flash content requires the free Adobe Flash Player.