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    Pictured above: Figure 4 of the article, "Repeated threat (without direct harm) alters metabolic capacity in select regions that drive defensive behavior," highlighted below. 

    Established in 1976, Neuroscience is the flagship journal of IBRO and is overseen by the IBRO Publications CommitteeElsevier publishes 28 issues per year. 

    The journal features papers describing the results of original research on any aspect of the scientific study of the nervous system. Any paper, however short, is considered for publication provided that it reports significant, new and carefully confirmed findings with full experimental details.

    READ THE CURRENT ISSUE OF IBRO Neuroscience (vol. 354)  published on 23 June 2017.

    Highlights from this issue include:

    Opioid neurotransmission modulates defensive behavior and fear-induced antinociception in dangerous environments

    (Norberto Cysne Coimbra, Fabrício Calvo, Rafael Carvalho Almada, Renato Leonardo Freitas, Tatiana Paschoalin-Maurin, Tayllon dos Anjos-Garcia, Daoud Hibrahim Elias-Filho, Walter Adriano Ubiali, Bruno Lobão-Soares, Irene Tracey)

    Using elevated mazes and a prey-versus-predator paradigm, researchers investigated the involvement of the endogenous opioid peptide-mediated system in the modulation of anxiety- and panic attack-induced responses and innate fear-induced antinociception in the present work. Wistar rats were intraperitoneally pretreated with either physiological saline or naloxone at different doses and were subjected to either the elevated plus- or T-maze test or confronted by Crotalus durissus terrificus, a venomous pit viper snake (commonly known as a South American rattlesnake). After completing all tests, the naloxone-treated groups exhibited less anxiety/fear-induced antinociception than the control group, as measured by the tail-flick test. These findings demonstrate the anxiolytic and panicolytic-like effects of opioid receptor blockade. In addition, the fearlessness behavior displayed by preys treated with naloxone at higher doses enhanced the defensive behavioral responses of venomous snakes.

    Region-specific aging of the human brain as evidenced by neurochemical profiles measured noninvasively in the posterior cingulate cortex and the occipital lobe using 1H magnetic resonance spectroscopy at 7 T

    (Małgorzata Marjańska, J. Riley McCarten, James Hodges, Laura S. Hemmy, Andrea Grant, Dinesh K. Deelchand, Melissa Terpstra)

    The concentrations of fourteen neurochemicals associated with metabolism, neurotransmission, antioxidant capacity, and cellular structure were measured noninvasively from two distinct brain regions using 1H magnetic resonance spectroscopy. Seventeen young adults (age 19–22 years) and sixteen cognitively normal older adults (age 70–88 years) were scanned. To increase sensitivity and specificity, 1H magnetic resonance spectra were obtained at the ultra-high field of 7 T and at ultra-short echo time. The concentrations of neurochemicals were determined using water as an internal reference and accounting for gray matter, white matter, and cerebrospinal fluid content of the volume of interest. Altogether, the resulting findings shed light on how the human brain ages differently depending on region.

    Murine model and mechanisms of treatment-induced painful diabetic neuropathy

    (Juliet M. Nicodemus, Cynthia Enriquez, Alexandra Marquez, Carlos J. Anaya, Corinne G. Jolivalt)

    Neuropathy is the most common complication of long-term diabetes and approximately 30% of these subjects develop chronic neuropathic pain. A distinct acute, severe form of neuropathic pain, called insulin neuritis or treatment-induced painful neuropathy of diabetes (TIND), may also occur shortly after initiation of intensive glycemic control. The pathological mechanisms leading to TIND, which is mostly unresponsive to analgesics, are not yet understood. In the current study, researchers developed chronic and acute insulin-induced neuropathic pain in mice with type 2 insulin-resistant diabetes. Furthermore, they determined that insulin-induced acute allodynia is independent of glycemia levels, can also be induced with Insulin-like Growth Factor 1 (IGF1) and be prevented by inhibition of AKT, providing evidence of an insulin/IGF1 signaling pathway-based mechanism for TIND. The mouse model is useful for the elucidation of mechanisms contributing to TIND and for the testing of new therapeutic approaches to treat TIND.

     

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