FAIR SCI Ahead: The Evolution of the Open Data Commons for Pre-Clinical Spinal Cord Injury Research.

Over the last 5 years, multiple stakeholders in the field of spinal cord injury (SCI) research have initiated efforts to promote publications standards and enable sharing of experimental data. In 2016, the National Institutes of Health/National Institute of Neurological Disorders and Stroke hosted representatives from the SCI community to streamline these efforts and discuss the future of data sharing in the field according to the FAIR (Findable, Accessible, Interoperable and Reusable) data stewardship principles. As a next step, a multi-stakeholder group hosted a 2017 symposium in Washington, DC entitled "FAIR SCI Ahead: the Evolution of the Open Data Commons for Spinal Cord Injury research.

CCDC141 Mutation Identified in Anosmic Hypogonadotropic Hypogonadism (Kallmann Syndrome) Alters GnRH Neuronal Migration.

The first mutation in a gene associated with a neuronal migration disorder was identified in patients with Kallmann Syndrome, characterized by hypogonadotropic hypogonadism and anosmia. This pathophysiological association results from a defect in the development of the GnRH and the olfactory system. A recent genetic screening of Kallmann Syndrome patients revealed a novel mutation in CCDC141.

Chloride Accumulators NKCC1 and AE2 in Mouse GnRH Neurons: Implications for GABAA Mediated Excitation.

A developmental "switch" in chloride transporters occurs in most neurons resulting in GABAA mediated hyperpolarization in the adult. However, several neuronal cell subtypes maintain primarily depolarizing responses to GABAA receptor activation. Among this group are gonadotropin-releasing hormone-1 (GnRH) neurons, which control puberty and reproduction.

Metabolic influences on reproduction: adiponectin attenuates GnRH neuronal activity in female mice.

Metabolic dysfunctions are often linked to reproductive abnormalities. Adiponectin (ADP), a peripheral hormone secreted by white adipose tissue, is important in energy homeostasis and appetite regulation. GnRH neurons are integral components of the reproductive axis, controlling synthesis, and release of gonadotropins.

Culturing embryonic nasal explants for developmental and physiological study.

Primary cultures obtained from embryonic nasal placodes can maintain olfactory neurons, olfactory ensheathing cells, and large numbers of gonadotropin releasing hormone-1 (GnRH) neurons. Depending on the age of the starting material, one can examine cell interactions important for placode formation or neuronal migration and axonal outgrowth. When generated at E11.

Neural crest and ectodermal cells intermix in the nasal placode to give rise to GnRH-1 neurons, sensory neurons, and olfactory ensheathing cells.

The origin of GnRH-1 cells and olfactory ensheathing cells has been controversial. Genetic Cre-lox lineage tracing of the neural crest (NC) versus ectodermal contribution to the developing nasal placode was performed using two complementary mouse models, the NC-specific Wnt1Cre mouse line and an ectodermal-specific Crect mouse line. Using these lines we prove that the NC give rise to the olfactory ensheathing cells and subpopulations of GnRH-1 neurons, olfactory and vomeronasal cells.

Behavioral comparisons of the tastes of L-alanine and monosodium glutamate in rats.

Recent research has implicated T1R1/T1R3 as the primary taste receptor in mammals for detecting L-amino acids, including L-monosodium glutamate (MSG) and L-alanine. Previous behavioral studies with rodents found only minimal evidence that these two substances share perceptual qualities, but those studies did not control for the taste of sodium associated with MSG. This study used several behavioral methods to compare the perceptual qualities of MSG and L-alanine in rats, using amiloride (a sodium channel blocker) to reduce the sodium component of MSG taste.

Monosodium glutamate and sweet taste: discrimination between the tastes of sweet stimuli and glutamate in rats.

Generalization of a conditioned taste aversion (CTA) is based on similarities in taste qualities shared by the aversive substance and another taste substance. CTA experiments with rats have found that an aversion to a variety of sweet stimuli will cross-generalize with monosodium glutamate (MSG) when amiloride, a sodium channel blocker, is added to all solutions to reduce the taste of sodium. These findings suggest that the glutamate anion elicits a sweet taste sensation in rats.