A thermal tolerance polygon over the range of Defactinib 18-30 degrees C resulted in a calculated area of 210.0 degrees C-2. The oxygen consumption rate increased significantly alpha=0.05 with increasing acclimation temperatures between 18 and 30 degrees C. Maximum and minimum temperature

quotients (Q(10)) were observed between 26-30 degrees C and 22-26 degrees C as 3.03 and 1.71, respectively. These results suggest that O. maya has an increased capability for adapting to moderate temperatures, and suggest increased culture potential in subtropical regions southeast of Mexico. (C) 2012 Elsevier Ltd. All rights reserved.”
“Hypobaric hypoxia (HH), an environmental stress resulting from ascent to high altitude, affects perception, memory, judgment, and attention, resulting in degradation IPI-549 of many aspects of normal functioning. Alpha 2A adrenergic agonist, guanfacine proved to be beneficial in the amelioration of neurological outcomes of many neuropsychiatric disorders involving adrenergic imbalance and neurodegeneration.

Adrenergic dysregulation and neuronal damage have been implicated in hypoxia-induced cognitive deficits, however, efficacy of guanfacine as a countermeasure for HH-induced cognitive decline remains to be evaluated. We, therefore, have studied the effect of this drug on the HH-induced cognitive deficits, adrenergic dysfunction and neuronal damage. Rats were exposed to HH at a simulated altitude of 25,000 feet for 7 days and received an IM injection

of either saline or guanfacine at a dose of 1 mg/kg. Adrenergic transmission was evaluated by biomarkers i.e. norepinephrine (NE), dopamine (DA) and tyrosine hydroxylase (TH) in medial prefrontal cortex (PFC) by biochemical and immunohistochemical assays. Spine and dendritic morphology of pyramidal neurons in layer ll of medial PFC was studied using Golgi Cox staining and Neurolucida neuronal tracing. The cognitive performance was assessed by Delayed Alternation Task using a T-Maze. There was a significant reduction in HH-induced increases in NE, DA and TH levels with guanfacine treatment. Guanfacine rescued HH-induced dendritic atrophy and selleck compound mushroom type spine loss. The spatial working memory deficits induced by HH were significantly ameliorated with guanfacine treatment. Furthermore, the cognitive performance showed a positive correlation with dendritic arbors and spine numbers. These results showed that the HH-induced cognitive decline is associated with adrenergic dysregulation and neuronal damage in layer II of medial PFC, and that guanfacine treatment during HH ameliorated these functional and morphological deficits. The study suggests a potential role of the alpha-2A adrenergic agonist, guanfacine, in amelioration of PFC dysfunction caused by high altitude exposure. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.