] c 8.9 ± 0.7% and 3.8 ± 0.3%, while decreasing normoxic whole-cell NMDAR currents by 41.1 ± 6.7% and 55.4 ± 10.2%, respectively. These changes were also blocked by 5HD or glibenclamide, BAPTA, or spermine. Blockade of mitochondrial Ca 2+ -uptake decreased normoxic NMDAR currents 47.0 ± 3.1% and this change was blocked by BAPTA but not by 5HD. Taken together, these data suggest mK ATP channel activation in the anoxic turtle cortex uncouples mitochondria and reduces mitochondrial Ca 2+ uptake via the uniporter, subsequently increasing [Ca 2+ ] c and decreasing NMDAR activity.

Sexually selected traits that are costly are predicted to be more condition dependent than nonsexually selected traits. Assuming resource limitation, increased allocation to a sexually selected trait may also come at a cost to other fitness components. To test these predictions, we varied adult food ration to manipulate condition in the colour dimorphic bug, Phymata americana. We compared the degree of condition dependence in a sexually selected trait expressed in males to a nonsexually selected trait expressed in males and females. We also evaluated the effects of condition on longevity of both sexes. We found that the expression of these colour pattern traits was strongly influenced by both diet and age. As expected, the strength of condition dependence was much more pronounced in the sexually selected, male‐limited trait but the nonsexual trait also exhibited significant condition dependence in both sexes. The sexually selected male trait also exhibited a higher coefficient of phenotypic variation than the nonsexually selected trait in males and females. Diet had contrasting effects on male and female longevity; increased food availability had positive effects on female lifespan but these effects were not detected in males, suggesting that males allocated limited resources preferentially to sexually selected traits. These results are consistent with the expectation that optimal allocation to various fitness components differs between the sexes.

Periods of restricted growth during early development are expected to have detrimental effects on subsequent metrics of fitness, most prominently increases in age and decreases in size at maturity. However, in some cases, animals may compensate by altering foraging effort, growth efficiency, or patterns of resource allocation between critical traits prior to maturation. Yet, even when compensation for age and size is complete, brief periods of restricted growth may carry costs persisting in the long term, and compensatory tactics may themselves be costly. We investigated the long-term costs of early growth restriction and mechanisms of compensatory growth in the damselfly Ischnura verticalis (Say, 1839). Larvae were temporarily exposed to one of three feeding regimes in the early stages of development, after which food levels were restored. In the period of unrestricted growth prior to emergence, partial compensation for structural size in the lowest food treatment was observed, while both resource-limited groups accelerated mass gain relative to controls. Changes in food consumption and food conversion efficiency were ruled out as mechanisms for accelerating growth following diet restriction. We tested for changes in resource allocation patterns that could explain the observed compensatory growth and found that adult body shape may depend on early growth conditions in females. There was no evidence of detrimental effects on immune function at emergence, although males tended to have higher phenoloxidase activity (a measure of immunocompetence) than females.

Unlike anoxia‐sensitive mammals the western painted turtle survives prolonged periods of anoxia. Likely key is the ability to acutely decrease N‐methyl‐D‐aspartate receptor (NMDAR) activity with the onset of anoxia. Recently, we have shown that mitochondrial KATP channels (mKATP) regulate NMDARs in the anoxic turtle cortex via a Ca2+‐based mechanism. We hypothesized that mKATP activation in anoxia partially uncouples the mitochondrial membrane potential (Δψm), reducing the activity of the Ca2+ uniporter and thereby altering cellular Ca2+ homeostasis and subsequently NMDAR activity. NMDAR activity was measured using the whole‐cell patch‐clamp technique and cellular Ca2+ was measured fluorescently. Mitochondrial uncoupling was measured via the rates of oxygen consumption and ATP synthesis and by changes in (Δψm. Activation of mKATP partially uncoupled mitochondria 9–14% and partially depolarized (Δψm. Ca2+ fluorescence increased and NMDAR currents decreased with anoxia, mKATP activation and uniporter blockade. These changes were abolished by activation of the uniporter. mKATP blockade abolished the anoxic and mKATP mediated changes but not those mediated by the uniporter. These data show that the anoxic attenuation of the NMDARs is mediated by mitochondrial Ca2+ handling, which is in turn modulated by mKATP activity. Supported by an NSERC Grant to LTB.