Remarkable variability between males and females occurs for an array of taste-guided behaviors in both rodents and humans. Sex differences have been noted for taste preference, detection thresholds, and reactivity to taste stimuli. Manipulating sex hormones during early postnatal development or altering the amount of circulating estrogen in adulthood can dramatically alter the pattern of these behaviors. Receptors for sex hormones appear to be prominent in several nuclei associated with central gustatory pathways, indicating that steroid hormones may modulate central taste processing. Electrophysiological recordings from the rat brainstem suggest that taste-elicited activity to sweet stimuli is organized by hormones during early development, and activity during bitter stimulation is altered by circulating ovarian hormones. Sex differences in gustatory function appear to emerge at the level of the taste bud. Among ovariectomized rats, estradiol treatment decreases activity in the chorda tympani nerve during NaCl stimulation. Although there is no evidence that chorda tympani responses to NaCl differ between intact male and female rats, glossopharyngeal nerve responses are lower in intact females for both NaCl and sodium acetate. Responses in the glossopharyngeal nerve to citric acid stimulation are also higher in female rats relative to males. These findings suggest that, in addition to differential central modulation of taste input based on sex, taste information from the periphery varies between males and females. Although the extent of sex differences in taste processing and the underlying causal mechanisms require further clarification, it is clear that studying one sex alone provides an incomplete picture of gustatory function. V C 2016 Wiley Periodicals, Inc.
The peripheral taste system of the adult rodent is highly resilient against damage, with morphological, behavioral, and functional recovery evident after regeneration of a transected nerve. If chorda tympani transection (CTX) occurs at early postnatal ages however, the nerve fails to regenerate and effects on tongue morphology and behavior are more severe and longer-lasting compared to adult denervation. To examine whether neonatal CTX induces functional changes in intact nerves, whole-nerve electrophysiology was performed on the glossopharyngeal (GL) and chorda tympani (CT) nerves of adult rats that received CTX at P10. Attenuation of NaCl-elicited GL responses were observed in CTX rats 2 months after surgery, with bilateral denervation causing the largest decreases in responses. When assessed 1 year after neonatal CTX, amiloride-sensitive responses to NaCl in the contralateral CT increased while amiloride-insensitive responses decreased. Responses to other tastants were consistent with control animals. This is the first evidence of long-term functional changes to the peripheral taste system after injury in rats fed a normal diet. This study further characterizes the developing peripheral taste system as highly susceptible to change following neural injury.
We have investigated the effect of oleic (18:1) and 4,7,10,13,16,19-docosahexaenoic (22:6 omega 3) acids on triglyceride (TG) accumulation, secretion and reuptake in rat hepatocytes in culture. We also calculated the percentage of total TG, TG-esterified 18:1 and TG-esterified 22:6 omega 3 that were secreted relative to the total accumulation (intra + extracellular TG). Both fatty acids were incorporated mainly in the intracellular TG fraction. Treatment with 18:1 but not with 22:6 omega 3 increased the quantity of TG secreted into the culture medium relative to controls. Treatment with 22:6 omega 3 caused a greater accumulation of intracellular TG than 18:1. This arises in part from the preferential retention of 22:6 omega 3-enriched TG by the hepatocytes. At 24 hr, there was no longer any difference in the net secretion of TG by 18:1 and 22:6 omega 3-treated cells, which may be a consequence of the reuptake of TG-esterified 18:1. There was no reuptake of TG-esterified 22:6 omega 3. We conclude that inhibition of hepatocyte TG synthesis is not obligatory for 22:6 omega 3-induced diminution of TG secretion.
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