The composition of carcass and noncarcass tissue growth was quantified by serial slaughter of 26 Angus x Hereford crossbred steers (initial age and weight 289 +/- 4 d and 245 +/- 4 kg) during continuous growth (CON) or compensatory growth (CG) after a period of growth restriction (.4 kg/d) from 245 to 325 kg BW. All steers were fed a 70% concentrate diet at ad libitum or restricted levels. Homogenized samples of 9-10-11th rib and noncarcass tissues were analyzed for nitrogen, fat, ash, and moisture. Growth rate from 325 to 500 kg BW was 1.54 and 1.16 kg/d for CG and CON steers. The weight of gut fill in CG steers was 10.8 kg less (P less than .05) before realimentation and 8.8 kg more (P less than .10) at 500 kg BW than in CON steers. The allometric accretive rates for carcass chemical components relative to the empty body were not affected by treatment. However, the accretive rates for CG steers were greater (P less than .01) for noncarcass protein (.821 vs .265), noncarcass water (.861 vs .507), and empty-body protein (.835 vs. .601) than for CON steers. Final empty-body fat was lower (P less than .001; 24.2 vs 32.4%) and empty-body protein higher (P less than .001; 16.6 vs 14.8%) in CG steers than in CON steers. Consequently, net energy requirements for growth (NEg) were approximately 18% lower for CG steers. We conclude that reduced NEg requirements and changes in gut fill accounted for most of the compensatory growth response exhibited in these steers.

Eight steers from a group of 14 were fed ad libitum from 240 to 510 kg live weight, gaining at 1.4 +/- .2 kg/d. The six other steers were diet-restricted and grew at .37 +/- .09 kg/d from 240 to 307 kg, prior to ad libitum realimentation on the same diet to a final weight of 510 kg. Blood samples taken during the growth phases from both treatments were analyzed for insulin-like growth factor-I (IGF-I), triiodothyronine (T3), thyroxine (T4), glucose (GLU), nonesterified fatty acids (NEFA), and blood urea nitrogen (BUN) and (or) growth hormone (GH). During restricted growth, mean serum concentrations of GH were elevated (45.6 vs 23.4 ng/ml; P less than .05), serum concentrations of IGF-I decreased (108 vs 167 ng/ml; P less than .05) compared with control steers with ad libitum access to feed. Levels of T4 and GLU also were lower (P less than .05) during restricted than during normal growth. During early realimentation, levels of GLU (P less than .05), IGF-I (P less than .01), T4 and BUN (P less than .01) increased. Levels of T3 remained unchanged, whereas concentration of NEFA declined (P less than .001). Blood urea nitrogen decreased during early realimentation despite a large increase in diet protein intake and in protein storage, suggesting an increased efficiency of nitrogen use for protein synthesis. During realimentation, IGF-I levels rose above those of control steers and remained higher at the final weight of 510 kg (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Background and Purpose: Currently, there is no effective drug to treat cocaine-use disorder, which affects millions of people worldwide. Benzodiazepines are potential therapeutic candidates, as microdialysis and voltammetry studies have shown that they can decrease dopamine concentrations in the nucleus accumbens of rodents and block the increase in dopamine levels and appetitive 50-kHz ultrasonic vocalizations (USVs) induced by amphetamine in rats.Experimental Approach: Here, we tested whether administration of 2.5-mgÁkg À1 diazepam (i.p.) in adult male rats could block the effects of 20-mgÁkg À1 cocaine (i.p.) on electrically evoked phasic dopamine signals in the nucleus accumbens measured by fast-scan cyclic voltammetry, as well as 50-kHz USV and locomotor activity.Key Results: Cocaine injection increased evoked dopamine signals up to threefold within 5 min, and the increase was significantly higher than baseline for at least 75 min. The injection of diazepam, 5 min after cocaine, attenuated the cocaine effect by nearly 50%, and this attenuation was maintained for at least 40 min. Behaviourally, cocaine increased the number of appetitive 50-kHz calls by about 12-fold. Diazepam significantly blocked this effect for the entire duration of the session. Also, cocainetreated rats were more active than controls and diazepam significantly attenuated cocaine-induced locomotion, by up to 50%. Conclusion and Implications:These results suggest that the neurochemical and psychostimulant effects of cocaine can be mitigated by diazepam.LINKED ARTICLES: This article is part of a themed issue on Building Bridges in Neuropharmacology. To view the other articles in this section visit http://onlinelibrary.