An experiment was conducted to investigate the effect of concentrations of certain blood nutrientsensitive metabolites and the resumption of postpartum ovarian cyclicity in 16 Sanga cows (mean BCS 5). Blood samples were taken from cows from weeks 1 to 13 (90 days) postpartum, processed and the plasma progesterone concentration measured to determine the resumption of postpartum ovarian cyclicity. The cows were classified as having resumed ovarian cyclicity when a plasma progesterone concentration of ≥1.0 ng/mL was recorded for two consecutive weekly samples. Based on the resumption of ovarian activity, cows were classified as early cycling, late cycling or non-cycling. The plasma glucose, cholesterol, total protein, albumin and globulin concentrations recorded were similar in the early cycling, late cycling and non-cycling cows. The mean blood glucose, cholesterol, total protein, albumin and globulin concentrations were 3.60 mmol/L, 2.47 mmol/L, 83.1 g/L, 29.9 g/L and 52.9 g/L, respectively. Plasma urea concentrations in late (6.57 ± 0.17 mmol/L) and non-cycling (6.59 ± 0.17 mmol/L) cows were higher than in the early cycling (5.99 ± 0.17 mmol/L) cows in weeks 1 to 13 postpartum. In addition, the plasma creatinine concentration in the early cycling cows was higher than in late cycling cows (101.8 ± 1.82 versus 94.0 ± 1.99 mmol/L). Cows with higher plasma concentrations of urea and lower creatinine concentrations were at risk of delayed resumption of postpartum ovarian cyclicity. Results suggest poor nutritional status, especially energy deficiency, as a major underlying factor suppressing the postpartum resumption of ovarian cyclicity.

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The physiological basis of seasonal breeding in the guinea fowl (Numida meleagris) still remains unknown, despite the socioeconomic importance of these birds, particularly in Ghana. A study involving a total of 50 local guinea cocks was conducted, and documented gross anatomical and histological differences in the reproductive organs of breeding and non-breeding male guinea fowls. The study also compared peripheral testosterone concentrations in breeding and non-breeding cocks. Seasonal differences in variables measured were determined using two-tailed t-test/Mann-Whitney U-test. All comparisons were made at 5% level of significance. Breeding males had significantly (P = 0.000) higher anatomical biometric parameters than their non-breeding counterparts. Also, breeding birds had thicker (P = 0.000) phalli than their non-breeding counterparts. Histologically, regressing testis was characterized by the presence of sloughed off cells and increased debris in the tubular lumen and within the excurrent duct system, collapsed tubules and reduction in tubular lumen. Germ and Sertoli cell populations and nuclear diameters and actual seminiferous tubular diameter and length in regressing testes were significantly (P = 0.000) lower than in active testes. Leydig cell nuclear diameters and populations were also significantly (P = 0.000) reduced. Relative volume of seminiferous tubules in the testis, testicular sperm production/mg testis and per testis and peripheral testosterone concentrations were all higher (P < 0.05) in breeding than non-breeding testis. The ducts in the epididymal region also saw significant (P < 0.05) reductions in luminal diameters in non-breeding birds. Significant regression in anatomical and histological structures of the guinea cock reproductive tract occurred during the non-breeding season, and lower peripheral testosterone concentrations may be responsible for this phenomenon.

These experiments were conducted to determine if 1) syndyphalin-33 (SD33), a mu-opioid receptor ligand, affects feed intake; 2) SD33 effects on feed intake are mediated by actions on opioid receptors; and 3) its activity can counteract the reduction in feed intake associated with administration of bacterial endotoxin. In Exp. 1, 5 mixed-breed, castrate male sheep were housed indoors in individual pens. Animals had ad libitum access to water and concentrate feed. Saline (SAL; 0.9% NaCl) or SD33 (0.05 or 0.1 micromol/kg of BW) was injected i.v., and feed intake was determined at 2, 4, 6, 8, 24, and 48 h after the i.v. injections. Both doses of SD33 increased (at least P < 0.01) feed intake at 48 h relative to saline. In Exp. 2, SAL + SAL, SAL + SD33 (0.1 micromol/kg of BW), naloxone (NAL; 1 mg/kg of BW) + SAL, and NAL + SD33 were injected i.v. Food intake was determined as in Exp. 1. The SAL + SD33 treatment increased (P = 0.022) feed intake at 48 h relative to SAL + SAL. The NAL + SAL treatment reduced (at least P < 0.01) feed intake at 4, 6, 8, 24, and 48 h, whereas the combination of NAL and SD33 did not reduce feed intake at 24 (P = 0.969) or 48 h (P = 0.076) relative to the saline-treated sheep. In Exp. 3, sheep received 1 of 4 treatments: SAL + SAL, SAL + 0.1 micromol of SD33/kg of BW, 0.1 microg of lipopolysaccharide (LPS)/kg of BW + SAL, or LPS + SD33, and feed intake was monitored as in Exp. 1. Lipopolysaccharide suppressed cumulative feed intake for 48 h (P < 0.01) relative to saline control, but SD33 failed to reverse the reduction in feed intake during this period. These data indicate that SD33 increases feed intake in sheep after i.v. injection, and its effects are mediated via opioid receptors. However, the LPS-induced suppression in feed intake cannot be overcome by the opioid receptor ligand, SD33.

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