Trauma rates and patterns in specific pathogen free (SPF) rhesus macaque (Macaca mulatta) groups.

There are some predictable patterns of trauma in captive rhesus macaque (Macaca mulatta) social groups. Several factors have been documented to contribute to these patterns, including group formation of unrelated animals, and the establishment of dominance ranks. Here, we report on how socially induced trauma in groups of rhesus monkeys is influenced by the breeding season, numbers of matrilines per group and matriline size. We analyzed 3 years of data collected from veterinary admittance logs for four groups in our specific pathogen free (SPF) breeding colony. Since the groups differed in time from formation, both the numbers of matrilines and the composition of those matrilines were different. Across the four groups, trauma rates were significantly higher during the fall breeding season than the spring and summer months when births occur. The group that was formed most recently, comprised of the greatest number of matrilines but fewest related animals, showed significantly higher rates of trauma than the older social groups. Further, the middle and lowest ranking families received signifincantly higher rates of trauma than the highest ranking families, suggesting a rank-related phenomenon. Additionally, there was a significant negative correlation between numbers of adult females in a matriline and rates of trauma observed in each matriline, but the numbers of adult females are significantly higher in the top ranked families compared to all of the other matrilines. These findings suggest that trauma rates increase during the breeding season and may be exacerbated in recently formed breeding groups that have smaller matrilines and reduced opportunities for social support to mitigate rank-related aggression. Management practices should be devised to ensure adequate matrilineal size to decrease rates of trauma in captive rhesus macaque groups.

Stimulatory adrenocortical effects of a selective estrogen receptor modulator in ovariectomized female macaques.

Here, we report the effects of estrogen and the selective estrogen receptor modulator (SERM) levormeloxifene on adrenocortical measures in ovariectomized female cynomolgus monkeys (Macaca fascicularis). Animals were randomized into one of five treatment groups, each containing 23 to 26 animals: (1) placebo, (2) 0.016 mg/kg 17ß-estradiol (E(2)), (3) 0.5 mg/kg levormeloxifene (L(1)), (4) 1.0 mg/kg levormeloxifene (L(2)), and (5) 5.0 mg/kg levormeloxifene (L(3)). Treatments were administered orally each day for 18 mo. All doses of levormeloxifene resulted in adrenal weights at least 50% greater than placebo (p < .0001 for all). The target dose of levormeloxifene (L(2)) resulted in higher serum concentrations of cortisol (+63%), dehydroepiandrosterone-sulfate (+73%), and androstenedione (+37%) compared with the placebo group (p < .05 for all). In contrast, E(2) resulted in no significant differences in adrenal weight or adrenocortical steroids. Oral E(2) and all SERM doses resulted in similar reductions in serum gonadotropins and at least threefold greater uterine weight versus placebo (p < .0001 for all). Results indicate that the SERM levormeloxifene, in contrast to E(2), may have robust stimulatory effects on adrenocortical hormones in a postmenopausal model. These findings warrant further investigation into long-term SERM effects on adrenocortical function.

Cortisol response to relocation stress in Garnett's bushbaby (Otolemur garnettii).

Relocation of research animals, either within a facility or from one facility to another, is assumed to be stressful. Development of appropriate research methodologies may be facilitated by understanding the extent and duration of the physiological response to relocation stress and whether the stress can be buffered by environmental or social factors, such as the presence of a cagemate. To characterize the response to relocation stress in Garnett's bushbaby, we assessed cortisol concentrations in nine female and six male bushbabies during relocation to a different facility; six of the animals were pair-housed at the time of the move and were moved with their respective cagemates. Fecal cortisol was assessed at three time points: 1) baseline (1 day prior to moving); 2) relocation (the day the animals were relocated); and 3) post-relocation (7 days after relocation). Cortisol concentrations were higher at the relocation time point than at baseline and post-relocation, which did not differ. Cortisol concentration did not differ as a function of having a cagemate during relocation. Although relocation resulted in a significant (P < 0.05) increase in cortisol excretion concentration, the levels returned to baseline within 7 days after the stressor.

Melatonin enhances the in vitro and in vivo repair of severed rat sciatic axons.

This study examines the effects of several experimental compounds [melatonin (MEL), cyclosporin A (CsA), glial-derived neurotrophic factor (GDNF), and methylprednisolone (MP)] on polyethylene glycol (PEG)-induced repair in vitro and/or in vivo by plasmalemmal fusion (PEG-fusion) of sciatic axons severed by crushing. As measured by conduction of compound action potentials (CAPs) through the lesion site, a significantly (p<0.025) higher percentage (75%) of crushed rat sciatic axons can be repaired in vitro by PEG-fusion following exposure to MEL compared to PEG-fusion of severed sciatic axons in control Krebs saline that contains calcium (CTL=20%). In contrast, no other experimental compound (GDNF: 45%; MP: 42%; CsA: 24%) produces a significant improvement in PEG-fusion success compared to CTL. Further, MEL produces significantly (p<0.001) larger peak CAP amplitudes conducted through the lesion site following PEG-fusion compared to CTL or any other experimental compound in vitro. Additionally, MEL significantly (p<0.025) increases the ability to PEG-fuse sciatic axons in vivo, compared to CTL. Finally, PEG-fusion success in vivo is significantly (p<0.01) greater in calcium-free CTL (CTL-Ca) compared to CTL.

Degeneration of mammalian PNS and CNS axons is accelerated by incubation with protein synthesis inhibitors.

Protein synthesis inhibitors (PSIs) increase the rate of degeneration, as measured by compound action potential (CAP) conduction, in segments of rat PNS and CNS axons. Sciatic axonal segments maintained in vitro in Krebs at 37-38 degrees C generate CAPs for 24 h compared to 8 h for axons exposed to Krebs containing two PSIs, 100 microM anisomycin and/or 35 microM cycloheximide. Spinal axonal segments at 37-38 degrees C generate CAPs for 3 h compared to 2 h for axons exposed to Krebs containing PSIs. While cooling (6-9 degrees C) slows degeneration rate, cooled sciatic axons exposed to PSIs exhibit lower peak CAPs compared to cooled control segments (P<0.005).

Cooling enhances in vitro survival and fusion-repair of severed axons taken from the peripheral and central nervous systems of rats.

Severed segments of rat peripheral (PNS; sciatic) and central nervous system (CNS; spinal) axons continue to conduct action potentials when maintained in vitro at 6-9 degrees C for up to 7 (sciatic axons) and 2 days (spinal axons), compared with only 36 h at 37-38 degrees C for sciatic axons and 6 h for spinal axons. These PNS and CNS axonal segments can be crushed and then treated with polyethylene glycol (PEG), resulting in a rapid reconnection (fusion) of the surviving axons at the crush site, as assessed by conduction of action potentials through the crush site within minutes after PEG administration. Severed PNS or CNS axons maintained in vitro at 6-9 degrees C prior to crushing can be successfully PEG-fused for up to 4 and 1.5 days, respectively, compared with only 24 (sciatic) and 3 h (spinal) at 37-38 degrees C. These data demonstrate that cooling significantly increases both the survival time of severed mammalian PNS and CNS axons and the time that severed axons can still be PEG-fused (rejoined) to rapidly re-establish axonal continuity in vitro.