Annual behavioral and biochemical patterns of black bears (Ursus americanus), grizzly bears (Ursus arctos horribilis), and polar bears (Ursus maritimus) were reviewed. We propose that black and grizzly bears show 4 annual physiological stages: Stage I-hibernation, in which lean body mass is preserved and body fat supplies energy; Stage II-walking hibernation, in which the biochemistry of hibernation is integrated with physical activity, but food and water intake are minimal; Stage Illnormal activity, in which patterns are consistent with those of nonhibernating mammals; and Stage IV-hyperphagia, which increases fat reserves for hibernation. For polar bears, using published reports and recently collected data, we propose that all 4 stages are possible and that polar bears appear able to shift between Stages I and II in both summer and winter, which permits successful adaptation to the arctic environment. lnt. Conf. Bear Res. and Manage. 5:284-290 Field and laboratory observations of behavior of black and grizzly bears have indicated that they pass through 4 annual biochemical and physiological stages. These have been designated as Stage I-hibernation, Stage II-walking hibernation, Stage III1-normal activity, and Stage IVhyperphagia (Nelson et al. 1979). The purpose of this paper is to further define the 4 stages and to determine, using the literature and experimental data, whether the polar bear corresponds. PHYSIOLOGICAL STAGES OF BLACK AND GRIZZLY BEARS Stage I-Hibernation Studies by Folk (1974) have shown that black and grizzly bears are hibernators in winter in the true sense, showing physiological patterns similar to those of deep hibernators: distinct decreases in heart rate, metabolic rate, and body temperature. However, hibernation in black and grizzly bears differs from that of deep hibernators in that bears hibernate at a near-normal body temperature, 31-35 C, and their dormancy is continuous from 3 to 7 months. Deep hibernators (bats, insectivores, and rodents) hibernate at near 0 C and undergo periodic arousals (Folk 1974). Although expending about 4,000 kcal per day (calculations based on body fat utilization rates),

RIOR REPORTS SUGGESTED THAT rapidly progressive, bilateral, asymmetric inner ear dysfunction may be caused by immunological attack or may be associated with autoimmune disorders. 1-3 McCabe 4 renewed interest in this disorder as a distinct clinical entity and motivated investigators to identify the most efficacious treatment regimens for management of this potentially reversible form of deafness. Initial experience with this disorder has underscored the risk of developing bilateral profound deafness and vestibulopathy if patients are left untreated or treated inadequately.On empirical grounds, glucocorticoids and cytotoxic agents were initially proposed as treatments. In a fol-

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American black bears, Ursus americanus, are seasonal breeders with a mating season in late spring to early summer. The objectives of this study were to determine whether there are seasonal changes in spermatogenesis and immunolocalization of testicular steroidogenic enzymes, and to correlate these changes with peripheral steroid concentrations. Three captive mature bears were maintained in open cages during the summer season and provided with chambers for denning during the winter. Testicular biopsies and blood samples were obtained from anaesthetized bears on 12 March, 15 June, 12 October and 15 January. Steroidogenic enzymes were immunolocalized using polyclonal antisera raised against bovine adrenal cholesterol side-chain cleavage cytochrome P450 (P450scc), human placental 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), porcine testicular 17 alpha-hydroxylase cytochrome P450 (P450c17) and human placental aromatase cytochrome P450 (P450arom). Spermatogenesis changed seasonally: spermatogonia and degenerating spermatocytes were observed in October; spermatogonia and primary spermatocytes were present in January; spermatogonia, spermatocytes and round spermatids were present in March; and spermatogonia through spermatozoa were present in June. P450scc and P450c17 were immunolocalized in spermatids and Leydig cells in June, whereas in October these enzymes were present only in Leydig cells. 3 beta HSD was localized in Leydig cells in June and October with more intense staining in June. Localization of P450arom changed seasonally: no immunostaining in October; positive immunostaining in Sertoli cells in January; more extensive immunostaining in Sertoli cells, peritubular-myoid cells and round spermatids in March; and strong immunostaining in Sertoli cells and round and elongating spermatids in June. Serum testosterone and oestradiol concentrations changed seasonally: testosterone and oestrogen were low in October and January, slightly higher in March, and high in June. The present study demonstrates that in the black bear seasonal changes in spermatogenesis are accompanied by changes in the immunolocalization of testicular steroidogenic enzymes that are correlated with changes in serum testosterone and oestradiol concentrations. The presence of P450arom in Sertoli cells at the beginning of testicular recrudescence suggests that aromatase and oestrogen may play a role in re-initiating spermatogenesis.

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