This study aimed to elucidate, for the first time, the effects of chronical oral treatment with zinc chloride on the depressant‐like behavior of Wistar rats and correlate them with the neuroendocrine profile promoted by our protocol. Two groups of male Wistar rats (200‐250 g) were treated with zinc chloride (15 mg/kg n=16) or isotonic saline (n=17) during 30 days. The rats were kept in a controlled room temperature with light/dark cycle and food ad libitum. After the treatment, both groups were submitted to a behavioral assessment in an open field (OF), elevated plus maze (EPM) and forced swim (FS) test for five minutes. Moreover, basal plasma corticosterone, triiodothyronine (T3), thyroxine (T4) were measured. Also, iodothyronine deiodinase type 2 (Dio2) activity in brown adipose tissue (BAT) and hippocampus were assessed. In view of our results, chronic treatment with orally zinc chloride does not alter the spontaneously locomotor activity as assessed by OF. However, zinc‐treated group showed anxiolytic effects as shown by less time of grooming (P<0,05), even though the episodes of grooming did not differ between groups. Corroborating the aforementioned anxiolytic effects on OF, zinc treatment reduced the time spent in closed arms (P<0,01) and the number of fecal pellets (P<0,05) on EPM. Yet, zinc‐treated group showed fewer immobilization time compared to control group on FS (P<0,05). Regarding to neuroendocrine profile, zinc‐treated group showed higher plasmatic T3 (P<0,01), however there were no differences on serum corticosterone and T4. Furthermore, there were no differences on Dio2 activity on BAT and hippocampus. We can conclude that chronically treatment with orally zinc chloride provides antidepressant‐like effects and discrete anxiolytic‐like effects during adulthood, presumably by raising plasma T3 level with no involvement of Dio2, taking into account that rodents with signs of depression‐like behavior often present hypothyroidism. Grant Funding Source: FAPERJ/CNPq
Hypothyroidism is the result of inadequate production of thyroid hormone or inadequate action of thyroid hormone in target tissues. Hypothyroidism can be seen secondary to hyperadrenocorticism with an overlapping clinical signs. We intend to demonstrate that clinical symptoms of hypothyroidism secondary to hyperadrenocorticism can be undetectable even if there is already evidence of hormonal disease. Male Wistar rats (~ 280g, n = 7) were submitted to daily subcutaneous administration of 200µg of adrenocorticotropic hormone (0.2ml ACTH 1‐24 synthetic 1mg/ml) or vehicle (NaCl 0,9% 0.2ml) for 7 days. At the end of the experiment, were obtained the values of plasmatic thyroid hormones (TH): T3 (Triiodothyronine) and T4 (Thyroxine) by chemiluminescence method; serum corticosterone, TSH (Thyroid Stimulating Hormone) and hypothalamic and pituitary type 2 deiodinase (D2) by radioimmunoassay technique. ACTH group obtained significant elevated level of corticosterone (p < 0.05) and low levels of HT (p < 0.0001). Despite, TSH levels showed no significant difference between groups, ie, compatible with hypothyroidism secondary to hypercortisolism. Additionally, D2 levels showed no significant differences between groups, demonstrating that those tissues did not represent important sources of reducing HT in our protocol. Although it has been demonstrated hormonal difference between the groups, no clinical signs were detected in ACTH group. These data suggest that the lack of symptoms of hypothyroidism and hyperadrenocorticism in this protocol can be attributed to early of the syndrome, once hormone values could be able to confirm both diseases. Grant Funding Source: Supported by FAPERJ, CNPq and CAPES
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