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EN
Disturbances in the serotonin (5-HT) system and the limbic-hypothalamo-pituitary-adrenal axis (LHPA) have been implicated in the pathophysiology of depression. It is well established that hippocampus is a central component of limbic circuitry that participates in the modulation of cognition, mood and behavior, and is involved in the control of the LHPA axis. Therefore, the hippocampus provides a unique environment to study the interplay between serotonergic system, antidepressants and corticosteroids. Activity of hippocampal cells can be modulated by 5-HT via inhibitory 5-HT1A and excitatory 5-HT4 receptors. Repeated treatment with antidepressants increases the responsiveness of hippocampal pyramidal neurons to the 5-HT1A and attenuates the responsiveness to the 5-HT4 receptor agonists, with a time course which correlates with the delayed onsed of the therapeutic effect of antidepressants in humans. Moreover, repeated corticosterone, which may constitute a model of a prolonged nonadaptable stress, has opposite effect on hippocampal responsiveness to the 5-HT1A and 5-HT4 receptor activation. Such an action results in an enhancement of the 5-HT-mediated inhibition by antidepressants and a reduction in the inhibitory effect of 5-HT by corticosterone which may be relevant to antidepressant/antiaxiety and proaxiety effects, respectively, of both treatments.
EN
The present investigation was performed to study the participation of the specific isozyme of mono-amineoxidase (MAO) during reserpine-modulated release of medullary catecholamines (CAM). This was carried out by pretreatments of pargyline and clorgyline followed by reserpine administration. The findings revealed that the pigeon adrenal contained predominantly MAO-A. Blockade of type B activity by pargyline caused a significant rise in adrenomedullary CAM content in reserpinized pigeons. However, clorgyline (an MAO-A inhibitor) administration followed by reserpine treatment showed no appreciable change in the medullary CAM level, suggesting that type B activity is mainly responsible for reserpine action on the adrenal medulla in the pigeon. In addition, reserpine was also able to decrease the glandular corticosterone content, while pargyline and clorgyline failed to alter this trend in reserpinized pigeons.
EN
Chronic stress and/or glucocorticoid administration produces atrophy of hippocampal neurons. However, evidence of the impact of glucocorticoids on glial cells, especially in both males and females, is limited. In the present study, we investigated the total percentage body weight, hippocampal volume and hippocampal astrocyte numbers following chronic corticosterone treatment in male and female Wistar rats. Males had greater left and right hippocampal volumes overall, but no effect on hippocampal volume was seen after corticosterone treatment. Total body weight was dose-dependently lower in both sexes, but the decrease was more prominent in male rats. Corticosterone treatment dose-dependently increased astrocyte numbers in the CA1 region, but not in the lateral and medial CA3 hippocampal regions. This increase was similar in both male and female rats. The astrogliosis observed following chronic corticosterone may have implications for extrasynaptic communication and neuron-glia interactions and is similar to changes in the astrocytic population observed in aged rats.
EN
This study aimed at verifying a hypothesis that St. John's wort (Hypericum perforatum) alleviates stress-induced memory impairments. Administration of Hypericum perforatum (350 mg kg-1 daily for 21 days) significantly enhanced recall of passive avoidance behavior (PAB), but had no effect on the acquisition of conditioned avoidance responses (CARs). Rats stressed chronically (2 h daily for 21 days) displayed diminished recall of the PAB and this effect was abolished by St John's wort. Chronic administration of the ?equivalent' to the stress dose of exogenous corticosterone (5 mg kg-1 daily for 21 days) also impaired recall of PAB, and this effect was also reversed by Hypericum perforatum. None of our treatments produced significant motor coordination impairments as tested in a ?chimney' test. It appears that H. perforatum prevents stress-induced deterioration of memory in rats.
EN
Adult male mice were kept for one week either one or four animals per cage. Some were maintained under the same social conditions for an additional 9 days (controls); their counterparts were either grouped (4 per cage) or isolated (1 per cage). Changes in housing conditions caused a significant increase of plasma corticosterone measured 30 minutes after separation or grouping of SWISS, C57C3H, and BALB/c but not of C57BL/6 mice. Peritoneal inflammation was induced by i.p. zymosan injection on day 9 after changes in housing conditions when corticosterone was again at its initial level in each group. Peritonitis-connected pain symptoms, exudatory PMN numbers, and cytokine (IL-1_ and MPC-1) and corticosterone levels were compared between animals living in stable social conditions with those shifted 9 days earlier from separation to the group or vice versa. These factors were unaffected by social stress in C57BL/6 mice and in SWISS animals transferred from the group to isolation. In all other instances at least two parameters were significantly different in the post-stressed and control animals, being either enhanced or inhibited. In conclusion, social stress had long-term consequences on the course of inflammation in three out of four investigated strains of mice.
EN
The aim of the current investigation was to ascertain the role of ACTH and adrenal hormones on adrenomedullary and glycemic functions in soft-shelled turtles, Lissemys punctata punctata. All the experiments were carried out on sexually immature animals. Findings revealed that: (1) ACTH administration (0.5 IU/1.0 IU/2.0 IU per 100 g body wt. daily for 10 days) in all doses stimulated adrenomedullary function by increasing medullary cell nuclear diameter with elevations of norepinephrine, epinephrine and blood sugar levels. Only moderate and higher doses (50 mug/100 mug per 100 g body wt. daily for 10 days) of dexamethasone suppressed adrenomedullary activity and blood sugar level by reversing the changes to those of ACTH; the responses were dose-dependent. But these changes were no longer observed after ACTH treatment in dexamethasone (DMS) recipients (DMS: 100mug / 100 g body wt daily for the first 10 days and ACTH: 0.5 IU / 100 g body wt daily for the next 10 days); (2) Only moderate and higher doses (50 mug/100 mug per 100 g body wt daily for 10 days) of corticosterone increased adrenomedullary activity and blood sugar level and the responses were also dose-dependent. But aldosterone treatment in all doses (same as for corticosterone) had no significant effect on the adrenal medulla or blood sugar level; (3) Only moderate and higher doses of norepinephrine or epinephrine (same as for corticosterone) caused adrenomedullary atrophy with depletions of norepinephrine and epinephrine levels but elevated the glycemic level. The findings are briefly discussed.
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