Effects of the Endocannabinoid Anandamide on the Efficiency of Noradrenergic Neurotransmission in the Amygdaloid Body in
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Effects of the Endocannabinoid Anandamide on the Efficiency of Noradrenergic Neurotransmission in the Amygdaloid Body in Acute Stress in Mice E. E. Anderzhanova,1,2 V. S. Kudrin,1 and S. T. Wotjak3
Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 105, No. 9, pp. 1122–1132, September, 2019. Original article submitted June 2, 2019. Revised version received July 3, 2019. Accepted July 3, 2019. The effects of endocannabinoid neurotransmission on corticosterone secretion by the adrenals and release of noradrenaline in the amygdaloid body during acute stress modeled in the elevated platform test were studied by intracerebral microdialysis in C57Bl/6N mice using the CB1 receptor antagonist rimonabant and the anandamide reuptake inhibitor AM-404. Increases in corticosterone secretion on exposure to rimonabant (3 mg/kg, p.o.) confirmed the role of CB1 receptors in controlling the activity of the hypothalamo-hypophyseal-adrenal (HHA) system and verified their influences on the amplitude but not the duration of hormone secretion. Stress was accompanied by a transient increase in noradrenaline release in the amygdaloid body. AM-404 (3 mg/kg, i.p.) suppressed but did not fully inhibit stress-induced noradrenaline release, decreasing it to control levels. The results obtained here provide evidence that the endocannabinoid anandamide is involved in regulating presynaptic noradrenaline release in the amygdaloid body in conditions of psychological stress. Keywords: acute stress, corticosterone, noradrenaline, endocannabinoids, AM-404, amygdaloid body, microdialysis.
The body’s complex response to stress includes changes to memory processes. The adaptive stress reaction can aid better recall of specific information relating to the stress factor and the context of the stress situation. This allows timely recognition of the threat in the future, and, thus, avoidance or reduction in that threat. Stress also affects the memorization of information which is not directly linked to the determinant of the stress but is temporally associated with it [1]. The final influences of stress on memorization are different (increases or decreases in or no effect on memory) and depend on the overall conditions. This includes the level of activation of the hypothalamo-hypophyseal-adrenal (HHA) system, the modality of the stress, the nature of the information remembered, and the psychophysiological state of the biological object. The effects of these and other
factors provides evidence that there can be an effect on the quantitative and qualitative characteristics of remembering. Studies of the mechanisms involved in mediating the interaction between corticosterone signaling and noradrenergic neurotransmission constitute an important component in studies of the psychophysiology of stress. This is determined by the need to find therapeutic agents which would not suppress memories for the stressor as much as eliminate the resultant adverse emotional response to the context of the stressful situation. In seeking targets fo
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