Involvement of hippocampal angiotensin 1 receptors in anxiety-like behaviour of olfactory bulbectomized rats

被引:13
作者
Tashev, Roman [1 ,2 ]
Ivanova, Margarita [3 ]
机构
[1] Med Univ Sofia, Dept Pathophysiol, Sofia, Bulgaria
[2] Bulgarian Acad Sci, Inst Neurobiol, Dept Behav Neurobiol, Sofia, Bulgaria
[3] Med Univ, Dept Physiol & Pathophysiol, Varna, Bulgaria
关键词
AT1; receptors; Hippocampus; Anxiety; Depression; Olfactory bulbectomy; ELEVATED PLUS-MAZE; CAPTOPRIL TREATMENT; MAJOR DEPRESSION; POSITIVE CELLS; CA1; AREA; BRAIN; STRESS; AT(1); ANTAGONIST; EXPRESSION;
D O I
10.1016/j.pharep.2018.03.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: Accumulated evidence suggests that the enhanced brain angiotensin II (Ang II) activity is associated with stress and anxiety. More recent reports demonstrated that Ang II function is elevated in depression, but the role of hippocampal Ang II and its receptors in this state is not well established. The present study investigated the effects of Ang II and losartan (a selective Ang II type 1 receptor antagonist) microinjected into the hippocampal CA1 area on the anxiety-like behavior in rats with a model of depression. Methods: The bilateral olfactory bulbectomy (OBX) was used as a model of depression. The stereotaxic technique was used for bilaterally (right and left) implantation of guide cannulas into CA1 hippocampal area of the OBX rats. The anxiety state of OBX rats was studied using the elevated plus-maze test. Results: Ghe bilateral infusion of Ang II (0.5 mg) did not change the anxiety-like behavior of OBX rats, while losartan (100 mg) showed an anxiolytic-like behavior, by increasing the number and time of open arms entries, the ratio of open/total entries and open/total time and decreasing the number and time of closed arm entries. Conclusions: These findings demonstrated that the inhibition of hippocampal AT1 receptors reduces the anxiety in OBX rats, which indicates involvement of AT1 receptors in the mechanisms of OBX-induced anxiety. (c) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:847 / 852
页数:6
相关论文
共 57 条
[1]  
Ahmed HI, 2011, AJBAS, V5, P738
[2]   Physiological and pathophysiological functions of different angiotensins in the brain [J].
Albrecht, Doris .
BRITISH JOURNAL OF PHARMACOLOGY, 2010, 159 (07) :1392-1401
[3]   Anxiogenic effects in the rat elevated plus-maze of 5-HT2C agonists into ventral but not dorsal hippocampus [J].
Alves, SH ;
Pinheiro, G ;
Motta, V ;
Landeira-Fernandez, J ;
Cruz, APM .
BEHAVIOURAL PHARMACOLOGY, 2004, 15 (01) :37-43
[4]   Peripheral administration of an angiotensin II AT1 receptor antagonist decreases the hypothalamic-pituitary-adrenal response to isolation stress [J].
Armando, I ;
Carranza, A ;
Nishimura, Y ;
Hoe, KL ;
Barontini, M ;
Terrón, JA ;
Falcón-Neri, A ;
Ito, T ;
Juorio, AV ;
Saavedra, JM .
ENDOCRINOLOGY, 2001, 142 (09) :3880-3889
[5]   Angiotensin II AT1 receptor blockade prevents the hypothalamic corticotropin-releasing factor response to isolation stress [J].
Armando, Ines ;
Volpi, Simona ;
Aguilera, Greti ;
Saavedra, Juan M. .
BRAIN RESEARCH, 2007, 1142 :92-99
[6]   Tissue Renin-Angiotensin-Aldosterone Systems: Targets for Pharmacological Therapy [J].
Bader, Michael .
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, 2010, 50 :439-465
[7]   Hypothalamic-pituitary-adrenocortical axis dysregulation in patients with major depression is influenced by the insertion/deletion polymorphism in the angiotensin I-converting enzyme gene [J].
Baghai, TC ;
Schule, C ;
Zwanzger, P ;
Minov, C ;
Zill, P ;
Ella, R ;
Eser, D ;
Oezer, S ;
Bondy, B ;
Rupprecht, R .
NEUROSCIENCE LETTERS, 2002, 328 (03) :299-303
[8]   Behavioral effects of angiotensin II microinjected into CA1 hippocampal area [J].
Belcheva, I ;
Georgiev, V ;
Chobanova, M ;
Hadjiivanova, C .
NEUROPEPTIDES, 1997, 31 (01) :60-64
[9]   Genetic variants in the angiotensin I-converting-enzyme (ACE) and angiotensin II receptor (AT1) gene and clinical outcome in depression [J].
Bondy, B ;
Baghai, TC ;
Zill, P ;
Schule, C ;
Eser, D ;
Deiml, T ;
Zwanzger, P ;
Ella, R ;
Rupprecht, R .
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, 2005, 29 (06) :1094-1099
[10]  
Braszko Jan J., 2003, Journal of Basic and Clinical Physiology and Pharmacology, V14, P323