PMID- 10064799
OWN - NLM
STAT- MEDLINE
DCOM- 19990422
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 821
IP  - 1
DP  - 1999 Mar 6
TI  - Anxiety-like behavior in mice lacking the angiotensin II type-2 receptor.
PG  - 150-9
AB  - The main biological role of angiotensin II type 2 receptor (AT2) has not been 
      established. We made use of targeted disruption of the mouse AT2 gene to examine 
      the role of the AT2 receptor in the central nervous system (CNS). AT2-deficient 
      mice displayed anxiety-like behavior compared with wild-type mice. However, 
      AT2-deficient mice showed no depressant-like activity and no change in 
      hexobarbital-induced sleeping time as compared with findings in wild-type mice. 
      Both noradrenergic and corticotropin-releasing factor (CRF) neuronal systems 
      appear to be involved in this anxiety-like behavior. Diazepam, captopril 
      (angiotensin I converting enzyme inhibitor), prazosin (alpha1 antagonist) 
      reversed the anxiety-like behavior in these AT2-deficient mice, whereas yohimbine 
      (alpha2 antagonist), phenylephrine (alpha1 agonist), clonidine (alpha2 agonist), 
      isoproterenol (beta1/beta2 agonist), propranolol (beta1/beta2 antagonist) and 
      alpha-helical CRF9-41 (CRF receptor antagonist) has no apparent effects on 
      anxiety-like behavior in AT2-deficient mice. In addition, concentrations of 
      plasma adrenocorticotropic hormone (ACTH) and corticosterone in AT2-deficient 
      mice did not differ from these in wild-type mice, hence, there are probably no 
      endocrine abnormalities involving the hypothalamic-pituitary-adrenal axis (HPA). 
      The amygdala appears to play an important role in many of the responses to fear 
      and anxiety. The number of [3H]prazosin but not [125I]CRF binding sites in the 
      amygdala was significantly reduced in AT2-deficient mice. These findings indicate 
      that the noradrenergic system is involved in mediating the anxiety-like behavior 
      in AT2-deficient mice.
CI  - Copyright 1999 Elsevier Science B.V.
FAU - Okuyama, S
AU  - Okuyama S
AD  - 1st Laboratory, Medicinal Research Laboratories, Taisho Pharmaceutical, 1-403, 
      Yoshinocho, Ohmiya 330-8530, Japan.
FAU - Sakagawa, T
AU  - Sakagawa T
FAU - Chaki, S
AU  - Chaki S
FAU - Imagawa, Y
AU  - Imagawa Y
FAU - Ichiki, T
AU  - Ichiki T
FAU - Inagami, T
AU  - Inagami T
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Anesthetics)
RN  - 0 (Receptors, Angiotensin)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenocorticotropic Hormone/blood
MH  - Anesthetics
MH  - Animals
MH  - Anxiety/*physiopathology
MH  - Behavior, Animal/*physiology
MH  - Corticosterone/blood
MH  - Darkness
MH  - Emotions/physiology
MH  - Feces
MH  - Female
MH  - Injections, Intraventricular
MH  - Light
MH  - Male
MH  - Maze Learning/physiology
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Motor Activity/physiology
MH  - Receptors, Angiotensin/*deficiency
EDAT- 1999/03/05 00:00
MHDA- 1999/03/05 00:01
CRDT- 1999/03/05 00:00
PHST- 1999/03/05 00:00 [pubmed]
PHST- 1999/03/05 00:01 [medline]
PHST- 1999/03/05 00:00 [entrez]
AID - S0006-8993(99)01098-7 [pii]
AID - 10.1016/s0006-8993(99)01098-7 [doi]
PST - ppublish
SO  - Brain Res. 1999 Mar 6;821(1):150-9. doi: 10.1016/s0006-8993(99)01098-7.