The effect of mGlu8 deficiency in animal models of psychiatric diseases

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The effect of mGlu8 deficiency in animal models of psychiatric diseases. / Fendt, M.; Bürki, H.; Imobersteg, S. et al.
In: Genes, Brain and Behavior, Vol. 9, No. 1, 02.2010, p. 33-44.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Fendt, M, Bürki, H, Imobersteg, S, van der Putten, H, McAllister, K, Leslie, JC, Shaw, D & Hölscher, C 2010, 'The effect of mGlu8 deficiency in animal models of psychiatric diseases', Genes, Brain and Behavior, vol. 9, no. 1, pp. 33-44. https://doi.org/10.1111/j.1601-183X.2009.00532.x

APA

Fendt, M., Bürki, H., Imobersteg, S., van der Putten, H., McAllister, K., Leslie, J. C., Shaw, D., & Hölscher, C. (2010). The effect of mGlu8 deficiency in animal models of psychiatric diseases. Genes, Brain and Behavior, 9(1), 33-44. https://doi.org/10.1111/j.1601-183X.2009.00532.x

Vancouver

Fendt M, Bürki H, Imobersteg S, van der Putten H, McAllister K, Leslie JC et al. The effect of mGlu8 deficiency in animal models of psychiatric diseases. Genes, Brain and Behavior. 2010 Feb;9(1):33-44. doi: 10.1111/j.1601-183X.2009.00532.x

Author

Fendt, M. ; Bürki, H. ; Imobersteg, S. et al. / The effect of mGlu8 deficiency in animal models of psychiatric diseases. In: Genes, Brain and Behavior. 2010 ; Vol. 9, No. 1. pp. 33-44.

Bibtex

@article{3abcf6bdf42b45b6b3d5fdf4cf474980,

title = "The effect of mGlu8 deficiency in animal models of psychiatric diseases",

abstract = "The metabotropic glutamate receptor subtype 8 (mGlu(8)) is presynaptically located and regulates the release of the transmitter. Dysfunctions of this mechanism are involved in the pathophysiology of different psychiatric disorders. mGlu(8) deficient mice have been previously investigated in a range of studies, but the results are contradictory and there are still many open questions. Therefore, we tested mGlu(8)-deficient animals in different behavioral tasks that are commonly used in neuropsychiatric research. Our results show a robust contextual fear deficit in mGlu(8)-deficient mice. Furthermore, novel object recognition, chlordiazepoxide-facilitated extinction of operant conditioning and the acoustic startle response were attenuated by mGlu(8) deficiency. We found no changes in sensory processing, locomotor activity, prepulse inhibition, phencyclidine-induced changes in locomotion or prepulse inhibition, operant conditioning, conditioned fear to a discrete cue or in animal models of innate fear and post-traumatic stress disorder. We conclude that mGlu(8) might be a potential target for disorders with pathophysiological changes in brain areas where mGlu(8) modulates glutamate and gamma-amino butyric acid (GABA) transmission. Our data especially point to anxiety disorders involving exaggerated contextual fear, such as generalized anxiety disorders, and to conditions with disturbed declarative memory.",

keywords = "Animals, Anxiety Disorders, Chlordiazepoxide, Conditioning (Psychology), Conditioning, Operant, Disease Models, Animal, Extinction, Psychological, Fear, Hyperkinesis, Maze Learning, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity, Pattern Recognition, Visual, Phencyclidine, Receptors, Metabotropic Glutamate, Startle Reaction",

author = "M. Fendt and H. B{\"u}rki and S. Imobersteg and {van der Putten}, H. and K. McAllister and Leslie, {J. C.} and D. Shaw and Christian H{\"o}lscher",

year = "2010",

month = feb,

doi = "10.1111/j.1601-183X.2009.00532.x",

language = "English",

volume = "9",

pages = "33--44",

journal = "Genes, Brain and Behavior",

issn = "1601-183X",

publisher = "Wiley-Blackwell",

number = "1",

}

RIS

TY - JOUR

T1 - The effect of mGlu8 deficiency in animal models of psychiatric diseases

AU - Fendt, M.

AU - Bürki, H.

AU - Imobersteg, S.

AU - van der Putten, H.

AU - McAllister, K.

AU - Leslie, J. C.

AU - Shaw, D.

AU - Hölscher, Christian

PY - 2010/2

Y1 - 2010/2

N2 - The metabotropic glutamate receptor subtype 8 (mGlu(8)) is presynaptically located and regulates the release of the transmitter. Dysfunctions of this mechanism are involved in the pathophysiology of different psychiatric disorders. mGlu(8) deficient mice have been previously investigated in a range of studies, but the results are contradictory and there are still many open questions. Therefore, we tested mGlu(8)-deficient animals in different behavioral tasks that are commonly used in neuropsychiatric research. Our results show a robust contextual fear deficit in mGlu(8)-deficient mice. Furthermore, novel object recognition, chlordiazepoxide-facilitated extinction of operant conditioning and the acoustic startle response were attenuated by mGlu(8) deficiency. We found no changes in sensory processing, locomotor activity, prepulse inhibition, phencyclidine-induced changes in locomotion or prepulse inhibition, operant conditioning, conditioned fear to a discrete cue or in animal models of innate fear and post-traumatic stress disorder. We conclude that mGlu(8) might be a potential target for disorders with pathophysiological changes in brain areas where mGlu(8) modulates glutamate and gamma-amino butyric acid (GABA) transmission. Our data especially point to anxiety disorders involving exaggerated contextual fear, such as generalized anxiety disorders, and to conditions with disturbed declarative memory.

AB - The metabotropic glutamate receptor subtype 8 (mGlu(8)) is presynaptically located and regulates the release of the transmitter. Dysfunctions of this mechanism are involved in the pathophysiology of different psychiatric disorders. mGlu(8) deficient mice have been previously investigated in a range of studies, but the results are contradictory and there are still many open questions. Therefore, we tested mGlu(8)-deficient animals in different behavioral tasks that are commonly used in neuropsychiatric research. Our results show a robust contextual fear deficit in mGlu(8)-deficient mice. Furthermore, novel object recognition, chlordiazepoxide-facilitated extinction of operant conditioning and the acoustic startle response were attenuated by mGlu(8) deficiency. We found no changes in sensory processing, locomotor activity, prepulse inhibition, phencyclidine-induced changes in locomotion or prepulse inhibition, operant conditioning, conditioned fear to a discrete cue or in animal models of innate fear and post-traumatic stress disorder. We conclude that mGlu(8) might be a potential target for disorders with pathophysiological changes in brain areas where mGlu(8) modulates glutamate and gamma-amino butyric acid (GABA) transmission. Our data especially point to anxiety disorders involving exaggerated contextual fear, such as generalized anxiety disorders, and to conditions with disturbed declarative memory.

KW - Animals

KW - Anxiety Disorders

KW - Chlordiazepoxide

KW - Conditioning (Psychology)

KW - Conditioning, Operant

KW - Disease Models, Animal

KW - Extinction, Psychological

KW - Fear

KW - Hyperkinesis

KW - Maze Learning

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Motor Activity

KW - Pattern Recognition, Visual

KW - Phencyclidine

KW - Receptors, Metabotropic Glutamate

KW - Startle Reaction

U2 - 10.1111/j.1601-183X.2009.00532.x

DO - 10.1111/j.1601-183X.2009.00532.x

M3 - Journal article

C2 - 19740090

VL - 9

SP - 33

EP - 44

JO - Genes, Brain and Behavior

JF - Genes, Brain and Behavior

SN - 1601-183X

IS - 1

ER -

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