Disrupting the melanin-concentrating hormone receptor 1 in mice leads to cognitive deficits and alterations of NMDA receptor function.

Adamantidis, Antoine Roger; Thomas, Elizabeth; Foidart, Agnès; Tyhon, Amélie; Coumans, Bernard; Minet, Arlette; Tirelli, Ezio; Seutin, Vincent; Grisar, Thierry; Lakaye, Bernard (2005). Disrupting the melanin-concentrating hormone receptor 1 in mice leads to cognitive deficits and alterations of NMDA receptor function. European journal of neuroscience, 21(10), pp. 2837-2844. Blackwell Science 10.1111/j.1460-9568.2005.04100.x

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In order to investigate the physiological properties of the melanin-concentrating hormone (MCH) we have generated and used mice from which the MCH receptor 1 gene was deleted (MCHR1(Neo/Neo) mice). Complementary experimental approaches were used to investigate alterations in the learning and memory processes of our transgenic model. The ability of the knockout strain to carry out the inhibitory passive avoidance test was found to be considerably impaired although no significant differences were observed in anxiety levels. This impaired cognitive property prompted us to explore modifications in N-methyl D-aspartate (NMDA) responses in the hippocampus. Intracellular recordings of CA1 pyramidal neurons in hippocampal slices from the MCHR1(Neo/Neo) mice revealed significantly decreased NMDA responses. Finally, using in situ hybridization we found a 15% reduction in NMDAR1 subunit in the CA1 region. These results show for the first time a possible role for MCH in the control of the function of the NMDA receptor.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology

UniBE Contributor:

Adamantidis, Antoine Roger

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0953-816X

Publisher:

Blackwell Science

Language:

English

Submitter:

Stefanie Hetzenecker

Date Deposited:

11 Jul 2018 15:38

Last Modified:

23 Oct 2019 23:54

Publisher DOI:

10.1111/j.1460-9568.2005.04100.x

PubMed ID:

15926931

BORIS DOI:

10.7892/boris.117274

URI:

https://boris.unibe.ch/id/eprint/117274

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