J 2008

Signaling through cGMP-Dependent Protein Kinase I in the Amygdala Is Critical for Auditory-Cued Fear Memory and Long-Term Potentiation

PAUL, Cindy; Florian SCHOEBERL; Pascal WEINMEISTER; Vincenzo MICALE; Carsten T WOTJAK et al.

Základní údaje

Originální název

Signaling through cGMP-Dependent Protein Kinase I in the Amygdala Is Critical for Auditory-Cued Fear Memory and Long-Term Potentiation

Autoři

PAUL, Cindy; Florian SCHOEBERL; Pascal WEINMEISTER; Vincenzo MICALE; Carsten T WOTJAK; Franz HOFMANN a Thomas KLEPPISCH

Vydání

JOURNAL OF NEUROSCIENCE, WASHINGTON, SOC NEUROSCIENCE, 2008, 0270-6474

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30000 3. Medical and Health Sciences

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 7.452

Označené pro přenos do RIV

Ne

Klíčová slova anglicky

amygdala; cGMP; PKG; fear conditioning; long-term memory; long-term potentiation

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 9. 8. 2012 07:33, Olga Křížová

Anotace

V originále

Long-term potentiation (LTP) of inputs relaying sensory information from cortical and thalamic neurons to principal neurons in the lateral amygdala (LA) is thought to serve as a cellular mechanism for associative fear learning. Nitric oxide (NO), a messenger molecule widely implicated in synaptic plasticity and behavior, has been shown to enhance LTP in the LA as well as consolidation of associative fear memory. Additional evidence suggests that NO-induced enhancement of LTP and amygdala-dependent learning requires signaling through soluble guanylyl cyclase (sGC) and cGMP-dependent protein kinase (cGK). Mammals possess two genes for cGK: the prkg1 gene gives rise to the cGK type I isoforms, cGKI alpha and cGKI beta, and the prkg2 gene encodes the cGK type II. Reportedly, both cGKI and cGKII are expressed in the amygdala, and cGKII is involved in controlling anxiety-like behavior. Because selective pharmacological tools for individual cGK isoforms are lacking, we used different knock-out mouse models to examine the function of cGKI and cGKII for LTP in the LA and pavlovian fear conditioning. We found robust expression of the cGKI specifically in the LA with cGKI beta as the prevailing isoform. We further show a marked reduction of LTP at both thalamic and cortical inputs to the LA and a selective impairment of auditory-cued fearmemoryin cGKI-deficient mutants. In contrast, cGKII null mutants lack these phenotypes. Our data suggest a function of cGKI, likely the beta isoform, in the LA, supporting synaptic plasticity and consolidation of fear memory.