Distribution of cGMP-dependent protein kinase type I and its isoforms in the mouse brain and retina

Feil, Susanne; Zimmermann, Patricia R.; Knorn, Anna-Maria; Brummer, Sabine; Schlossmann, Jens; Hofmann, Franz; Feil, Robert

doi:10.1016/j.neuroscience.2005.06.051

Cited by 66 publications

(61 citation statements)

References 19 publications

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“…There are two isoforms of the cGKI, I␣ and I␤, that differ in their N-terminal domain and cGMP sensitivity. For the amygdala, we detected an expression pattern of the two cGKI isoforms reminiscent of that observed in the cortex and olfactory bulb (Feil et al, 2005b) with cGKI␤ as the principal isoform. In contrast, the cGKI␣ protein highly expressed in cerebellar tissue was virtually absent in the amygdala (Fig.…”

Section: Discussionmentioning

confidence: 59%

“…In this study, we used different knock-out models for cGKI and cGKII to elucidate this issue. Data from in situ hybridization and immunohistochemical analyses suggested that neurons of the amygdala express both cGKI and cGKII (El-Husseini et al, 1995Werner et al, 2004;Feil et al, 2005b), and activity of cGKII plays a role for anxiety-like behavior (Werner et al, 2004). Hitherto, detailed information regarding expression of the cGKI␣ and cGKI␤ in the amygdala is missing.…”

Section: Introductionmentioning

confidence: 99%

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

Paul¹,

Schöberl²,

Weinmeister³

et al. 2008

J. Neurosci.

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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␣ and cGKI␤, 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␤ 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 fear memory in cGKI-deficient mutants. In contrast, cGKII null mutants lack these phenotypes. Our data suggest a function of cGKI, likely the ␤ isoform, in the LA, supporting synaptic plasticity and consolidation of fear memory.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

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

Paul¹,

Schöberl²,

Weinmeister³

et al. 2008

J. Neurosci.

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“…Pharmacological and genetic studies have indicated that cGMP could be the central mediator of the effects NO͞cGMP in several brain regions (41)(42)(43). cGMP has several target proteins, including cGMP-regulated cation channels and cGMPdependent PKs.…”

Section: Discussionmentioning

confidence: 99%

“…cGMP has several target proteins, including cGMP-regulated cation channels and cGMPdependent PKs. Two cGMP-PK genes (types 1 and 2) that have been described in mammals are widely distributed in the brain (42,44). cGMP has been implicated in neuronal maturation (45)(46)(47), directional guidance of growth cones (48)(49)(50), and learning and memory tasks (51)(52)(53).…”

Section: Discussionmentioning

confidence: 99%

Phosphodiesterase genes are associated with susceptibility to major depression and antidepressant treatment response

Wong

Whelan²,

Deloukas

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

139

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Cyclic nucleotide phosphodiesterases (PDEs) constitute a family of enzymes that degrade cAMP and cGMP. Intracellular cyclic nucleotide levels increase in response to extracellular stimulation by hormones, neurotransmitters, or growth factors and are downregulated through hydrolysis catalyzed by PDEs, which are therefore candidate therapeutic targets. cAMP is a second messenger implicated in learning, memory, and mood, and cGMP modulates nervous system processes that are controlled by the nitric oxide (NO)͞cGMP pathway. To investigate an association between genes encoding PDEs and susceptibility to major depressive disorder (MDD), we genotyped SNPs in 21 genes of this superfamily in 284 depressed Mexican Americans who participated in a prospective, double-blind, pharmacogenetic study of antidepressant response, and 331 matched controls. Polymorphisms in PDE9A and PDE11A were found to be associated with the diagnosis of MDD. Our data are also suggestive of the association between SNPs in other PDE genes and MDD. Remission on antidepressants was significantly associated with polymorphisms in PDE1A and PDE11A. Thus, we found significant associations with both the diagnosis of MDD and remission in response to antidepressants with SNPs in the PDE11A gene. We show here that PDE11A haplotype GAACC is significantly associated with MDD. We conclude that PDE11A has a role in the pathophysiology of MDD. This study identifies a potential CNS role for the PDE11 family. The hypothesis that drugs affecting PDE function, particularly cGMP-related PDEs, represent a treatment strategy for major depression should therefore be tested.gene association ͉ pharmacogenetics ͉ cGMP ͉ SNP ͉ Mexican American

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“…Alternative mRNA splicing of PKG-1 produces a type 1␣ PKG (75 kDa) and a type 1␤ PKG (78 kDa), which only share 36% identity in their first 70 -100 amino-terminal residues (8,9). PKG-1 has been detected at high concentrations in all types of vascular smooth muscle cells (VSMC) (5). PKG-2 has been detected in renal, adrenal, intestinal, pancreatic, and brain cells but not in cardiac and vascular cells.…”

mentioning

confidence: 99%

Nitration of Tyrosine 247 Inhibits Protein Kinase G-1α Activity by Attenuating Cyclic Guanosine Monophosphate Binding

Aggarwal

Groß

Rafikov

et al. 2014

Journal of Biological Chemistry

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Background: PKG-1␣ nitration plays an important role in the development of pulmonary hypertension. Results: We identified Tyr 247 as the key residue susceptible to nitration and inhibition of PKG-1␣. Conclusion: Nitration attenuates PKG activity by reducing its affinity for cGMP. Significance: Preventing the nitration of PKG-1␣ could prevent the phenotypic remodeling in the blood vessels during the development of a number of cardiovascular diseases.

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Distribution of cGMP-dependent protein kinase type I and its isoforms in the mouse brain and retina

Cited by 66 publications

References 19 publications

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

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

Phosphodiesterase genes are associated with susceptibility to major depression and antidepressant treatment response

Nitration of Tyrosine 247 Inhibits Protein Kinase G-1α Activity by Attenuating Cyclic Guanosine Monophosphate Binding

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