Evidence for distinct forms of compulsivity in the SAPAP3 mutant-mouse model for obsessive-compulsive disorder.
Javier
September 20, 2020
Specific mechanisms underlying the compulsive behaviors of obsessive-compulsive disorder (OCD) is unknown. It has been suggested that these compulsivity may have its origin in cognitive dysfunction such as impaired information processing feedback – received after completion of goal-directed action. Signal attenuation (SA) models such task processing deficits in animals by weakening the strength of the relationship between food and the gift audiovisual feedback (signal) served after the performance operant response. The compulsive as resulting from the SA respond well characterized in mice, but so far not established in rats, a species strong genetic OCD existing models.
Thus, first, we show that the task of SA can be implemented in mice and showed that the damping feedback related reward responses produce similar behavior in C57BL6 mice as reported previously in mice. Secondly, we tested the hypothesis that SAPAP3 KO mice (SAPAP3 – / -), prone to show some OCD-like disorders including excessive treatment, showed an increase in compulsive-like behaviors in their task of SA compared with wild-type littermates (WT). However, measures compulsivity-related tasks in SAPAP3 – / – and WT did not produce a significant difference, following either SA or for the extinction of “ordinary” of instrumental behavior.
Thus, compulsive-like behaviors instrumental follows distortion feedback is not potential in compulsive care mice, involving in particular that a) deficits common in the processing of feedback is not related to the treatment of excessive SAPAP3 – / -, and b) a different manifestation of compulsivity may be driven by independent mechanisms.Significance Statement signal attenuation (SA) duty is established for a rat behavioral paradigm that promotes compulsivity.
First, we show that SA tasks can also be applied to the processing of feedback tests on mice. Second, we investigate if SAPAP3 mutant mice, a model of animal genetic highly validated for obsessive-compulsive disorder (OCD), exhibit compulsive respond to the task exacerbated SA. However, we did not find an increased compulsivity feedback-induced mutant SAPAP3. Thus, our results indicate the presence of various types of compulsivity (ie, genetically induced behavior compared compulsivity) possibly boosted by an independent mechanism.
Evidence for distinct forms of compulsivity in the SAPAP3 mutant-mouse model for obsessive-compulsive disorder.
The effect of reduced connexin43 function in the development of the skull in Cx43I130T / + mouse mutant models oculodentodigital dysplasia.
Oculodentodigital dysplasia (ODDD) is a disease caused by mutations in the gene that encodes GJA1 gap-junctional protein connexin43 (Cx43). ODDD affects multiple organs, but the typical craniofacial anomalies. However, details about the time the phenotypic presentation of this disorder and their correspondence with potential cellular changes is not complete.
Here, we do the first assessment of the development of the craniofacial phenotype ODDD in Cx43I130T / + mouse model and showed that the phenotypic features commonly found in commonly found in patients with these disorders arise in mice between E17.5 and birth and becoming deeper with age. Using mice heterozygous for the mutation I130T of Gja1 we provide a detailed analysis of the craniofacial phenotype in this ODDD models using shape analysis based on micro-CT images.
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EUR 540
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EUR 2215
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EUR 680
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5x40Tests
EUR 2835
Tissue cDNA, First Strand, Human Adult Normal, Stomach, Fundus, BioGenomics
MBS651912-10Tests
MyBiosource
10Tests
EUR 540
Tissue cDNA, First Strand, Human Adult Normal, Stomach, Fundus, BioGenomics
MBS651912-5x10Tests
MyBiosource
5x10Tests
EUR 2215
Tissue cDNA, First Strand, Human Adult Normal, Salivary gland, BioGenomics
MBS652022-10Tests
MyBiosource
10Tests
EUR 540
Tissue cDNA, First Strand, Human Adult Normal, Salivary gland, BioGenomics
MBS652022-5x10Tests
MyBiosource
5x10Tests
EUR 2215
Tissue cDNA, First Strand, Human Diseased, Lupus, Spinal cord, BioGenomics
MBS652411-40Tests
MyBiosource
40Tests
EUR 995
Tissue cDNA, First Strand, Human Diseased, Lupus, Spinal cord, BioGenomics
MBS652411-5x40Tests
MyBiosource
5x40Tests
EUR 4250
Tissue cDNA, First Strand, Human Adult Normal, Stomach, Cardia, BioGenomics
MBS652430-10Tests
MyBiosource
10Tests
EUR 540
Tissue cDNA, First Strand, Human Adult Normal, Stomach, Cardia, BioGenomics
MBS652430-5x10Tests
MyBiosource
5x10Tests
EUR 2215
Tissue cDNA, First Strand, Human Adult Normal, Uterus, Corpus, BioGenomics
MBS652435-10Tests
MyBiosource
10Tests
EUR 540
The results showed that in addition to differences in facial bone morphology no significant differences in the basic shape of the skull. mutant mice display delayed ossification at E17.5 and birth, especially in the facial bones and the skull vault but normal ossification at three months. Our immunohistochemical analysis showed that the palatine bone osteoblast differentiation is delayed in Cx43I130T / + mice compared to their wildtype littermates, which contribute to the possibility of phenotypic variation observed in the facial bones.