Neuronal M3 muscarinic acetylcholine receptors are essential for somatotroph proliferation and normal somatic growth.

Gautam D, Jeon J, Starost MF, Han SJ, Hamdan FF, Cui Y, Parlow AF, Gavrilova O, Szalayova I, Mezey E, Wess J

Proceedings of the National Academy of Sciences of the United States of America30 Mar 2009Cited by 30 (Europe PMC)

PMID19332789PMCIDPMC2662962DOI10.1073/pnas.0900977106PepBankPUB-19332789

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice lacking brain M3 muscarinic receptors, treatment with CJC‑1295 rescued the growth deficit.
In plain wordsIn mice with a growth deficit from missing brain M3 receptors, CJC‑1295 treatment rescued the growth deficit.
Peptide
CJC-1295 (with DAC)
Outcome
DecreaseGrowth deficit (dwarf phenotype)
Study
mousen: not reported in source
Br-M3-KO mice (brain-specific M3 receptor knockout)
Outcome group
Growth hormone and IGF-1 · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Remarkably, treatment of Br-M3-KO mice with CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br-M3-KO mice by restoring normal pituitary size and normal serum GH and IGF-1 levels.
1 context sentence(design, population, supporting numbers)
Summary · context
We report the surprising observation that mutant mice that selectively lack the M(3) muscarinic acetylcholine receptor subtype in the brain (neurons and glial cells; Br-M3-KO mice) showed a dwarf phenotype associated with a pronounced hypoplasia of the anterior pituitary gland and a marked decrease…
Report a problemFND-1933278901
02AnimalAnimal study (in vivo)Efficacy outcome
In mice lacking brain M3 muscarinic receptors, treatment with CJC‑1295 restored normal pituitary size.
In plain wordsIn mice missing brain M3 receptors, CJC‑1295 treatment restored normal pituitary size.
Peptide
CJC-1295 (with DAC)
Outcome
IncreasePituitary size
Study
mousen: not reported in source
Br-M3-KO mice (brain-specific M3 receptor knockout)
Outcome group
Growth hormone and IGF-1 · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Remarkably, treatment of Br-M3-KO mice with CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br-M3-KO mice by restoring normal pituitary size and normal serum GH and IGF-1 levels.
1 context sentence(design, population, supporting numbers)
Summary · context
We report the surprising observation that mutant mice that selectively lack the M(3) muscarinic acetylcholine receptor subtype in the brain (neurons and glial cells; Br-M3-KO mice) showed a dwarf phenotype associated with a pronounced hypoplasia of the anterior pituitary gland and a marked decrease…
Report a problemFND-1933278902
03AnimalAnimal study (in vivo)Efficacy outcome
In mice lacking brain M3 muscarinic receptors, treatment with CJC‑1295 restored normal serum GH levels.
In plain wordsIn mice missing brain M3 receptors, CJC‑1295 treatment restored normal blood levels of growth hormone.
Peptide
CJC-1295 (with DAC)
Outcome
IncreaseSerum GH level
Study
mousen: not reported in source
Br-M3-KO mice (brain-specific M3 receptor knockout)
Outcome group
Growth hormone and IGF-1 · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Remarkably, treatment of Br-M3-KO mice with CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br-M3-KO mice by restoring normal pituitary size and normal serum GH and IGF-1 levels.
1 context sentence(design, population, supporting numbers)
Summary · context
We report the surprising observation that mutant mice that selectively lack the M(3) muscarinic acetylcholine receptor subtype in the brain (neurons and glial cells; Br-M3-KO mice) showed a dwarf phenotype associated with a pronounced hypoplasia of the anterior pituitary gland and a marked decrease…
Report a problemFND-1933278903
04AnimalAnimal study (in vivo)Efficacy outcome
In mice lacking brain M3 muscarinic receptors, treatment with CJC‑1295 restored normal serum IGF-1 levels.
In plain wordsIn mice missing brain M3 receptors, CJC‑1295 treatment restored normal blood levels of IGF-1.
Peptide
CJC-1295 (with DAC)
Outcome
IncreaseSerum IGF-1 level
Study
mousen: not reported in source
Br-M3-KO mice (brain-specific M3 receptor knockout)
Outcome group
Growth hormone and IGF-1 · Endocrine and hormones
Studied dose
Dose not stated
Source sentences
Summary
Remarkably, treatment of Br-M3-KO mice with CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br-M3-KO mice by restoring normal pituitary size and normal serum GH and IGF-1 levels.
1 context sentence(design, population, supporting numbers)
Summary · context
We report the surprising observation that mutant mice that selectively lack the M(3) muscarinic acetylcholine receptor subtype in the brain (neurons and glial cells; Br-M3-KO mice) showed a dwarf phenotype associated with a pronounced hypoplasia of the anterior pituitary gland and a marked decrease…
Report a problemFND-1933278904

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
9 Oct 2026, 18:17 UTC
Study results updated
Version 1
9 Oct 2026, 03:13 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

MeSH terms

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