ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Haploinsufficiency in peptidylglycine alpha-amidating monooxygenase leads to altered synaptic transmission in the amygdala and impaired emotional responses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- New insights into the pharmacogenomics of antidepressant response from the GENDEP and STAR*D studies: rare variant analysis and high-density imputation.The pharmacogenomics journal · 2018Pooled it
- Impaired peptide amidation and risk of incident dementia in the Malmoe preventive project cohort.Alzheimer's research & therapy · 2026Article
- Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025Review
- Comparative Single-Cell Transcriptome Analysis of c-Met Receptor Expressing and Non-Expressing Projection Neurons in the Developing Frontal and Visual Cortices.Developmental neuroscience · 2025Article
- Peptidylglycine alpha-amidating monooxygenase is important in mice for beta-cell cilia formation and insulin secretion but promotes diabetes risk through beta-cell independent mechanisms.Molecular metabolism · 2025Article
- Germline loss-of-functionmedRxiv : the preprint server for health sciences · 2023Article
- Germline loss-of-functionFrontiers in endocrinology · 2023Article
- Cell-type specific knockout of peptidylglycine α-amidating monooxygenase reveals specific behavioral roles in excitatory forebrain neurons and cardiomyocytes.Genes, brain, and behavior · 2021Article
- Stress-Related Neuronal Clusters in Sublenticular Extended Amygdala of Basal Forebrain Show Individual Differences of Positions.Frontiers in neural circuits · 2020Article
- A Novel Bio-Psychosocial-Behavioral Treatment Model of Panic Disorder.Psychiatry investigation · 2019Article
- Early eukaryotic origins for cilia-associated bioactive peptide-amidating activity.Journal of cell science · 2016Article
- Molecular basis of neurodegeneration and neurodevelopmental defects in Menkes disease.Neurobiology of disease · 2015Review
- Genetic determinants of amidating enzyme activity and its relationship with metal cofactors in human serum.BMC endocrine disorders · 2014Article
- Pam heterozygous mice reveal essential role for Cu in amygdalar behavioral and synaptic function.Annals of the New York Academy of Sciences · 2014Article
- In vivo and in vitro analyses of amygdalar function reveal a role for copper.Journal of neurophysiology · 2014Article
- Peptidylglycine α-amidating monooxygenase heterozygosity alters brain copper handling with region specificity.Journal of neurochemistry · 2013Article
- Genome-wide association for fear conditioning in an advanced intercross mouse line.Behavior genetics · 2012Article
- The clinical implications of mouse models of enhanced anxiety.Future neurology · 2011Article
- Signaling from the secretory granule to the nucleus.Critical reviews in biochemistry and molecular biologyReview
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The mammalian amygdala expresses various neuropeptides whose signaling has been implicated in emotionality. Many neuropeptides require amidation for full activation by peptidylglycine α-amidating monooxygenase (PAM), a transmembrane vesicular cuproenzyme and regulator of the secretory pathway. Mice heterozygous for the Pam gene (PAM(+/-)) exhibit physiological and behavioral abnormalities related to specific peptidergic pathways. In the present study, we evaluated emotionality and examined molecular and cellular responses that characterize neurophysiological differences in the PAM(+/-) amygdala. PAM(+/-) mice presented with anxiety-like behaviors in the zero maze that were alleviated by diazepam. PAM(+/-) animals were deficient in short- and long-term contextual and cued fear conditioning and required higher shock intensities to establish fear-potentiated startle than their wild-type littermates. Immunohistochemical analysis of the amygdala revealed PAM expression in pyramidal neurons and local interneurons that synthesize GABA. We performed whole-cell recordings of pyramidal neurons in the PAM(+/-) amygdala to elucidate neurophysiological correlates of the fear behavioral phenotypes. Consistent with these observations, thalamic afferent synapses in the PAM(+/-) lateral nucleus were deficient in long-term potentiation. This deficit was apparent in the absence and presence of the GABA(A) receptor antagonist picrotoxin and was abolished when both GABA(A) and GABA(B) receptors were blocked. Both evoked and spontaneous excitatory signals were enhanced in the PAM(+/-) lateral nucleus. Phasic GABAergic signaling was also augmented in the PAM(+/-) amygdala, and this difference comprised activity-independent and -dependent components. These physiological findings represent perturbations in the PAM(+/-) amygdala that may underlie the aberrant emotional responses in the intact animal.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.