| 2022 |
ADCYAP1+ neurons in the nucleus of the solitary tract and area postrema (NTS-AP) are both necessary and sufficient for sickness behavior responses to LPS (anorexia, adipsia, lethargy, temperature changes): activation of these neurons fully recapitulates LPS-induced sickness, while inhibition significantly diminishes all behavioral responses. |
Chemogenetic activation/inhibition of ADCYAP1+ neurons in TRAP2 mice combined with single-nucleus RNA sequencing to identify LPS-activated neural populations; whole-brain activity mapping (FOS expression) |
Nature |
High |
36071158
|
| 2006 |
Loss of Adcyap1 (PACAP) in mice causes hyperlocomotion and prepulse inhibition deficits; the paradoxical antihyperkinetic effect of amphetamine in Adcyap1−/− mice depends on serotonin 1A (5-HT1A) receptor signaling, and amphetamine increases c-Fos-positive neurons in the prefrontal cortex of these mice, suggesting PACAP normally modulates 5-HT1A-mediated inhibitory prefrontal control of motor activity. |
Genetic knockout (Adcyap1−/− mice), prepulse inhibition assay, pharmacological manipulation (amphetamine, 5-HT1A agonist 8-OH-DPAT, fluoxetine), c-Fos immunohistochemistry |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
Medium |
16687500
|
| 2006 |
Adcyap1−/− mice exhibit intense jumping behavior that is suppressed by the SSRI fluoxetine and the serotonin precursor 5-hydroxytryptophan, and these mice show reduced brain 5-HIAA, indicating that PACAP supports serotonergic tone that limits abnormal motor behavior. |
Genetic knockout (Adcyap1−/− mice), pharmacological treatment (fluoxetine, 5-HTP), neurochemical measurement of 5-HIAA |
Annals of the New York Academy of Sciences |
Medium |
16888223
|
| 2008 |
Adcyap1−/− mice have markedly reduced white adipose tissue mass, hypoinsulinemia, and increased insulin sensitivity accompanied by decreased adipocyte differentiation marker aP2 and reduced plasma resistin, indicating that PACAP promotes energy storage, adipogenesis, and insulin secretion in vivo. |
Genetic knockout (Adcyap1−/− mice), glucose and insulin tolerance tests, fat mass measurement, adipocyte marker mRNA expression (aP2), plasma hormone and adipokine measurements, high-fat diet challenge |
Journal of pharmacological sciences |
Medium |
18446003
|
| 2009 |
Forced overexpression of Adcyap1 in insulinoma NIT-1 cells protected them from cytokine-triggered apoptosis, establishing ADCYAP1 as a downstream mediator of DcR3-mediated islet beta cell survival. |
Plasmid-mediated overexpression of Adcyap1 in NIT-1 insulinoma cells, cytokine-induced apoptosis assay; DNA microarray identified Adcyap1 upregulation (>700-fold) in DcR3-transgenic islets |
Journal of immunology (Baltimore, Md. : 1950) |
Medium |
20007581
|
| 2020 |
ADCYAP1 (PACAP) is the most strongly upregulated gene in skin during peripheral nerve regeneration after carpal tunnel release; PACAP signals through its G-protein coupled receptor (PAC1R) expressed on human iPSC-derived sensory neurons and dose-dependently enhances axon outgrowth in vitro. |
Transcriptional profiling of serial skin biopsies (pre/post carpal tunnel surgery), human iPSC-derived sensory neuron culture with PACAP treatment, neurite length measurement in vitro |
Brain : a journal of neurology |
Medium |
32651949
|
| 2023 |
Adcyap1/PACAP38 is an intrinsic protective factor in dorsal root ganglion neurons linking neuropathic pain suppression and axonal regeneration: intrathecal PACAP38 mitigates mechanical hyperalgesia and facilitates axon regeneration, while Adcyap1 siRNA knockdown or PAC1R antagonist (PACAP6-38) both worsen pain and delay regeneration in a rat spared nerve crush model. |
scRNA-seq of rat DRGs, intrathecal PACAP38 administration, siRNA knockdown of Adcyap1, PAC1R antagonist (PACAP6-38) treatment; behavioral pain testing (mechanical hyperalgesia), axonal regeneration assessment |
BMC biology |
Medium |
37880634
|
| 2011 |
The ADCYAP1 promoter is hypermethylated in cervical cancer cells and CIN lesions, silencing ADCYAP1 expression; this silencing is reversed by treatment with a DNA methyltransferase inhibitor (5-aza-2'-deoxycytidine) and/or histone deacetylase inhibitor (trichostatin A), establishing promoter hypermethylation as a mechanism of ADCYAP1 transcriptional repression in cervical cancer. |
Methylation analysis of CpG islands in ADCYAP1 promoter in cancer cell lines and tissue samples; pharmacological demethylation/HDAC inhibitor treatment followed by gene expression measurement |
Oncology reports |
Medium |
21109983
|
| 2025 |
Gα13 overexpression in medial prefrontal cortex pyramidal neurons downregulates Adcyap1, reducing cAMP/PKA signaling and impairing NMDA receptor function; pharmacological activation with PACAP-38 rescues social deficits and restores synaptic function in Gα13-OE mice, placing ADCYAP1/PACAP downstream of Gα13 in a mPFC cAMP/PKA/NMDAR pathway controlling social behavior. |
CRISPR/Cas9-mediated Gα13 overexpression in mPFC pyramidal neurons; RNA-seq identifying Adcyap1 downregulation; pharmacological rescue with PACAP-38; fiber photometry; Golgi staining; whole-cell patch clamp; three-chamber socialization test |
Schizophrenia bulletin |
Medium |
40843621
|
| 2025 |
A Kölliker-Fuse nucleus subpopulation co-expressing Adcyap1 (PACAP) and VGluT1 (Slc17a7) forms calyceal terminals around PKCδ+/GluD1+ extended amygdala neurons and becomes Fos-positive rapidly after acute hypotension, preceding vasopressin-mediated endocrine responses, suggesting PACAP/glutamate co-transmission mediates rapid autonomic compensation to falling blood pressure. |
Fos immunohistochemistry at 60 and 120 min after hydralazine-induced hypotension in rats; confocal immunohistochemistry of PACAP+ terminals around EA neurons; RNAscope in situ hybridization for Adcyap1/Slc17a7 co-expression in KF |
bioRxivpreprint |
Low |
bio_10.1101_2025.10.16.682741
|