ArticleScientific reports2016
CALHM1 deficiency impairs cerebral neuron activity and memory flexibility in mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- The CALHM1 blocker CGP37157 increases seizure severity during status epilepticus in adult mice.Purinergic signalling · 2025Article
- AAV-mediated peripheral scFv's administration to reduce cerebral tau in adult P301S transgenic mice: Mono-vs. combination therapy.Molecular therapy. Methods & clinical development · 2025Article
- Biology, function and structure of the calcium homeostasis modulator family.The Journal of physiology · 2025Review
- Non-Drug and Non-Invasive Therapeutic Options in Alzheimer's Disease.Biomedicines · 2025Review
- Control of astrocytic CaBiological research · 2024Article
- S-acylation of Ca2+ transport proteins: molecular basis and functional consequences.Biochemical Society transactions · 2024Review
- Kinesin-2 motors differentially impact biogenesis of extracellular vesicle subpopulations shed from sensory cilia.iScience · 2022Article
- Intramolecular Disulfide Bonds for Biogenesis of CALHM1 Ion Channel Are Dispensable for Voltage-Dependent ActivationMolecules and cells · 2021Article
- Human CALHM5: Insight in large pore lipid gating ATP channel and associated neurological pathologies.Molecular and cellular biochemistry · 2021Review
- On the molecular nature of large-pore channels.Journal of molecular biology · 2021Review
- Proteomic and Transcriptomic Analyses Reveal Pathological Changes in the Entorhinal Cortex Region that Correlate Well with Dysregulation of Ion Transport in Patients with Alzheimer's Disease.Molecular neurobiology · 2021Article
- Review
- Article
- Structure and assembly of calcium homeostasis modulator proteins.Nature structural & molecular biology · 2020Article
- CALHM1/CALHM3 channel is intrinsically sorted to the basolateral membrane of epithelial cells including taste cells.Scientific reports · 2019Article
- Drug Development for Alzheimer's Disease: Microglia Induced Neuroinflammation as a Target?International journal of molecular sciences · 2019Review
- Large-Scale Validation of the Paddling Pool Task in the Clockmaze for Studying Hippocampus-Based Spatial Cognition in Mice.Frontiers in behavioral neuroscience · 2019Article
- Blockade and knock-out of CALHM1 channels attenuate ischemic brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Chemical synapses without synaptic vesicles: Purinergic neurotransmission through a CALHM1 channel-mitochondrial signaling complex.Science signaling · 2018Article
- CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes.Neuron · 2018Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
CALHM1 is a cell surface calcium channel expressed in cerebral neurons. CALHM1 function in the brain remains unknown, but recent results showed that neuronal CALHM1 controls intracellular calcium signaling and cell excitability, two mechanisms required for synaptic function. Here, we describe the generation of Calhm1 knockout (Calhm1(-/-)) mice and investigate CALHM1 role in neuronal and cognitive functions. Structural analysis revealed that Calhm1(-/-) brains had normal regional and cellular architecture, and showed no evidence of neuronal or synaptic loss, indicating that CALHM1 deficiency does not affect brain development or brain integrity in adulthood. However, Calhm1(-/-) mice showed a severe impairment in memory flexibility, assessed in the Morris water maze, and a significant disruption of long-term potentiation without alteration of long-term depression, measured in ex vivo hippocampal slices. Importantly, in primary neurons and hippocampal slices, CALHM1 activation facilitated the phosphorylation of NMDA and AMPA receptors by protein kinase A. Furthermore, neuronal CALHM1 activation potentiated the effect of glutamate on the expression of c-Fos and C/EBPβ, two immediate-early gene markers of neuronal activity. Thus, CALHM1 controls synaptic activity in cerebral neurons and is required for the flexible processing of memory in mice. These results shed light on CALHM1 physiology in the mammalian brain.
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Registered trials
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.