Endocannabinoid and nitric oxide-dependent IGF-I-mediated synaptic plasticity at mice barrel cortex
Entity
UAM. Departamento de Anatomía, Histología y NeurocienciaPublisher
MDPIDate
2022-05-14Citation
10.3390/cells11101641
Cells 11.10 (2022): 1641
ISSN
2073-4409 (online)DOI
10.3390/cells11101641Funded by
This research was funded by MINECO and MICINN grants number BFU2016-80802-P AEI/FEDER, UE (MINECO) and PID2020-119358GB-I00/AEI/10.13039/501100011033 (MICINN).The APC was funded by PID2020-119358GB-I00/AEI/10.13039/501100011033 (MICINN)Project
Gobierno de España.BFU2016-80802-P; Gobierno de España.PID2020-119358GB-I00Editor's Version
https://doi.org/10.3390/cells11101641Subjects
endocannabinoids; IGF-I; nitric oxide; spike timing-dependent plasticity; MedicinaRights
© 2022 by the authorsAbstract
Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory. IGF-I increases the spiking and induces synaptic plasticity in the mice barrel cortex (Noriega-Prieto et al., 2021), favoring the induction of the long-term potentiation (LTP) by Spike Timing-Dependent Proto-cols (STDP) (Noriega-Prieto et al., 2021). Here, we studied whether these IGF-I effects depend on endocannabinoids (eCBs) and nitric oxide (NO). We recorded both excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) evoked by stimulation of the basal dendrites of layer II/III pyramidal neurons of the Barrel Cortex and analyzed the effect of IGF-I in the presence of a CB1 R antagonist, AM251, and inhibitor of the NO synthesis, L-NAME, to prevent the eCBs and the NO-mediated signaling. Interestingly, L-NAME abolished any modulatory effect of the IGF-I-induced excitatory and inhibitory transmission changes, suggesting the essential role of NO. Surprisingly, the inhibition of CB1Rs did not only block the potentiation of EPSCs but reversed to a depression, highlighting the remarkable functions of the eCB system. In conclusion, eCBs and NO play a vital role in deciding the sign of the effects induced by IGF-I in the neocortex, suggesting a neuromodulatory interplay among IGF-I, NO, and eCBs
Files in this item
Google Scholar:Noriega Prieto, José Antonio
-
Maglio, Laura Eva
-
Ibáñez-Santana, Sara
-
Fernández de Sevilla García, David
This item appears in the following Collection(s)
Related items
Showing items related by title, author, creator and subject.
-
VHL promotes immune response against renal cell carcinoma via NF-κB–dependent regulation of VCAM-1
Labrousse Arias, David; Martínez Alonso, Emma; Corral-Escariz, María; Bienes Martínez, Raquel; Berridy, Jaime; Serrano-Oviedo, Leticia; Conde, Elisa; García Bermejo, María Laura; Giménez Bachs, José M.; Salinas-Sánchez, Antonio S.; Sánchez Prieto, Ricardo; Yao, Masahiro; Lasa Benito, Marina Paloma; Calzada, María J.
2017-02-24