The endocannabinoid system drives neural progenitor proliferation
(2005) In FASEB Journal 19(9). p.1704-1704- Abstract
- The discovery of multipotent neural progenitor (NP) cells has provided strong support for the existence of neurogenesis in the adult brain. However, the signals controlling NP proliferation remain elusive. Endocannabinoids, the endogenous counterparts of marijuana-derived cannabinoids, act as neuromodulators via presynaptic CB1 receptors and also control neural cell death and survival. Here we show that progenitor cells express a functional endocannabinoid system that actively regulates cell proliferation both in vitro and in vivo. Specifically, NPs produce endocannabinoids and express the CB1 receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase ( FAAH). CB1 receptor activation promotes cell proliferation and... (More)
- The discovery of multipotent neural progenitor (NP) cells has provided strong support for the existence of neurogenesis in the adult brain. However, the signals controlling NP proliferation remain elusive. Endocannabinoids, the endogenous counterparts of marijuana-derived cannabinoids, act as neuromodulators via presynaptic CB1 receptors and also control neural cell death and survival. Here we show that progenitor cells express a functional endocannabinoid system that actively regulates cell proliferation both in vitro and in vivo. Specifically, NPs produce endocannabinoids and express the CB1 receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase ( FAAH). CB1 receptor activation promotes cell proliferation and neurosphere generation, an action that is abrogated in CB1-deficient NPs. Accordingly, proliferation of hippocampal NPs is increased in FAAH-deficient mice. Our results demonstrate that endocannabinoids constitute a new group of signaling cues that regulate NP proliferation and thus open novel therapeutic avenues for manipulation of NP cell fate in the adult brain. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/231573
- author
- Aguado, T ; Monory, K ; Palazuelos, J ; Stella, N ; Cravatt, B ; Lutz, B ; Marsicano, G ; Kokaia, Zaal LU ; Guzman, M and Galve-Roperh, I
- organization
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- cannabinoid, CB1 receptor, NP
- in
- FASEB Journal
- volume
- 19
- issue
- 9
- pages
- 1704 - 1704
- publisher
- Wiley
- external identifiers
-
- wos:000230923000013
- scopus:26444557412
- pmid:16037095
- ISSN
- 1530-6860
- DOI
- 10.1096/fj.05-3995fje
- language
- English
- LU publication?
- yes
- id
- 7abb9c4e-caed-4e77-813e-6f21f4f08b20 (old id 231573)
- date added to LUP
- 2016-04-01 16:02:58
- date last changed
- 2023-09-04 11:20:55
@article{7abb9c4e-caed-4e77-813e-6f21f4f08b20, abstract = {{The discovery of multipotent neural progenitor (NP) cells has provided strong support for the existence of neurogenesis in the adult brain. However, the signals controlling NP proliferation remain elusive. Endocannabinoids, the endogenous counterparts of marijuana-derived cannabinoids, act as neuromodulators via presynaptic CB1 receptors and also control neural cell death and survival. Here we show that progenitor cells express a functional endocannabinoid system that actively regulates cell proliferation both in vitro and in vivo. Specifically, NPs produce endocannabinoids and express the CB1 receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase ( FAAH). CB1 receptor activation promotes cell proliferation and neurosphere generation, an action that is abrogated in CB1-deficient NPs. Accordingly, proliferation of hippocampal NPs is increased in FAAH-deficient mice. Our results demonstrate that endocannabinoids constitute a new group of signaling cues that regulate NP proliferation and thus open novel therapeutic avenues for manipulation of NP cell fate in the adult brain.}}, author = {{Aguado, T and Monory, K and Palazuelos, J and Stella, N and Cravatt, B and Lutz, B and Marsicano, G and Kokaia, Zaal and Guzman, M and Galve-Roperh, I}}, issn = {{1530-6860}}, keywords = {{cannabinoid; CB1 receptor; NP}}, language = {{eng}}, number = {{9}}, pages = {{1704--1704}}, publisher = {{Wiley}}, series = {{FASEB Journal}}, title = {{The endocannabinoid system drives neural progenitor proliferation}}, url = {{http://dx.doi.org/10.1096/fj.05-3995fje}}, doi = {{10.1096/fj.05-3995fje}}, volume = {{19}}, year = {{2005}}, }