| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Physiology, University of Maryland, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: Masako.Isokawa{at}utb.edu.
Endogenous cannabinoids (eCBs) are produced and mobilized in a cytosolic calcium ([Ca2+]i) - dependent manner, and they regulate excitatory and inhibitory neurotransmitter release by acting as retrograde messengers. An indirect but real time bioassay for this process on GABAergic transmission is DSI (depolarization-induced suppression of inhibition). The magnitude of DSI correlates linearly with depolarization-induced increase of [Ca2+]i that is thought to be initiated by Ca2+ influx through voltage-gated Ca2+ channels. However, the identity of Ca2+ sources involved in eCB-mobilization in DSI remains undetermined. Here we show that, in CA1 pyramidal cells, DSI-inducing depolarizing voltage steps caused Ca2+ induced Ca2+ release (CICR) by activating the ryanodine receptor (RyR) Ca2+-release channel. CICR was reduced, and the remaining rise in [Ca2+]i was less effective in generating DSI, when the RyR antagonists, ryanodine or ruthenium red, were applied intracellularly, or the Ca2+ stores were depleted by the Ca2+-ATPase inhibitors, cyclopiazonic acid or thapsigargin. The CICR-dependent effects were most prominent in cultured or immature acute slices, but were also detectable in slices from adult tissue. Thus, we suggest that voltage-gated Ca2+ entry raises local [Ca2+]i sufficiently to activate nearby RyRs, and that the resulting CICR plays a critical role in initiating eCB mobilization. RyR may be a key molecule for the depolarization-induced production of eCBs that inhibit GABA release in the hippocampus.
This article has been cited by other articles:
|
|
 |
|
  R. Kellogg, K. Mackie, and A. Straiker Cannabinoid CB1 Receptor-Dependent Long-Term Depression in Autaptic Excitatory Neurons J Neurophysiol, August 1, 2009; 102(2): 1160 - 1171. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Manita and W. N. Ross Synaptic Activation and Membrane Potential Changes Modulate the Frequency of Spontaneous Elementary Ca2+ Release Events in the Dendrites of Pyramidal Neurons J. Neurosci., June 17, 2009; 29(24): 7833 - 7845. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kano, T. Ohno-Shosaku, Y. Hashimotodani, M. Uchigashima, and M. Watanabe Endocannabinoid-Mediated Control of Synaptic Transmission Physiol Rev, January 1, 2009; 89(1): 309 - 380. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Adermark and D. M. Lovinger Retrograde endocannabinoid signaling at striatal synapses requires a regulated postsynaptic release step PNAS, December 18, 2007; 104(51): 20564 - 20569. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Makara, I. Katona, G. Nyiri, B. Nemeth, C. Ledent, M. Watanabe, J. de Vente, T. F. Freund, and N. Hajos Involvement of Nitric Oxide in Depolarization-Induced Suppression of Inhibition in Hippocampal Pyramidal Cells during Activation of Cholinergic Receptors J. Neurosci., September 19, 2007; 27(38): 10211 - 10222. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Carter and X.-J. Wang Cannabinoid-Mediated Disinhibition and Working Memory: Dynamical Interplay of Multiple Feedback Mechanisms in a Continuous Attractor Model of Prefrontal Cortex Cereb Cortex, September 1, 2007; 17(suppl_1): i16 - i26. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Straiker and K. Mackie Metabotropic suppression of excitation in murine autaptic hippocampal neurons J. Physiol., February 1, 2007; 578(3): 773 - 785. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Sang and C. Chen Lipid Signaling and Synaptic Plasticity Neuroscientist, October 1, 2006; 12(5): 425 - 434. [Abstract] [PDF]
|
|
|
|
|
|
S. D. Brenowitz, A. R. Best, and W. G. Regehr Sustained elevation of dendritic calcium evokes widespread endocannabinoid release and suppression of synapses onto cerebellar Purkinje cells. J. Neurosci., June 21, 2006; 26(25): 6841 - 6850. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
