Skip to main content
. Author manuscript; available in PMC: 2010 Jun 28.
Published in final edited form as: J Neurosci. 2009 May 20;29(20):6568–6579. doi: 10.1523/JNEUROSCI.0181-09.2009

Figure 5. Regulation of somatodendritic DA release by mGluR1 activation of IP3R-gated intracellular Ca2+ stores.

Figure 5

a. Average [DA]o versus time profiles in SNc evoked by local stimulation (30 pulses, 10 Hz) in the absence and presence of a membrane permeable IP3R inhibitor 2-APB (left panel, 100 μM, n = 8). b. Summary of the effect of 2-APB on peak [DA]o; control peak [DA]o was taken as 100%. Inhibition of IP3Rs by 2-APB decreased evoked [DA]o (n = 8, ***p < 0.001 vs. control), indicating involvement of Ca2+ mobilization from IP3R-gated stores in somatodendritic DA release. c. Average [DA]o versus time profiles in SNc in the absence and presence of an mGluR1 agonist DHPG (left panel, 1 μM, n = 8) or the mGluR1 antagonist CPCCOEt (right panel, 100 μM, n = 9). d. Summary of the effect of DHPG and CPCCOEt on peak [DA]o; control peak [DA]o was taken as 100%. Activation of the IP3R-dependent mGluR1 pathway by DHPG significantly increased evoked [DA]o (n = 8, *p < 0.05 vs. control) implicating a role for mGluR1-gated Ca2+ stores in somatodendritic DA release. Blockade of mGluR1s with CPCCOEt decreased evoked [DA]o (n = 9, ***p < 0.001), indicating that endogenously released glutamate normally facilitates somatodendritic DA release via activation of mGluR1s. e. Average [DA]o versus time profiles in SNc with CPCCOEt (100 μM) after pretreatment with the IP3R antagonist 2-APB (left panel, 100 μM, n = 6) or the SERCA inhibitor CPA (right panel, 30 μM, n = 6). f. Summary of the effect of CPCCOEt in 2-APB or CPA on peak [DA]o; control peak [DA]o in either 2-APB or CPA alone was taken as 100%. Suppression of evoked [DA]o by CPCCOEt was prevented by pretreatment with 2-APB (n = 6, p > 0.05, CPCCOEt + 2-APB vs. 2-APB alone) or CPA (n = 6, p > 0.05, CPCCOEt + CPA vs. CPA alone), demonstrating that activation of mGluR1s by endogenously released glutamate involves mobilization of Ca2+ from IP3R-gated ER stores.