Modulation of Calcium-Dependent Inactivation of L-Type Ca2+ Channels via β-Adrenergic Signaling in Thalamocortical Relay Neurons
Figure 4
β2AR specifically modulates CDI in TC neurons of dLGN.
(A) Representative current traces recorded under control conditions (upper left panel) and during extracellular application of specific β2AR agonist salmeterol (10 µM) plus antagonists for the other two types of receptor (CGP 20712 dihydrochloride-β1 antagonist and SR 59230A hydrochloride-β3-antagonist, 100 µM each; lower left panel) elicited by the indicated pulse protocol (middle left panel). The bar graph (right panel) represents Dinact under different recording conditions (as indicated). The mean value of four cells recorded under control conditions was taken for comparison with four cells recorded under 10 µM salmeterol plus 100 µM β1+β3 antagonists. Data are presented as means ± SEM of several independent experiments. **P<0.01. Significance of salmeterol plus antagonists versus control was calculated by Student's t test. The degree of inactivation is given by the normalized current amplitude of the mean postpulse I/V at +10 mV. (B) Immunocytochemical analysis of primary cultures of the dorsal thalamus using MAP2 specific antibody (left upper panel, red) and β2AR specific antibody (left down panel, green). The merged picture revealed the co-expression of these two proteins in somatic regions and proximal dendrites. Enlarged inlay represents magnification of the area indicated by the rectangle. Yellow dots represent places were these two proteins are in close proximity. Data shown are representative pictures from several independent immunostainings and preparations of neurons. In all cases, omission of primary antibodies resulted in no fluorescence signal above background (negative control).