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Fig. 9. The soma, responsible for inhibitory responses of spontaneous firing to glutamate, works together with the PDCs, to produce the typical burst-pause firing patterns in DA neurons. (A) A dissociated DA neuron was loaded with NP-EGTA and Fluo 4-AM. Serial photolysis of a small area along a dendrite led to localized cytosolic Ca2+ rises. Serial fluorescence images from the white box are magnified and overlapped. Dendritic Ca2+ changes in the uncaging regions are presented according to the distance from the soma, with the corresponding firing patterns recorded in the soma. Photolysis points are indicated by blue dotted lines. (B) Relative changes in the normalized hyperpolarization of membrane potential according to the distance from the soma. (C) The duration of postfiring pauses is plotted versus distance from the soma (n = 4). (D, E) When Ca2+ uncaging on the same site of a dendrite was repeated with different degrees, higher [Ca2+] rises caused longer pauses in spontaneous firing and stronger hyperpolarization of the membrane potential. Right, the relationship between the hyperpolarization of membrane potential and dendrite Ca2+ changes (n = 5, r = 0.76). (F) Strong glutamate uncaging in the local dendritic region induced different types of Ca2+ increases between the stimulated dendritic region (green) and the soma (blue). Spontaneous firing and evoked bursts were measured with a patch pipette at the soma (gray trace). (G) The recoveries of the elevated Ca2+ levels in the soma and stimulated dendritic region when the first spontaneous firing reappeared after glutamate uncaging (soma = 60.07 ± 7.35%, proximal = 2.77 ± 1.07%, n = 7). (H) Functional somatodendritic organization of the pacemaking and firing system in multipolar DA neurons. Highly excitable PDCs not only drive pacemaking but also serve as an integration site for evoked firings. PDCs, proximal dendritic compartments; DA, dopamine.
Korean J Physiol Pharmacol 2024;28:165-181
© Korean J Physiol Pharmacol