scholarly journals Dopamine Receptor Activation Can Reduce Voltage-Gated Na+ Current by Modulating Both Entry Into and Recovery From Inactivation

2004 ◽  
Vol 92 (5) ◽  
pp. 3134-3141 ◽  
Author(s):  
Yuki Hayashida ◽  
Andrew T. Ishida

We tested whether dopamine receptor activation modulates the voltage-gated Na+ current of goldfish retinal ganglion cells, using a fast voltage-clamp amplifier, perforated-patch whole cell mode, and a physiological extracellular Na+ concentration. As found in other cells, activators of D1-type dopamine receptors and of protein kinase A reduced the amplitude of current activated by depolarizations from resting potential without altering the current kinetics or activation range. However, D1-type dopamine receptor activation also accelerated the rate of entry into inactivation during subthreshold depolarizations and slowed the rate of recovery from inactivation after single, brief depolarizations. Our results provide the first evidence in any preparation that D1-type receptor activation can produce both of these latter effects.

2003 ◽  
Vol 90 (6) ◽  
pp. 3888-3901 ◽  
Author(s):  
Sherwin C. Lee ◽  
Yuki Hayashida ◽  
Andrew T. Ishida

Spiking in central neurons depends on the availability of inward and outward currents activated by depolarization and on the activation and priming of currents by hyperpolarization. Of these processes, priming by hyperpolarization is the least described. In the case of T-type Ca2+ current availability, the interplay of hyperpolarization and depolarization has been studied most completely in expression systems, in part because of the difficulty of pharmacologically separating the Ca2+ currents of native neurons. To facilitate understanding of this current under physiological conditions, we measured T-type current of isolated goldfish retinal ganglion cells with perforated-patch voltage-clamp methods in solutions containing a normal extracellular Ca2+ concentration. The voltage sensitivities and rates of current activation, inactivation, deactivation, and recovery from inactivation were similar to those of expressed α1G (CaV3.1) Ca2+ channel clones, except that the rate of deactivation was significantly faster. We reproduced the amplitude and kinetics of measured T currents with a numerical simulation based on a kinetic model developed for an α1G Ca2+ channel. Finally, we show that this model predicts the increase of T-type current made available between resting potential and spike threshold by repetitive hyperpolarizations presented at rates that are within the bandwidth of signals processed in situ by these neurons.


2009 ◽  
Vol 29 (47) ◽  
pp. 15001-15016 ◽  
Author(s):  
Y. Hayashida ◽  
C. V. Rodriguez ◽  
G. Ogata ◽  
G. J. Partida ◽  
H. Oi ◽  
...  

2011 ◽  
Vol 52 (8) ◽  
pp. 5515 ◽  
Author(s):  
Preethi S. Ganapathy ◽  
Richard E. White ◽  
Yonju Ha ◽  
B. Renee Bozard ◽  
Paul L. McNeil ◽  
...  

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5713-5724 ◽  
Author(s):  
K.L. McCabe ◽  
E.C. Gunther ◽  
T.A. Reh

Neurons in both vertebrate and invertebrate eyes are organized in regular arrays. Although much is known about the mechanisms involved in the formation of the regular arrays of neurons found in invertebrate eyes, much less is known about the mechanisms of formation of neuronal mosaics in the vertebrate eye. The purpose of these studies was to determine the cellular mechanisms that pattern the first neurons in vertebrate retina, the retinal ganglion cells. We have found that the ganglion cells in the chick retina develop as a patterned array that spreads from the central to peripheral retina as a wave front of differentiation. The onset of ganglion cell differentiation keeps pace with overall retinal growth; however, there is no clear cell cycle synchronization at the front of differentiation of the first ganglion cells. The differentiation of ganglion cells is not dependent on signals from previously formed ganglion cells, since isolation of the peripheral retina by as much as 400 μm from the front of ganglion cell differentiation does not prevent new ganglion cells from developing. Consistent with previous studies, blocking FGF receptor activation with a specific inhibitor to the FGFRs retards the movement of the front of ganglion cell differentiation, while application of exogenous FGF1 causes the precocious development of ganglion cells in peripheral retina. Our observations, taken together with those of previous studies, support a role for FGFs and FGF receptor activation in the initial development of retinal ganglion cells from the undifferentiated neuroepithelium peripheral to the expanding wave front of differentiation.


Neuroscience ◽  
2019 ◽  
Vol 408 ◽  
pp. 400-417 ◽  
Author(s):  
Allison M. Cleymaet ◽  
Shannon K. Gallagher ◽  
Ryan E. Tooker ◽  
Mikhail Y. Lipin ◽  
Jordan M. Renna ◽  
...  

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Spring R Farrell ◽  
Luis Perez Sevilla Mueller ◽  
Allison Sargoy ◽  
Nicholas Brecha ◽  
Steven Barnes

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