scholarly journals Role of the Hyperpolarization‐Activated Cation Current ( I h ) in Pacemaker Activity in Area Postrema Neurons of Rat Brain Slices

2003 ◽  
Vol 552 (1) ◽  
pp. 135-148 ◽  
Author(s):  
Makoto Funahashi ◽  
Yoshihiro Mitoh ◽  
Atsushi Kohjitani ◽  
Ryuji Matsuo
1980 ◽  
Vol 190 (2) ◽  
pp. 333-339 ◽  
Author(s):  
M C W Minchin

1. Protoveratrine A increased the release of gamma-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 microM. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 microM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for gamma-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated gamma-aminobutyrate release also inhibited 22Na+ uptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced gamma-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.


1998 ◽  
Vol 112 (supplement) ◽  
pp. 148-152
Author(s):  
Keisuke Migita ◽  
Nobuaki Hori ◽  
Ryo Saito ◽  
Kenji Honda ◽  
Yukio Takano ◽  
...  

1991 ◽  
Vol 204 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Matsuda Toshio ◽  
Shimizu Isao ◽  
Baba Akemichi

1998 ◽  
Vol 256 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Keisuke Migita ◽  
Nobuaki Hori ◽  
Jun-ichiro Manako ◽  
Ryo Saito ◽  
Yukio Takano ◽  
...  

2007 ◽  
Vol 1165 ◽  
pp. 50-59 ◽  
Author(s):  
Naoki Kodama ◽  
Makoto Funahashi ◽  
Yoshihiro Mitoh ◽  
Shogo Minagi ◽  
Ryuji Matsuo

2006 ◽  
Vol 95 (2) ◽  
pp. 619-626 ◽  
Author(s):  
Takashi Okamoto ◽  
Mark T. Harnett ◽  
Hitoshi Morikawa

Ethanol stimulates the firing activity of midbrain dopamine (DA) neurons, leading to enhanced dopaminergic transmission in the mesolimbic system. This effect is thought to underlie the behavioral reinforcement of alcohol intake. Ethanol has been shown to directly enhance the intrinsic pacemaker activity of DA neurons, yet the cellular mechanism mediating this excitation remains poorly understood. The hyperpolarization-activated cation current, Ih, is known to contribute to the pacemaker firing of DA neurons. To determine the role of Ih in ethanol excitation of DA neurons, we performed patch-clamp recordings in acutely prepared mouse midbrain slices. Superfusion of ethanol increased the spontaneous firing frequency of DA neurons in a reversible fashion. Treatment with ZD7288, a blocker of Ih, irreversibly depressed basal firing frequency and significantly attenuated the stimulatory effect of ethanol on firing. Furthermore, ethanol reversibly augmented Ih amplitude and accelerated its activation kinetics. This effect of ethanol was accompanied by a shift in the voltage dependence of Ih activation to more depolarized potentials and an increase in the maximum Ih conductance. Cyclic AMP mediated the depolarizing shift in Ih activation but not the increase in the maximum conductance. Finally, repeated ethanol treatment in vivo induced downregulation of Ih density in DA neurons and an accompanying reduction in the magnitude of ethanol stimulation of firing. These results suggest an important role of Ih in the reinforcing actions of ethanol and in the neuroadaptations underlying escalation of alcohol consumption associated with alcoholism.


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