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18. Sites and Regulation of L-Type Ca2+ Channel Cav1.2 Phosphorylation in Brain.

Author

Shin, Seok Kyo, Li, Hai Ying, Cho, Kun, Cho, Young Wuk, Lee, Jung-Ha, and Park, Kang-Sik

Subjects
CALCIUM channels, PHOSPHORYLATION, MYOCARDIUM, NEUROPLASTICITY, MASS spectrometry
Abstract

Cav1.2 channel phosphorylation plays an important role in regulating neuronal plasticity by action potential-dependent Ca2+ entry. Most studies of Cav1.2 regulation by phosphorylation have been reported in heart and muscles. Here, we identified phosphorylation sites of neuronal Cav1.2 channel protein purified from rat brain using mass spectrometry. The functional characterization of these phosphorylation sites showed altered voltage-dependent biophysical properties of the channel, without affecting current density. These results show that neuronal Cav1.2 channel is regulated by phosphorylation in a complex mechanism involving multiple phosphorylation sites. [ABSTRACT FROM AUTHOR]

Published
2022
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23. Reversal of neuropathic pain in diabetes by targeting glycosylation of [Ca.sub.v]3.2 T-type calcium channels

Author

Orestes, Peihan, Osuru, Hari Prasad, McIntire, William E., Jacus, Megan O., Salajegheh, Reza, Jagodic, Miljen M., Choe, WonJoo, Lee, JeongHan, Lee, Sang-Soo, Rose, Kirstin E., Poiro, Nathan, DiGruccio, Michael R., Krishnan, Katiresan, Covey, Douglas F., Lee, Jung-Ha, Barrett, Paula Q., Jevtovic-Todorovic, Vesna, and Todorovic, Slobodan M.

Subjects
Diabetes -- Complications and side effects -- Care and treatment -- Research, Calcium channels -- Physiological aspects -- Genetic aspects -- Research, Peripheral nerve diseases -- Causes of -- Development and progression -- Care and treatment -- Research, Health
Abstract

It has been established that [Ca.sub.v]3.2 T-type voltage-gated calcium channels (T-channels) play a key role in the sensitized (hyperexcitable) state of nociceptive sensory neurons (nociceptors) in response to hyperglycemia associated with diabetes, which in turn can be a basis for painful symptoms of peripheral diabetic neuropathy (PDN). Unfortunately, current treatment for painful PDN has been limited by nonspecific systemic drugs with significant side effects or potential for abuse. We studied in vitro and in vivo mechanisms of plasticity of [Ca.sub.v]3.2 T-channel in a leptin-deficient (ob/ob) mouse model of PDN. We demonstrate that posttranslational glycosylation of specific extracellular asparagine residues in [Ca.sub.v]3.2 channels accelerates current kinetics, increases current density, and augments channel membrane expression. Importantly, deglycosylation treatment with neuraminidase inhibits native T-currents in nociceptors and in so doing completely and selectively reverses hyperalgesia in diabetic ob/ob mice without altering baseline pain responses in healthy mice. Our study describes a new mechanism for the regulation of [Ca.sub.v]3.2 activity and suggests that modulating the glycosylation state of T-channels in nociceptors may provide a way to suppress peripheral sensitization. Understanding the details of this regulatory pathway could facilitate the development of novel specific therapies for the treatment of painful PDN. Diabetes 62:3828-3838, 2013, Despite significant advances in glucose monitoring and insulin therapy, people with diabetes remain hyperglycemic during significant portions of the day, placing them at increased risk for the development of diabetes [...]

Published
2013
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37. Molecular characterization of a neuronal low-voltage-activated T-type calcium channel

Author

Perez-Reyes, Edward, Cribbs, Leanne L., Daud, Asif, Lacerda, Antonio E., Barclay, Jane, Williamson, Magali P., Fell, Margaret, Rees, Michele, and Lee, Jung-Ha.

Subjects
Calcium channels -- Research, T cells -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The identification of a neuronal T-type channel is reported, using a cloning strategy. An expressed sequence tag (EST) was expressed, which was then used to clone a full-length complementary DNA from rate brain. The human gene was mapped to chromosome 17q22 and the mouse gene to chromosome 11. It is concluded that the channel is a low-voltage-activated T-type calcium channel.

Published
1998

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