Abstract: The present invention provides a method of bioluminescence-driven optogenetic control of excitable cells. The excitable cell expresses a light-gated ion channel, and a luminescent protein can be expressed either in the excitable cell or in another cell proximal to the excitable cell. The methods of the invention can be used to desynchronize local activity of excitable cells in a mammalian tissue. The methods of the invention can be used to treat a disease or condition in a mammal, the disease or condition being related to bursting. The disease or condition can be Parkinson's disease, epilepsy, a sleep disorder, or a sensory-related disease or condition (e.g., attention deficit disorder or pain). The invention also provides a conjugate of containing a voltage-gated ion channel and a luminescent protein.

Abstract: The present invention provides a method of bioluminescence-driven optogenetic control of excitable cells. The excitable cell expresses a light-gated ion channel, and a luminescent protein can be expressed either in the excitable cell or in another cell proximal to the excitable cell. The methods of the invention can be used to desynchronize local activity of excitable cells in a mammalian tissue. The methods of the invention can be used to treat a disease or condition in a mammal, the disease or condition being related to bursting. The disease or condition can be Parkinson's disease, epilepsy, a sleep disorder, or a sensory-related disease or condition (e.g., attention deficit disorder or pain). The invention also provides a conjugate of containing a voltage-gated ion channel and a luminescent protein.

Abstract: The invention pertains to a human N-type calcium channel isoform, h?1B+SFVG, which is involved in central nervous system signaling, and nucleic acids relating thereto. The present invention also includes fragments and biologically functional variants of the human h?1B+SFVG channel. Also included are human N-type calcium channel h?1B+SFVG subunit inhibitors which inhibit human N-type calcium channel h?1B+SFVG subunit activity by inhibiting the expression or function of human N-type calcium channel h?1B+SFVG subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitors in the treatment and/or diagnosis of disease, such as in methods for treating stroke, pain, e.g., neuropathic pain, and traumatic brain injury.

Abstract: The invention pertains to a human N-type calcium channel isoform, h?1B+SFVG, which is involved in central nervous system signaling, and nucleic acids relating thereto. The present invention also includes fragments and biologically functional variants of the human h?1B+SFVG channel. Also included are human N-type calcium channel h?1B+SFVG subunit inhibitors which inhibit human N-type calcium channel h?1B+SFVG subunit activity by inhibiting the expression or function of human N-type calcium channel h?1B+SFVG subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitors in the treatment and/or diagnosis of disease, such as in methods for treating stroke, pain, e.g., neuropathic pain, and traumatic brain injury.

Abstract: The invention pertains to a human N-type calcium channel isoform, h?1B+SFVG, which is involved in central nervous system signaling, and nucleic acids relating thereto. The present invention also includes fragments and biologically functional variants of the human h?1B+SFVG channel. Also included are human N-type calcium channel h?1B+SFVG subunit inhibitors which inhibit human N-type calcium channel h?1B+SFVG subunit activity by inhibiting the expression or function of human N-type calcium channel h?1B+SFVG subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitors in the treatment and/or diagnosis of disease, such as in methods for treating stroke, pain, e.g., neuropathic pain, and traumatic brain injury.

Abstract: The invention pertains to N-type calcium channel isoforms containing exon 37a (Cav2.2e[37a]), which are specifically expressed in nociceptive neurons, and nucleic acids relating thereto. Also included are methods for identifying antagonists of Cav2.2e[37a] subunit activity that act by inhibiting the expression or function of the subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitor molecules in the treatment and/or diagnosis of disease, such as in methods for treating pain, particularly neuropathic pain.

Abstract: The invention pertains to a human N-type calcium channel isoform, h&agr;1B+SFVG, which is involved in central nervous system signaling, and nucleic acids relating thereto. The present invention also includes fragments and biologically functional variants of the human h&agr;1B+sFvGchannel. Also included are human N-type calcium channel h&agr;1B+SFVG subunit inhibitors which inhibit human N-type calcium channel h&agr;1B+SFVG subunit activity by inhibiting the expression or function of human N-type calcium channel h&agr;1B+SFVG subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitors in the treatment and/or diagnosis of disease, such as in methods for treating stroke, pain, e.g., neuropathic pain, and traumatic brain injury.

Abstract: The invention pertains to a human N-type calcium channel isoform, h&agr;1B+SFVG, which is involved in central nervous system signaling, and nucleic acids relating thereto. The present invention also includes fragments and biologically functional variants of the human h&agr;1B+SFVG channel. Also included are human N-type calcium channel h&agr;1B+SFVG subunit inhibitors which inhibit human N-type calcium channel h&agr;1B+SFVG subunit activity by inhibiting the expression or function of human N-type calcium channel h&agr;1B+SFVG subunit. The invention further relates to methods of using such nucleic acids, polypeptides, and inhibitors in the treatment and/or diagnosis of disease, such as in methods for treating stroke, pain, e.g., neuropathic pain, and traumatic brain injury.