Abstract: Neuroprotective peptides derived from the voltage-gated potassium channel Kv2.2 are described. The peptides promote dispersal of the cognate channel Kv2.1 in neurons, thereby blocking pro-apoptotic potassium efflux, and preserving cell viability after apoptotic injury. Methods of preventing and treating neuronal damage, such as neuronal damage following ischemic stroke, by administering the neuroprotective peptides are described. Fusion of the neuroprotective peptides to a cell-penetrating peptide to promote cellular uptake is also described.

Abstract: Peptides capable of enhancing N-methyl D-aspartate (NMDA) receptor activity by inhibiting binding of the NMDA receptor GluN2A to zinc transporter 1 (Zn1) are described. The GluN2A-derived peptides can be used to in the treatment of disorders associated with NMDA receptor hypofunction, such as schizophrenia.

Abstract: Neuroprotective peptides derived from the voltage-gated potassium channel Kv2.2 are described. The peptides promote dispersal of the cognate channel Kv2.1 in neurons, thereby blocking pro-apoptotic potassium efflux, and preserving cell viability after apoptotic injury. Methods of preventing and treating neuronal damage, such as neuronal damage following ischemic stroke, by administering the neuroprotective peptides are described. Fusion of the neuroprotective peptides to a cell-penetrating peptide to promote cellular uptake is also described.

Abstract: Disclosed herein are small molecule compounds capable of disrupting Kv2.1-syntaxin binding. The compounds are useful for treating a variety of neurological disorders, diseases, and injuries.

Abstract: Peptides capable of interfering with the Kv2.1-mediated apoptotic K+ current surge that leads to neuronal cell death are described. The disclosed peptides are derived from the C-terminal region of Kv2.1, which mediates binding to the SNARE protein syntaxin. Disruption of Kv2.1 binding to syntaxin inhibits the apoptotic K+ current surge that leads to neuronal cell death. The present disclosure provides methods of inhibiting binding of Kv2.1 to syntaxin in a cell (in vitro or in vivo), such as for neuroprotection following cerebral ischemia, stroke, or traumatic brain injury, or during the course of a neurodegenerative disease, or any other condition associated with neuronal cell death.

Abstract: Peptides capable of interfering with the Kv2.1-mediated apoptotic K+ current surge that leads to neuronal cell death are described. The disclosed peptides are derived from the C-terminal region of Kv2.1, which mediates binding to the SNARE protein syntaxin. Disruption of Kv2.1 binding to syntaxin inhibits the apoptotic K+ current surge that leads to neuronal cell death. The present disclosure provides methods of inhibiting binding of Kv2.1 to syntaxin in a cell (in vitro or in vivo), such as for neuroprotection following cerebral ischemia, stroke, or traumatic brain injury, or during the course of a neurodegenerative disease, or any other condition associated with neuronal cell death.

Abstract: A method of resisting neurological damage caused by overstimulation of the NMDA receptor of nerve cells by glutamate includes exposing the NMDA receptors to an oxidizing agent to thereby diminish overall activity of the receptors following activation by glutamate. The oxidizing agent preferably is a material selected from the group consisting of pyrroloquinoline quinone and topa hydantoin.

Abstract: A method for resisting neurological damage caused by overstimulation of the MDA receptor of nerve cells by glutamate includes exposing the NMDA receptors to an oxidizing agent to thereby diminish overall activity of the receptors following activation by glutamate. The oxidizing agent preferably is a material selected from the group consisting of pyrroloquinoline quinone and topa hydantoin.