Differential Plasticity in Auditory and Prefrontal Cortices, and Cognitive-Behavioral Deficits Following Noise-Induced Hearing Loss.

Excessive exposure to loud noise causes hearing loss and neural plasticity throughout the auditory pathway. Recent studies have identified that non-auditory regions, such as the hippocampus, are also susceptible to noise exposure; however, the electrophysiological and behavioral consequences of noise-induced hearing loss on the prefrontal cortex (PFC) are unclear. Using chronically-implanted electrodes in awake rats, we investigated neural plasticity in the auditory and prefrontal cortices in the days following noise exposure via metrics associated with spontaneous neural oscillations and the 40-Hz auditory steady-state response (ASSR).

Depletion of plasma membrane-associated phosphoinositides mimics inhibition of TRPM7 channels by cytosolic Mg, spermine, and pH.

Transient receptor potential cation channel subfamily M member 7 (TRPM7) is an ion channel/protein kinase belonging to the TRP melastatin and eEF2 kinase families. Under physiological conditions, most native TRPM7 channels are inhibited by cytoplasmic Mg, protons, and polyamines. Currents through these channels (I) are robustly potentiated when the cell interior is exchanged with low Mg-containing buffers.

Inactivation of TRPM7 kinase in mice results in enlarged spleens, reduced T-cell proliferation and diminished store-operated calcium entry.

T lymphocytes enlarge (blast) and proliferate in response to antigens in a multistep program that involves obligatory cytosolic calcium elevations. Store-operated calcium entry (SOCE) pathway is the primary source of Ca in these cells. Here, we describe a novel modulator of blastogenesis, proliferation and SOCE: the TRPM7 channel kinase.

A novel path to chronic proprioceptive disability with oxaliplatin: Distortion of sensory encoding.

Persistent neurotoxic side effects of oxaliplatin (OX) chemotherapy, including sensory ataxia, limit the efficacy of treatment and significantly diminish patient quality of life. The common explanation for neurotoxicity is neuropathy, however the degree of neuropathy varies greatly among patients and appears insufficient in some cases to fully account for disability. We recently identified an additional mechanism that might contribute to sensory ataxia following OX treatment.