Meeting Abstract

S1.5  Tuesday, Jan. 4  Persistent inward currents in mouse spinal motoneurons: subcellular origins, postnatal development and neuropathology. QUINLAN, K.A.*; HECKMAN, C.J.; Northwestern University Feinberg School of Medicine; Northwestern University Feinberg School of Medicine katharina-quinlan@northwestern.edu

Persistent inward currents (PICs) have been described in neurons from many experimental preparations, from adult turtle and cat to embryonic cultured mouse spinal neurons. They are are low-voltage activated, slowly-inactivating currents mediated by Na⁺ and Ca²⁺ channels (Nav1.1 & 1.6 and Cav 1.3 channels most likely). PICs are both central to intrinsic excitability and highly dependent on the extrinsic environment, such that a neuron will not fire repetitively while PICs are blocked and are profoundly influenced by the presence of neuromodulators and the state of disease or injury. Specifically, PICs are upregulated in an animal model of spinal cord injury and the mouse model of amyotrophic lateral sclerosis (ALS), the SOD1^G93A mouse. This talk will discuss PICs in diseased and non-diseased states in spinal motoneurons, covering recent results on the Na⁺ and Ca²⁺ PIC in SOD1^G93A motoneurons, both of which show a progressively increased amplitude in SOD1^G93A motoneurons during postnatal development. In addition, recent results obtained through the use of 2 photon microscopy and Ca²⁺ sensitive dyes on the dendritic origins of the Ca²⁺ PIC and its modification by serotonin and other neuromodulators will be presented in the context of its contribution to intrinsic excitability and overall network activity.