title: Expression of L-type calcium channel alpha(1)-1.2 and alpha(1)-1.3 subunits on rat sacral motoneurons following chronic spinal cord injury.
abstract: In the presence of the monoamines serotonin and norepinephrine, motoneurons readily generate large persistent inward currents (PICs). The resulting plateau potentials amplify and sustain motor output. Monoaminergic input to the cord originates in the brainstem and the sharp reduction in monoamine levels that occurs following acute spinal cord injury greatly decreases motoneuron excitability. However, recent studies in the adult sacral cord of the rat have shown that motoneurons reacquire the ability to generate PICs and plateau potentials within 1-2 months following spinal transection. Ca(v)1.3 L-type calcium channels are involved in generating PICs in both healthy and injured animals. Additionally, expression of Ca(v)1.2 and Ca(v)1.3 L-type calcium channels is altered in several pathological conditions. Therefore, in this paper we analyzed the expression of L-type calcium channel alpha(1) subunits within the motoneuron pool following a complete transection of the spinal cord at the level of the sacral vertebra (S)2 segment. The analysis was done both caudally (S4 segment) and rostrally [thoracic vertebra (T)6 segment] from the injury site. The S4 segment was significantly reduced in diameter when compared with control animals, and this reduction was more evident in the white matter. Ca(v)1.2 alpha(1) subunit expression significantly increased (26%) in the motoneuron pool located caudally but not rostrally from the injury site. In contrast, the expression of Ca(v)1.3 alpha(1) subunit remained unchanged in both S4 and T6 segments. The differential expression of the two alpha(1) subunits in spinal injury suggests that Ca(v)1.2 and Ca(v)1.3 channels have different functions in neuronal adaptation following spinal cord injury.
authors.affiliation: Department of Physiology, Northwestern University Feinberg School of Medicine, Morton 5-666, 303 East Chicago Avenue (M211), Chicago, IL 60611, USA. ran806@northwestern.edu
authors.forename: R
authors.initials: R
authors.lastname: Anelli
authors.forename: L
authors.initials: L
authors.lastname: Sanelli
authors.forename: D J
authors.initials: DJ
authors.lastname: Bennett
authors.forename: C J
authors.initials: CJ
authors.lastname: Heckman
mesh_terms: D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000378:metabolism*; D002908:Chronic Disease; D004525:Efferent Pathways / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D008564:Membrane Potentials / Q000502:physiology; D009046:Motor Neurons / Q000378:metabolism*; D021122:Protein Subunits / Q000378:metabolism; D051381:Rats; D012447:Sacrum; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology
chemical_list: D015306:Biogenic Monoamines; D015220:Calcium Channels; D020746:Calcium Channels, L-Type; C419385:L-type calcium channel alpha(1C); D021122:Protein Subunits; C093712:Cacna1d protein, rat