Motoneurones are known to die (1) during embryonic development (naturally occurring cell death), (2) early in postnal development after axonal injury, and (3) as a consequence of disease such as SMA. Interactions with the target emerges as an important factor for survival of developing montoneurones. The evidence for the target dependence od of developing motoneurones will be presented and the mechanisms by which the muscle may regulate motoneurone survival discussed. Results that argue for the following proposal will be given: with maturation of the CNS motor activity in all mammals increases as do the functional demands on the motoneurones. The target muscle's role is to induce changes in the motoneurone to make it competent to respond to increased amounts of glutamate from excitatory inputs and thus allow it to carry out the tasks associated with its increased activity. A failure of the muscle to induce these changes in the motonerone's phenotype in time may lead to motoneurone death. In addition new approaches that could (1) improve motoneurone survival, and (2) use embryonic grafts to replace the lost cells will be discussed.
The influence of a pair of stimuli running in time sequence between 5-10 ms (a doublet) on the basic parameters of antidromic action potentials was studied in rat motoneurones. Electrophysiological experiments were based on stimulation of axons in the sciatic nerve and intracellular recording of antidromic action potentials from individual motoneurones located in L4-L5 segments of the spinal cord. The following parameters were analyzed after application of a single stimulus and a doublet: amplitude and duration of the antidromic spike, amplitude, total duration, time to minimum, half-decay time of the afterhyperpolarization (AHP). It was demonstrated that application of a pair of stimuli resulted in: (1) a prolongation of action potentials, (2) a prolongation of the total duration and half-decay time of the AHP, (3) a decline of the time to minimum of the AHP, (4) an increase of the AHP amplitude of the spike evoked by the second stimulus. Significant differences in AHP parameters were found either in fast or slow motoneurones. We suppose that doublet-evoked changes in the AHP amplitude and duration are linked to intrinsic properties of individual motoneurones and may lead to the prolongation of the time interval to subsequent motoneuronal discharges during voluntary activity.
Locomotor exercise increases neurotrophin BDNF and its receptor TrkBFL expression in the lumbar spinal cord. Involvement of BDNF/TrkBFL in synaptic transmission raises the questions which intracellular compartments are involved in this upregulation and whether exercise leads to redistribution of these proteins related to the duration of exercise. We have investigated the influence of short-term (7 days) locomotor exercise (ST) on intracellular distribution of BDNF and TrkBFL in the rat lumbar spinal cord comparing it with the effects of long-term (28 days) exercise (LT) described earlier. Immunofluorescence (IF) of proteins was analyzed with confocal microscopy. ST exercise caused a redistribution of perikaryonal BDNF IF toward periphery resulting in an increase of dendritic signal. In contrast to an enhancement of perikaryonal BDNF staining following LT, no increase of BDNF IF in cell bodies was observed after ST. An increase of TrkBFL IF in oligodendrocytes was consistent with that caused by LT. The fibers of TrkBFL IF oligodendrocytes surrounding the largest neurons were in close apposition to neuronal membrane. We propose that ST exercise causes (1) BDNF translocation to dendrites and/or local dendritic synthesis to serve increased synaptic activity (2) sensitization of oligodendroglia to BDNF mediated responses.
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