Recruitment of cat motoneurons in the absence of homonymous afferent feedback.

This study provides the first test in vivo of the hypothesis that group Ia muscle-stretch afferents aid in preventing reversals in the orderly recruitment of motoneurons. This hypothesis was tested by studying recruitment of motoneurons deprived of homonymous afferent input. Recruitment order was measured in decerebrate, paralyzed cats from dual intra-axonal records obtained simultaneously from pairs of medial gastrocnemius (MG) motoneurons. Pairs of MG motor axons were recruited in eight separate trials of the reflex discharge evoked by stimulation of the caudal cutaneous sural (CCS) nerve. Some reports suggest that reflex recruitment by this cutaneous input should bias recruitment against order by the size principle in which the axon with the slower conduction velocity (CV) in a pair is recruited to fire before the faster CV axon. Recruitment was studied in three groups of cats: ones with the MG nerve intact and untreated (UNTREATED); ones with the MG nerve cut (CUT); and ones with the MG nerve cut and bathed at its proximal end in lidocaine solution (CUT+). The failure of electrical stimulation to initiate a dorsal root volley and the absence of action potentials in MG afferents demonstrated the effective elimination of afferent feedback in the CUT+ group. Recruitment order by the size principle predominated and was not statistically distinguishable among the three groups. The percentage of pairs recruited in reverse order of the size principle was actually smaller in the CUT+ group (6%) than in CUT (15%) or UNTREATED (19%) groups. Thus homonymous afferent feedback is not necessary to prevent recruitment reversal. However, removing homonymous afferent input did result in the expression of inconsistency in order, i.e., switches in recruitment sequence from one trial to the next, for more axon pairs in the CUT+ group (33%) than for the other groups combined (13%). Increased inconsistency in the absence of increased reversal of recruitment order was approximated in computer simulations by increasing time-varying fluctuations in synaptic drive to motoneurons and could not be reproduced simply by deleting synaptic current from group Ia homonymous afferents, regardless of how that current was distributed to the motoneurons. These findings reject the hypothesis that synaptic input from homonymous group Ia afferents is necessary to prevent recruitment reversals, and they are consistent with the assertion that recruitment order is established predominantly by properties intrinsic to motoneurons.

Factors regulating AMPA-type glutamate receptor subunit changes induced by sciatic nerve injury in rats.

Excitatory glutamatergic neurotransmission at Ia afferent-motoneuron synapses is enhanced shortly after physically severing or blocking impulse propagation of the afferent and/or motoneuron axons. We considered the possibility that these synaptic changes occur because of alterations in the number or properties of motoneuron alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors. Therefore, we quantitatively analyzed glutamate receptor (GluR)1, GluR2/3, and GluR4 AMPA subunit immunoreactivity (ir) in motoneurons 3, 7, or 14 days after axotomy or continuous tetrodotoxin (TTX) block of the sciatic nerve. GluR1-ir remained low in experimental and control motoneurons with either treatment and at any date. However, there was a large reduction of GluR2/3-ir (peak at 7 days >60% reduced) and a smaller, but statistically significant, reduction of GluR4-ir (around 10% reduction at days 3, 7, and 14) in axotomized motoneurons. TTX sciatic blockade did not affect AMPA subunit immunostainings. Axonal injury or interruption of the trophic interaction between muscle and spinal cord, but not activity disruption, appears therefore more likely responsible for altering AMPA subunit immunoreactivity in motoneurons. These findings also suggest that synaptic plasticity induced by axotomy or TTX block, although similar in the first week, could be related to different mechanisms. The effects of axotomy or TTX block on motoneuron expression of the metabotropic glutamate receptor mGluR1a were also studied. mGluR1a-ir was also strongly decreased after axotomy but not after TTX treatment. The time course of the known stripping of synapses from the cell somas of axotomized motoneurons was studied by using synaptophysin antibodies and compared with AMPA and mGluR1a receptor changes. Coverage by synaptophysin-ir boutons was only clearly decreased 14 days post axotomy and not at shorter intervals or after TTX block.