Influences on the gamma-muscle-spindle system from muscle afferents stimulated by increased intramuscular concentrations of arachidonic acid.

There is evidence that static muscular contractions induce a release of arachidonic acid (AA) in the working muscle and that increased concentration of AA in a muscle increases the discharge rate of a subpopulation of groups III and IV muscular afferents. It is also known that activity in groups III and IV muscle afferents may activate gamma-motoneurones to both homo- and heteronymous muscles. The aim of the present study was to investigate if increased concentration of AA in one muscle may influence the activity in primary and secondary muscle spindle afferents (MSAs) from the chemically affected muscle and from surrounding muscles, via fusimotor reflexes. The experiments were made on five cats anaesthetized with alpha-chloralose. The triceps surae (GS) and the posterior biceps and semitendinosus (PBSt) muscles were subjected to sinusoidal stretches. Simultaneous recordings of 2-12 MSAs from these muscles were made and the mean rate of firing and the modulation for each MSA were determined. Responses of 36 MSAs (17 PBSt and 19 GS) were recorded. The responsiveness of the MSAs to injections of AA (0.3-1.0 mg; 0.3-1 ml) was 86% (n = 36) for injections into the arterial supply of the ipsilateral GS muscle and 45% (n = 20) for injections to the contralateral GS muscle. Out of 14 secondary MSAs, only one was unresponsive to ipsilateral AA injections while two of eight were unresponsive to contralateral AA injection. The majority of responses were compatible with predominantly static or mixed dynamic and static fusimotor activation. None of the effects were compatible with inhibition of fusimotor activity. The duration of the effects were usually 2-4 min. However, on some occasions the elevations in MSA activity persisted for up to 1 h. Local anaesthesia of the nerve to the injected muscle always abolished the effects of the injections and control injections of the solution in which the AA was dissolved were ineffective in changing the MSA responses. I.v. injections occasionally induced effects on the MSAs, but such effects were significantly different from those caused by close arterial muscle injections. Thus, increased concentration of AA may excite primary and secondary MSAs from homo- as well as heteronymous muscles, including contralateral muscles, most probably via fusimotor reflexes evoked by activity in chemosensitive muscle afferents.