Nicotine-induced reflex depression of alpha motoneuron activity in the absence of fusimotor-spindle feedback.
The effects of nicotine on the stretch reflex and on electrically induced monosynaptic and cutaneous polysynaptic reflex responses at a lumbosacral level were studied in lightly anesthetized (chloralose-urethane) cats in which the regional fusimotor-spindle loops had been interrupted by ventral rhizotomy. Doses of 15-40 mug/kg injected into the superior vena cava or the right atrium produced depression of the reflex responses in extensor and flexor alpha motoneurons after latent periods of 1-3 sec, while gamma activity was initially accelerated. The early phase of this alpha depression was abolished by bilateral vagotomy. Sebacylcholine (a nicotinic agent) and acetylcholine also caused depression of evoked alpha activity in the absence of spindle feedback. It is concluded that nicotine activates a viscerosomatic reflex by exciting sensory receptors in the cardiopulmonary region and that alpha motor depression results independent of the changes in gamma activity. However, alpha depression with delayed onset can still be elicited by nicotine after vagotomy and Renshaw blockade, and this effect is also duplicated by sebacylcholine and abolished by hexamethonium. In the doses used, spindle or skin afferents were not excited by nicotine. Thus, two more mechanisms are described by which nicotine can depress alpha activity. Both are reflex in nature, one implicating vagal, the other nonvagal peripheral receptors.[1]References
- Nicotine-induced reflex depression of alpha motoneuron activity in the absence of fusimotor-spindle feedback. Ginzel, K.H., Estavillo, J., Eldred, E. J. Neurosci. Res. (1975) [Pubmed]
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