Abstract
The injection of l-3,4-dihydroxyphenylalathne (dopa) into acute spinal cats facilitated monosynaptic transmission as indicated by a marked increase in the size of the monosynaptic reflex and a decrease in stimulus-response latency. This was accompanied by a depression of polysynaptic and dorsal root reflexes. The responses to dopa were dose-dependent with minimal effects observed with 5 mg/kg and maximal responses after 40 to 60 mg/kg. The effects of dopa required 15 to 20 minutes to reach a maximum and lasted for 1 to 4 hours, depending on the dose. Pargyline potentiated both the degree and duration of the effects of dopa. The action of dopa on intemneuronal pathways was complex. The excitatory effect of group II and III fibers on the motoneurons was strongly depressed by 10 to 30 mg/kg of dopa as shown by the marked depression of the polysynaptic reflex evoked by high-voltage sural nerve stimulation. These doses of dopa did not affect, or slightly increased the inhibition between opposing muscle groups observed at 2-to 20-msec intervals after a conditioning volley from an antagonistic nerve. Since this inhibition is largely mediated by group II and Ill flexor reflex afferents it is concluded that 10 to 30 mg/kg of dopa selectively depressed group II and III excitatory pathways. Blockade of the group II and III inhibitory pathways occurred with higher doses of dopa. The dorsal root reflex was significantly depressed by dopa, but presynaptic inhibition (as measured by long latency inhibition between nerves of antagonistic muscles) was only slightly depressed by dopa. Concurrently with these changes in reflexes, dopa increased spinal cord catecholamine levels. The injection of 20 mg/kg of dopa increased cord content of dopamine from 0.26 to 8.5 µg/g and norepinephrine from 0.45 to 0.61 µg/g. Thus, dopamine must be considered as a possible mediator of the action of dopa.
Footnotes
- Received March 17, 1969.
- Accepted February 1, 1970.
- © 1970, by The Williams & Wilkins Company
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