Cholinergic contribution to excitation in a spinal locomotor central pattern generator in XXXX embryos.

@entity1238 @entity3280 @entity535 @entity6959 @entity3409 @entity6325 @entity2607 @entity2899
1. We have investigated whether in @entity1238 embryos, spinal interneurons of the central pattern generator (CPG) receive cholinergic or electrical excitatory input during swimming. The functions of cholinergic excitation during swimming were also investigated. 2. Intracellular recordings were made from rhythmically active presumed premotor interneurons in the dorsal third of the spinal cord. After locally blocking inhibitory potentials with 2 microM strychnine and 40 microM bicuculline, the reliability of spike firing and the amplitude of fast, on-cycle, excitatory postsynaptic potentials (EPSPs) underlying the single on-cycle spikes were measured during fictive swimming. 3. The nicotinic antagonists @entity2899 and @entity6325 (DH beta E, both 10 microM) reversibly reduced the reliability of the spike firing during swimming and reduced the amplitude of the on-cycle EPSP by 16%. DH beta E also reduced the EPSP amplitude in spinalized embryos by 22%. These results indicate that interneurons receive rhythmic cholinergic excitation from a source within the spinal cord. 4. Combined applications of nicotinic and excitatory @entity535 (EAA) antagonists or @entity3409 ( @entity3280 , 100-200 microM) resulted in complete block of the fast EPSP, suggesting that interneurons do not receive electrical excitation. 5. The nicotinic antagonists @entity6959 and @entity2899 (both 5 microM) reduced the duration of episodes of fictive swimming recorded from the ventral roots, in spinal embryos. When applied in the middle of a long episode, @entity2899 decreased the swimming frequency, ruling out an effect on the initiation pathway. The cholinesterase inhibitor @entity2607 (10 microM) increased the duration of swimming episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
