Journal of neurophysiology
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Comparative Study
Presynaptic A1 inhibitory/A2A facilitatory adenosine receptor activation balance depends on motor nerve stimulation paradigm at the rat hemidiaphragm.
1. Adenosine modulates acetylcholine (ACh) release from the rat motor nerve terminals. Tonic activation of presynaptic A1 inhibitory and/or A2A facilitatory adenosine receptors is regulated by the concentration of the nucleoside at the synapse. ⋯ In contrast, the inhibitory effect of the A1 receptor agonist R-N6-phenylisopropyladenosine was significantly attenuated in both stimulation conditions. 6. In conclusion, the results suggest that high-intensity, high-frequency motor nerve stimulation critically influences endogenous adenosine formation and the A1/A2A receptor activation balance, i.e., it potentiates the tonic adenosine A2A-receptor-mediated facilitation of ACh release, whereas activation of the inhibitory A1 receptors becomes less effective. A model is proposed that attempts to further elucidate adenosine's involvement in synaptic transmission adaptation.
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1. Primary afferent depolarization (PAD) can be evoked by sensory volleys, supraspinal commands, or the activity of spinal locomotor networks (locomotor-related PAD). In this study we investigated the effect of locomotor-related PAD and of sensory-evoked PAD on the monosynaptic transmission between the group IA muscle afferents and motoneurons in the lumbosacral spinal cord. 2. ⋯ We conclude from these results that the locomotor-related PAD did not contribute significantly to the modulation of transmission in the monosynaptic reflex pathway of the cat during fictive locomotion. On the other hand, the results confirmed that PAD evoked by sensory input decreases group IA afferent transmission efficiently most probably by presynaptic inhibition. The results suggest therefore that, during real locomotion, sensory feedback induced by the moving limbs or perturbations will evoke an important presynaptic inhibition of the release from group IA primary afferent terminals.
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1. The introduction of a period of darkness between the disappearance of an initial fixation target and the appearance of a peripheral saccade target produces a general reduction in saccadic reaction time (SRT)-known as the gap effect- and often very short latency express saccades. To account for these phenomena, premotor processes may be facilitated by release of visual fixation and advanced preparation of saccadic programs. ⋯ These findings indicate that training-dependent express saccades are restricted to a specific spatial location dictated by the training target, and their incidence is facilitated by high predictability of target presentation, long-duration foreperiod, absence of visual fixation, eccentric initial eye position opposite to the saccade direction, and express saccade occurrence in the previous trial. The release of fixation afforded by the gap accounts for the general gap effect, but has only a modulatory influence on express saccade generation. We conclude that advanced motor preparation of saccadic programs generally reduces SRT and is primarily responsible for the occurrence of express saccades, which therefore may be caused mainly by neuronal changes restricted to a specific locus-coding for the trained movemen