Figure 6

Simplified diagram proposal summarizing the OT effects seen in lamina I-II at the light of our present study. Our results indicate that OT, which is physiologically released by hypothalamospinal fibers terminating in lamina I-II, activates a subpopulation of glutamatergic neurons (a) and, in particular, stimulates receptors present on presynaptic glutamatergic synaptic terminals (b). We also show that population of OT-sensitive glutamatergic neurons recruits the whole population of GABAergic neurons (c) resulting in an elevated GABAergic inhibitory tone in lamina II (represented as a green box). The dissection of the spinal action of OT can now unify previous observations which were in apparent contradiction. First, a network driven increase in GABAergic inhibition is likely to explain the specific inhibition of action potential triggered by the nociceptive activation of C and Aδ fibers [21,24]. In this case, a direct presynaptic inhibition of these fibers may be responsible for this effect (d). Alternatively, it remains possible that a specific C/Aδ network is inhibited through presynaptic fibre of neuronal inhibition (d). It remains that neurons, receiving convergent sensory inputs are not the direct target for OT effect since only C/Aδ fibre activity is reduced (e). Second, our findings and mechanism proposal fully answer to the questions left open after the work of Robinson et al [18], i.e. the presynaptic inhibition of glutamate release after stimulation of the dorsal roots and the postsynaptic effect on Lamina I-II neurons (OT sensitive neurons). Abbreviations: E: excitatory glutamatergic neurons; I: inhibitory GABAergic neurons.