Figure 4.

The microcircuit of the superior colliculus. Reduced GABA_B inhibition causes pronged burst duration firing in both the sensory and premotor neurons. A postulated mechanism for both abnormal temporal discrimination and cervical dystonia. Diagram of the local circuit underlying GABA_B receptor-mediated regulation of bursts in the superior colliculus [adapted from an original study kindly provided by Professor Tadashi Isa, from Ref. (82)]. Post-synaptic GABA_B receptors expressed in both NFV and WFV cells and presynaptic GABA_B receptors located on glutamatergic synaptic terminals in the SLSC are activated by synaptically released GABA during bursts of SLSC GABAergic neurons. GABA_B inhibition normally curtails the discharge of both the sensory and premotor neurons. When GABA_B receptors are blocked, burst duration in sensory neurons, the SLSC, may be prolonged in an NMDA receptor-dependent manner. Under conditions of reduced GABA_B inhibition, this prolonged bursting may spread to the DLSC involving the oculomotor and cephalomotor premotor neurons. This prolonged bursting is postulated to result in excessive cephalomotor neuronal activity and result in cervical dystonia. DLSC, intermediate and deep laminae of the superior colliculus; GABA, gamma-aminobutyric acid; NMDA, n-methyl-D-aspartate; NFV, narrow field vertical cell; SLSC, superficial lamina of superior colliculus; WFV, wide field vertical.