Hu_1989_Neurosci_31_1

The mode of action of afferents arising from the brainstem peribrachial region at the midbrain-pontine junction on neurons recorded from the reticular thalamic sector adjacent to the lateral geniculate nucleus (perigeniculate cells) was investigated at the intracellular level in the cat. Experiments were performed in cats under barbiturate or urethane anaesthesia and in non-anaesthetized deafferented animals. Most cats were pretreated with reserpine (1-2 mg/kg) and were also acutely deprived of their retinal and cortical visual inputs. It was found that peribrachial stimulation produced a short train of fast-rising depolarizations followed by a long-lasting period of hyperpolarization in all perigeniculate neurons. Although the latest part of the early depolarizations preceding the hyperpolarization resulted from a parallel activation of lateral geniculate relay neurons by peribrachial afferents, those occurring at shortest latencies appear to result from a direct excitation produced by peribrachial afferents. Furthermore, these early excitatory postsynaptic potentials persisted under deep barbiturate anaesthesia, a condition that prevents activation of thalamic relay neurons by peribrachial stimulation. The evoked hyperpolarization decreased with membrane hyperpolarization, was associated with a 40-50% increase in membrane conductance and was insensitive to Cl injections. It was no longer observed within one hour after i.v. injection of scopolamine. However, the depolarizing responses were not depressed by this muscarinic antagonist. Iontophoretic applications of scopolamine also removed peribrachial-evoked inhibition of synaptic responses triggered by optic chiasma stimulation. The peribrachial input exerted a powerful control on the oscillatory behavior of perigeniculate neurons. Spindle oscillations which are generated within the reticular thalamic complex were readily blocked by peribrachial stimulation. It is then concluded that the transition from an oscillatory to a relay mode of operation in the thalamus is controlled at least in part by a muscarinic inhibition of reticular thalamic neurons. The synaptic mechanism responsible for the early depolarization remains to be elucidated.