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. 2010 Nov 10;105(1):423–433. doi: 10.1152/jn.00876.2010

Fig. 1.

Fig. 1.

A: medullary slices contain hypoglossal motoneurons (XII MNs; inset) that receive spontaneous rhythmic respiratory input from pre-Bötzinger complex (preBötC) inspiratory neurons via premotor neurons in the intermediate medullary reticular formation (IRt). XII motoneurons (MNs) innervate the tongue muscles and the XII MN population activity can be recorded in XII nerve rootlets, while simultaneously recording whole cell current (Im) from single XII MNs. 5SP, spinal trigeminal nucleus; NA, nucleus ambiguous; IO, inferior olive; V4, fourth ventricle. B: long-duration voltage-clamp recording of a rhythmically active XII MN, showing the effects of nicotine (0.5 μM) superfusion into the recording chamber. Note the slight nicotine-evoked depolarizing inward current, the increase in XII nerve burst frequency, and the increase in excitatory postsynaptic currents (EPSCs) in the interburst interval compared with control and wash. C: bath application of glutamate receptor antagonists (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801; 20 μM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20 μM) abolishes rhythmic, respiratory-related inward currents and EPSCs in voltage-clamped XII MNs. D: voltage-clamp recording showing that bath application of nicotinic acetylcholine receptor (nAChR) blockers dihydro-β-erythroidine hydrobromide (DH-β-E, 0.2 μM) and α-bungarotoxin (α-Bgtx; 0.1 μM) causes reductions in XII MN synaptic activity in the interburst period and also decreases the frequency of phasic inspiratory modulated inward drive currents.