Fig. 3. Role of α7subunit–containing nicotinic receptors in ketamine responses. α Bungarotoxin (αBgTx), a selective antagonist of nicotinic receptors containing the α7subunit, did not alter the nicotine-evoked inward current (A ) or increase in miniature glutamatergic synaptic event (mini) amplitude (B ), but did block the nicotine-evoked alteration in mini frequency (C ). These results are consistent with the findings that nicotinic receptors containing α7subunits are predominantly located presynaptically and alter the probability of transmitter release. Inclusion of ketamine in the perfusate continued to inhibit the nicotine-evoked inward current (D ), but the effect of ketamine on the nicotine-evoked increase in mini frequency was occluded by the presence of αBgTx (F ). Neither ketamine nor αBgTx had an effect on mini amplitude (E ).

Fig. 3. Role of α7subunit–containing nicotinic receptors in ketamine responses. α Bungarotoxin (αBgTx), a selective antagonist of nicotinic receptors containing the α7subunit, did not alter the nicotine-evoked inward current (A ) or increase in miniature glutamatergic synaptic event (mini) amplitude (B ), but did block the nicotine-evoked alteration in mini frequency (C ). These results are consistent with the findings that nicotinic receptors containing α7subunits are predominantly located presynaptically and alter the probability of transmitter release. Inclusion of ketamine in the perfusate continued to inhibit the nicotine-evoked inward current (D ), but the effect of ketamine on the nicotine-evoked increase in mini frequency was occluded by the presence of αBgTx (F ). Neither ketamine nor αBgTx had an effect on mini amplitude (E ).

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