Modulation of neurotransmission by nicotinic receptors in the mouse ventral lateral geniculate nucleus (LGNv)

The objective was to examine the role of nicotinic acetylcholine receptors (nAChRs) in the mouse LGNv. The rodent LGNv contains high densities of nAChRs (J. Neurosci. 7: , 1987) and is innervated by cholinergic fibers from the pedunculopontine tegmentum (J. Comp. Neurol. 299:, 1990). Whole‐cell patch clamp electrophysiology was carried out in brain slices prepared from 5–21 day old mice. Atropine (1 μM) was present at all times to block muscarinic responses. The LGNv receives a major glutamatergic input from the optic tract. Electrical stimulation of this tract with a small bipolar electrode resulted in a biphasic response in LGNv neurons held at −40 mV with potassium gluconate internal pipette solution. An initial monosynaptic glutamatergic inward current was followed by a slower GABAergic outward current. Application of acetylcholine (ACh; 1 mM by U‐tube) produced a marked increase (greater than 2‐fold) in the optic tract‐evoked glutamatergic response in LGNv neurons. This response appeared to be due to presynaptic nAChRs located on glutamatergic terminals. Postsynaptic nAChRs were present on LGNv somata/dendrites, since ACh caused a direct inward current in most neurons. Both pre‐ and postsynaptic nAChR responses were blocked by 10 μM dihydro‐beta‐erythroidine (DHBE). The morphology of some LGNv neurons was examined using biocytin in the patch electrodes. Immunohistochemistry using an antibody to the vesicular ACh transporter (VAChT) revealed considerable cholinergic fibers and nerve endings in the LGNv.