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J. W. Phillis, A. K. Tebcis and D. H. York

1. The dorsal lateral geniculate nucleus (LGN) of the cat stains densely for acetylcholinesterase, which is present in intra-axonal and extracellular locations.

2. Acetylcholine (ACh), cholinomimetic drugs, anticholinesterases and ACh antagonists were administered iontophoretically to neurones in the LGN.

3. ACh excited eighty-six of 184 (46·7%) geniculate neurones and depressed seven (3·8%).

4. The excitatory response to ACh was frequently larger than that to L-glutamate and had a comparable time course.

5. There was a considerable variation in the proportion of ACh sensitive cells in different animals. ACh firing was facilitated by optic nerve or visual stimulation.

6. Carbamylcholine was the most active of the choline esters tested, frequently exceeding ACh in potency. The other choline esters and nicotine were consistently less active than ACh.

7. Anticholinesterases, eserine, neostigmine and edrophonium potentiated the action of ACh, and often caused excitation. Eserine caused an initial small enhancement in the amplitude of the focal potential evoked by optic nerve stimulation followed by a reduction in amplitude and prolongation of duration of the potential.

8. Atropine and benzoquinonium effectively prevented the ACh excitation of many cells. Dihydro--erythroidine failed to cause a significant reduction in the magnitude of the ACh response. All three ACh antagonists failed to reduce the excitant effects of optic nerve or visual stimulation.

9. Stimulation of the mesencephalic reticular formation caused either an enhancement or a reduction in the excitability of ACh sensitive neurones in the LGN. Benzoquinonium abolished the excitatory effects of reticular formation stimulation.

10. The findings presented in this paper suggest that ACh is the transmitter released by terminals of nerves of the reticular formation projection to the LGN.