A study of cholinoceptive cells in the lateral geniculate nucleus

Abstract

SUMMARY1. 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-,8-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 ofACh sensitive neurones in the LGN. Benzoquinonium abolished the excitatory effects of reticular formation stimulation.

Further Studies on the Mode of Action of Psychotomimetic Drugs: Antagonism of the Excitatory Actions of 5‐hydroxytryptamine by Methylated Derivatives of Tryptamine

“…LSD and LSD-like drugs do, however, appear to have some effects which are similar to the effects of increasing 5-HT activity in the CNS (Anden et al, 1968(Anden et al, , 1971Fuxe et al, 1972). LSD has frequently been reported to inhibit neurones which 5-HT inhibits (Curtis & Davis, 1962;Phillis, Tebecis & York, 1967;Aghajanian et al, 1972), although the 'mimicking' of 5-HT inhibitory effects by LSD and psychotomimetic tryptamines is not a universal finding (Boakes et al, 1970;present investigation). Nevertheless, mimicking of 5-HT inhibitory effects on neurones in some brain areas may explain some of the actions of these drugs; this possibility is not incompatible with the findings of antagonism of 5-HT excitation in other areas.…”

Brain stem stimulation and the acetylcholine‐evoked inhibition of neurones in the feline nucleus reticularis thalami

“…On the other hand, it has been reported that MRF-evoked excitations of long-latency and duration in the lateral geniculate nucleus (Phillis, Tebecis & York, 1967), ventrobasal complex (McCance et al 1968) and the cerebral cortex (Spehlmann & Smathers, 1974) Since the late phase of MRF-evoked inhibition of nucleus reticularis cells is often atropine sensitive and mimics the characteristic burstpromoting properties of ACh on these neurones, we suggest that stimulation of the MRF activates an inhibitory cholinergic pathway to the nucleus reticularis. In much the same way, others have shown that ACh-inhibited neurones of the cerebral cortex are also inhibited by MRF stimulation (Phillis & York, 1967), and it has been postulated that the ACh-inhibited neurones of the cortex function to inhibit the more deeply situated projecting pyramidal neurones (Krnjevic, 1974). Thus, analogous feed-back pathways may exist in the thalamus and cortex, in which collaterals of the projecting neurones of both structures activate a recurrent inhibitory interneurone that is itself under cholinergic inhibitory control mediated by the MRF.…”

Antagonism by Some Antihistamines of the Amino Acid‐evoked Responses Recorded From the Lobster Muscle Fibre and the Frog Spinal Cord

“…Microiontophoretically applied histamine depresses the firing of feline brain and spinal neurones (Krnjevic & Phillis, 1963;Phillis, Tebecis & York, 1968a,b;Haas, Anders & Hosli, 1973); however, these effects are often non-specifically antagonized by histamine H1-and H2-receptor blockers (Phillis et al, 1968a;Haas & Bucher, 1975;Haas, Wolf & Nussbaumer, 1975). This non-specificity has been tentatively attributed either to a blockade of axonal conduction (i.e.…”

“…This non-specificity has been tentatively attributed either to a blockade of axonal conduction (i.e. a local anaesthetic effect; Reuse, 1948;Phillis et al, 1968a) or to a direct 'non-selective' action on the neuronal membrane (Haas, 1974); furthermore the ability of the antihistamines to block receptors other than the histamine receptor is well known (Goodman & Gilman, 1975).…”