Inhibition from the brain stem of inhibitory interneurones of the cat's dorsal lateral geniculate nucleus.

Abstract

SUMMARY1. Brain-stem control of inhibitory circuits in the dorsal lateral geniculate nucleus (d.l.g.n.) of the cat was studied with extracellular recordings from functionally identified interneurones and with intracellular recordings from principal cells.2. Perigeniculate neurones, the recurrent inhibitory interneurones of the d.l.g.n., were inhibited by low-threshold stimulation within a wide bilateral field of the brainstem reticular formation extending from the rostral mesencephalon to the caudal medulla oblongata. The inhibition had a latency of 10-12 ms for stimulation sites in the mesencephalon and a duration of about 100 ms. The brain-stem stimulation evoked large hyperpolarizing potentials in intracellularly recorded perigeniculate neurones, indicating that the effect was due to post-synaptic inhibition.3. Intrageniculate interneurones, the feed-forward inhibitory interneurones of the d.l.g.n., were inhibited with a similar time course from the same region of the brain stem.4. Both feed-forward and recurrent inhibitory post-synaptic potentials (i.p.s.p.s) in principal cells were depressed by a preceding stimulation of brain-stem sites effective for the interneurones. The depression had about the same time course as the inhibition of the interneurones and it occurred without a concomitant change in the membrane potential of the recorded principal cells.5. A small depolarizing potential, with a latency of 10-20 ms, was observed in some principal cells after brain-stem stimulation. The potential reversed polarity when i.p.s.p.s were reversed by current injection into the recorded cell indicating that it was due to disinhibition of the principal cells.6. The possible neuronal pathway for the inhibition of the d.l.g.n. interneurones is considered and it is proposed that the effect is mediated by a group of neurones located in the caudal mesencephalon and the rostral pons close to the fibres of the brachium conjunctivum.

Muscarinic Regulation of Dendritic and Axonal Outputs of Rat Thalamic Interneurons: A New Cellular Mechanism for Uncoupling Distal Dendrites

“…An early in vivo study has shown that activation of brainstem cholinergic cells, which project to the thalamic nuclei, can induce a large hyperpolarization in geniculate interneurons (Ahlsén et al, 1984), caused presumably by activation of a potassium conductance (McCormick and Pape, 1988). Here, we show that in addition to a potassium conductance, activation of muscarinic receptors also enhances I h and I CAN .…”

“…Activation of the cholinergic input from the brainstem, which occurs during arousal, affects sensory transmission in the thalamus (Sillito et al, 1983;Francesconi et al, 1988;Heggelund, 1994, 1995;Uhlrich et al, 1995). In particular, inhibitory sharpening of sensory information is dramatically altered during the activation (Ahlsén et al, 1984;Hu et al, 1989;Murphy et al, 1994). In vitro studies have shown that various neuromodulators change the membrane potential of reticular and thalamocortical cells (Steriade et al, 1997), which switches their firing patterns by inactivating or deinactivating a low-threshold calcium current crucial for burst firing (Huguenard, 1996).…”

Actions of acetylcholine in the guinea‐pig and cat medial and lateral geniculate nuclei, in vitro.

“…Possible involvement of ACh in the ascending control of arousal Electrophysiological recording (Steriade, Oakson & Ropert, 1982), stimulation (Moruzzi & Magoun, 1949;Symmes & Anderson, 1967;Satinsky, 1968;Foote et al 1974;Kitsikis & Steriade, 1981;Ahlsen, Lindstr6m, & Lo, 1984;Francesconi et al 1984) and lesion (Watson, Heilman, Miller & King, 1974) experiments (also see reviews by Steriade, 1970;Singer, 1977;Burke & Cole, 1978) have indicated the presence of an ascending brain-stem system which has the ability to control the level of neuronal excitability in both the thalamus and cerebral cortex. The possibility that the brain-stem influences may be mediated, at least in part, by the activation of ACh-releasing neurones has been suggested by a number of investigators (Singer, 1977;Steriade & Deschenes, 1984;Sherman & Koch, 1986).…”

The variability of the maintained discharge of cat dorsal lateral geniculate cells.

“…Dubin & Cleland, 1977;Lindstrom, 1982), and the third from intrageniculate interneurones (Dubin & Cleland, 1977;but see Friedlander, Lin, Stanford & Sherman, 1981). An indirect input through both the perigeniculate nucleus and the intrageniculate interneurones comes from the mesencephalic reticular formation (Singer, 1977;Ahlsen, Lindstrom & Lo, 1984). It has been suggested that the variability of relay cells depends upon activity in the reticular formation (e.g.…”