An Excitatory Action of Iontophoretically Administered Lithium on Mammalian Central Neurones

Haas, Helmut L.; Ryall, R. W.

doi:10.1111/j.1476-5381.1977.tb07740.x

Cited by 11 publications

(4 citation statements)

References 18 publications

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“…In two cells Lit decreased the baseline firing, although it did not lead to a potentiation but to reductions in the responsiveness to DA. In only two other neurons was there a gradual increase in the firing frequency (Haas and Ryall, 1977), but the reductions in DA effects were still observed, as previously documented for Li + and noradrenaline in the hippocampus (Segal, 1974) andcerebellum (Siggins et al, 1979). Throughout this study the units were recorded for prolonged periods of time (60-180 min) and such variations of base-line firing could be independent of Lit.…”

Section: Resultssupporting

confidence: 80%

Acute effects of lithium on dopaminergic responses: Iontophoretic studies in the rat visual cortex

Gottberg

Montreuil

Reader

1988

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The interactions between lithium and cortical dopaminergic receptors were investigated using the iontophoretic technique to record and apply dopaminergic compounds, GABA, acetylcholine and LiCl on neurons in the primary visual cortex of the rat. The main responses to dopamine (DA) or to the D1 agonist (+/- )SKF38393 on spontaneously-active (SA) or visually-driven (VD) units was a prolonged decrease in firing and a reduction in the responsiveness to pulses of acetylcholine. The D1 antagonist SCH23390, applied iontophoretically or intravenously, blocked or attenuated the inhibitory responses to both DA and (+/- )SKF38393. The D2 agonist quinpirole (LY171555) either produced only slight excitations or had no effects on both VD and SA units. The concomitant application of lithium blocked the inhibitory responses to DA and to (+/- )SKF38393 but did not modify the responsiveness to LY171555. In addition, the DA- and (+/- )SKF38393-induced decreases in responsiveness to acetylcholine were also suppressed by lithium. These effects were on dopaminergic mechanisms, since the excitatory responses to acetylcholine alone as well as the inhibitions caused by GABA were unchanged by the application of lithium. These results imply that the modifications in sensitivity to dopaminergic agents induced by lithium are mediated by dopamine D1 receptors and are discussed in relation to adenylate-cyclase.

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Section: Resultssupporting

confidence: 80%

Acute effects of lithium on dopaminergic responses: Iontophoretic studies in the rat visual cortex

Gottberg

Montreuil

Reader

1988

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“…We have, thus far, been unable to detect an effect of these cholinergic agents on myo-inositol levels (Allison, 1978).The ability of atropine to block the lithium effect on myo-inositol and M I P levels as well as the ability of cholinergic agents to produce a small increase in M l P levels suggests that the action of lithium may be mediated by cholinergic mechanisms. Indeed, Haas and Ryall (1977) have shown that lithium facilitates transmission when administered iontophoretically to cholinoceptive Renshaw cells and supraspinal neurons in several regions of brain. The role of lithium as a cholinergic agent has been challenged, however (e.g., Vizi, 1975).The possible mediation of the lithium effect through cholinergic mechanisms can be investigated by determining whether the lithium-induced decrease in myoinositol levels is localized in layers of the cerebral cortex known to contain cholinoceptive cells.…”

mentioning

confidence: 99%

“…The ability of atropine to block the lithium effect on myo-inositol and M I P levels as well as the ability of cholinergic agents to produce a small increase in M l P levels suggests that the action of lithium may be mediated by cholinergic mechanisms. Indeed, Haas and Ryall (1977) have shown that lithium facilitates transmission when administered iontophoretically to cholinoceptive Renshaw cells and supraspinal neurons in several regions of brain. The role of lithium as a cholinergic agent has been challenged, however (e.g., Vizi, 1975).…”

mentioning

confidence: 99%

The Effects of Lithium on myo‐Inositol Levels in Layers of Frontal Cerebral Cortex, in Cerebellum, and in Corpus Callosum of the Rat

Allison

Boshans

Hallcher

et al. 1980

Journal of Neurochemistry

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Six hours after a single injection of lithium chloride (10 mequiv./kg), the concentration of myo-inositol in the cerebral cortex of the rat is reduced by 30% (Allison and Stewart, 1971). A similar decrease in myo-inositol concentration has been found in rat hypothalamus, hippocampus, caudate nucleus, and adrenal: however, the cerebellum is unaffected (Allison, itnprrblisli~d wsirlts). Under the same conditions, lithium chloride produces a 20-fold i n c w m e in the concentration of myo-inositol 1phosphate (MIP) in rat cerebral cortex . Atropine, an antimuscarinic agent, blocks both the lithium-induced fall in the level of myo-inositol and the increase in concentration of my-inositol I-phosphate Allsion et al., 1976). Furthermore, both the cholinesterase inhibitor physostigmine and the cholinomimetic pilocarpine produce a 1.8-2.8fold elevation in the M l P levels of rat cerebral cortex. We have, thus far, been unable to detect an effect of these cholinergic agents on myo-inositol levels (Allison, 1978).The ability of atropine to block the lithium effect on myo-inositol and M I P levels as well as the ability of cholinergic agents to produce a small increase in M l P levels suggests that the action of lithium may be mediated by cholinergic mechanisms. Indeed, Haas and Ryall (1977) have shown that lithium facilitates transmission when administered iontophoretically to cholinoceptive Renshaw cells and supraspinal neurons in several regions of brain. The role of lithium as a cholinergic agent has been challenged, however (e.g., Vizi, 1975).The possible mediation of the lithium effect through cholinergic mechanisms can be investigated by determining whether the lithium-induced decrease in myoinositol levels is localized in layers of the cerebral cortex known to contain cholinoceptive cells. Krnjevic and Phillis (1963) have shown in cats, rabbits, and monkeys that acetylcholine-sensitive cell bodies are found predominantly in the cerebral cortex layers lying between 0.8 and 1.3 mm below the surface and that few are found in more superficial layers. In addition to studying layers of the cerebral cortex we wished to examine cerebellar layers to determine if the apparent absence of a lithium-induced decrease in myo-inositol levels observed in whole cerebellum was due to the masking of a localized decrease by a larger mass of unreactive tissue. MATERIALS AND METHODS Treatment o f A n ima IsMale Sprague-Dawley rats (Harlan Industries, Indianapolis, Indiana) weighing 200 to 250 g were injected subcutaneously with 0.75 M-LiCI (10 meqikg). The rats were decapitated 6 h after treatment. Control groups either received 0.75 M-NaCI (10 meqikg) or were untreated. Preparcition of Tissue SamplesSamples of frontal cortex corresponding to the areas encompassed by the planes VI and ss (Sugita, 1917) were mounted on aluminum rods and frozen in Freon 12 cooled by liquid nitrogen within 120 sec of the time of decapitation. Cerebellar tissue was similarly prepared. Coronal serial sections, 10-pm thick, were cut in a cryostat at -15°C. E v ...

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“…Researchers have also found variation in muscarinic receptor binding in the presence of lithium ( Hruska et al., 1984 ; Gibbons et al., 2015 ). Pre-treatment with LiCl has been reported to increase acetylcholine release, with some studies observing a six-fold increase in the hippocampus ( Haas and Ryall, 1977 ; Jope, 1979 ; Hillert et al., 2014 ). This results in more acetylcholine crossing the synaptic cleft and reaching the postsynaptic membrane where it activates M1 muscarinic receptors.…”

Section: A New Hope: the Lithium-pilocarpine Model Of Sementioning

confidence: 99%

The evolution of the pilocarpine animal model of status epilepticus

Juvale

Has

2020

Heliyon

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The pilocarpine animal model of status epilepticus is a well-established, clinically translatable model that satisfies all of the criteria essential for an animal model of status epilepticus: a latency period followed by spontaneous recurrent seizures, replication of behavioural, electrographic, metabolic, and neuropathological changes, as well as, pharmacoresistance to anti-epileptic drugs similar to that observed in human status epilepticus. However, this model is also characterized by high mortality rates and studies in recent years have also seen difficulties in seizure induction due to pilocarpine resistant animals. This can be attributed to differences in rodent strains, species, gender, and the presence of the multi-transporter, P-glycoprotein at the blood brain barrier. The current paper highlights the various alterations made to the original pilocarpine model over the years to combat both the high mortality and low induction rates. These range from the initial lithium-pilocarpine model to the more recent Reduced Intensity Status Epilepticus (RISE) model, which finally brought the mortality rates down to 1%. These modifications are essential to improve animal welfare and future experimental outcomes.

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An Excitatory Action of Iontophoretically Administered Lithium on Mammalian Central Neurones

Cited by 11 publications

References 18 publications

Acute effects of lithium on dopaminergic responses: Iontophoretic studies in the rat visual cortex

Acute effects of lithium on dopaminergic responses: Iontophoretic studies in the rat visual cortex

The Effects of Lithium on myo‐Inositol Levels in Layers of Frontal Cerebral Cortex, in Cerebellum, and in Corpus Callosum of the Rat

The evolution of the pilocarpine animal model of status epilepticus

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