Effect of different lithium priming schedule on pilocarpine-induced
status epilepticus in rats

Chaudhary, Geeta; Malhotra, J; Chaudhari, Juhi; Gopinath, G.; Gupta, Yamini

doi:10.1358/mf.1999.21.1.527014

Cited by 8 publications

(4 citation statements)

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“…It decelerates generation of AP evoked by prolonged membrane depolarization, i.e., affects the electrical activity of the neurons in an opposite manner if compared with an epileptogenic agent, pilocarpine. The inability of Li ' to independently (with no additional influences applied) induce epileptiform effects in rats has been also demonstrated in in vivo experiments [8]. This is why our data allow us to believe that LF, when applied in isolation, does not act as an epileptogenic agent.…”

Section: Resultssupporting

confidence: 74%

Effect of lithium ions on the accommodation characteristics of neurons from theCA1 hippocampal zone

Yavorskii

Lukyanetz

2000

Neurophysiology

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Section: Resultssupporting

confidence: 74%

Effect of lithium ions on the accommodation characteristics of neurons from theCA1 hippocampal zone

Yavorskii

Lukyanetz

2000

Neurophysiology

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“…Here, we used the established lithium-pilocarpine protocol (Honchar et al, 1983;Kofman et al, 1993;Leite et al, 2002;Ormandy et al, 1991) to specifically verify whether acute lithium affects the muscarinic modulation of long-range connectivity. In support of our experimental design, the effects of acute lithium are known to be optimal within 2-24 h (Chaudhary et al, 1999). Moreover, acute lithium has been shown to modulate LTD-and LTP-like forms of cortical plasticity in humans (Voytovych et al, 2012), and to enhance LTP in the rodent hippocampus in vitro (Son et al, 2003).…”

Section: Limitations and Future Directionsmentioning

confidence: 57%

Lithium modulates the muscarinic facilitation of synaptic plasticity and theta-gamma coupling in the hippocampal-prefrontal pathway

Ruggiero

Rossignoli

Lopes-Aguiar

et al. 2018

Experimental Neurology

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Mood disorders are associated to functional unbalance in mesolimbic and frontal cortical circuits. As a commonly used mood stabilizer, lithium acts through multiple biochemical pathways, including those activated by muscarinic cholinergic receptors crucial for hippocampal-prefrontal communication. Therefore, here we investigated the effects of lithium on prefrontal cortex responses under cholinergic drive. Lithium-treated rats were anesthetized with urethane and implanted with a ventricular cannula for muscarinic activation, a recording electrode in the medial prefrontal cortex (mPFC), and a stimulating electrode in the intermediate hippocampal CA1. Either of two forms of synaptic plasticity, long-term potentiation (LTP) or depression (LTD), were induced during pilocarpine effects, which were monitored in real time through local field potentials. We found that lithium attenuates the muscarinic potentiation of cortical LTP (<20 min) but enhances the muscarinic potentiation of LTD maintenance (>80 min). Moreover, lithium treatment promoted significant cross-frequency coupling between CA1 theta (3-5 Hz) and mPFC low-gamma (30-55 Hz) oscillations. Interestingly, lithium by itself did not affect any of these measures. Thus, lithium pretreatment and muscarinic activation synergistically modulate the hippocampal-prefrontal connectivity. Because these alterations varied with time, oscillatory parameters, and type of synaptic plasticity, our study suggests that lithium influences prefrontal-related circuits through intricate dynamics, informing future experiments on mood disorders.

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“…It is well known that pretreatment with LiCl potentiates the SE-inducing effect of pilocarpine in rats as well as in mice (Jope et al, 1986;Clifford et al, 1987;Bersudsky et al, 1994;Chaudhary et al, 1999;Shaldubina et al, 2007). The underlying mechanism is not completely understood.…”

Section: Discussionmentioning

confidence: 99%

Pilocarpine-Induced Convulsive Activity Is Limited by Multidrug Transporters at the Rodent Blood-Brain Barrier

Römermann

Löscher

Bankstahl

2015

J Pharmacol Exp Ther

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As a result of the growing availability of genetically engineered mouse lines, the pilocarpine post-status epilepticus (SE) model of temporal lobe epilepsy is increasingly used in mice. A discrepancy in pilocarpine sensitivity in FVB/N wild-type versus P-glycoprotein (PGP)-deficient mice precipitated the investigation of the interaction between pilocarpine and two major multidrug transporters at the blood-brain barrier. Doses of pilocarpine necessary for SE induction were determined in male and female wild-type and PGP-deficient mice. Brain and plasma concentrations were measured following low (30-50 mg×kg 21 i.p.) and/or high (200 mg×kg 21 i.p.) doses of pilocarpine in wild-type mice, and mice lacking PGP, breast cancer resistance protein (BCRP), or both transporters, as well as in rats with or without pretreatment with lithium chloride or tariquidar. Concentration equilibrium transport assays (CETA) were performed using cells overexpressing murine PGP or BCRP. Lower pilocarpine doses were necessary for SE induction in PGP-deficient mice. Brain-plasma ratios were higher in mice lacking PGP or PGP and BCRP, which was also observed after pretreatment with tariquidar in mice and in rats. Lithium chloride did not change brain penetration of pilocarpine. CETA confirmed transport of pilocarpine by PGP and BCRP. Pilocarpine is a substrate of PGP and BCRP at the rodent blood-brain barrier, which restricts its convulsive action. Future studies to reveal whether strain differences in pilocarpine sensitivity derive from differences in multidrug transporter expression levels are warranted.

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Effect of different lithium priming schedule on pilocarpine-induced status epilepticus in rats

Cited by 8 publications

References 0 publications

Effect of lithium ions on the accommodation characteristics of neurons from theCA1 hippocampal zone

Effect of lithium ions on the accommodation characteristics of neurons from theCA1 hippocampal zone

Lithium modulates the muscarinic facilitation of synaptic plasticity and theta-gamma coupling in the hippocampal-prefrontal pathway

Pilocarpine-Induced Convulsive Activity Is Limited by Multidrug Transporters at the Rodent Blood-Brain Barrier

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