Dexamethasone modifies the behavioral effects induced by clonidine in mice

Capasso, Anna; Giannuario, A. Di; Loizzo, Alberto; Pieretti, Stefano; Sorrentino, L.

doi:10.1016/0306-3623(95)02144-2

Cited by 9 publications

(2 citation statements)

References 38 publications

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“…In humans, the α2-receptor agonist clonidine, which is used therapeutically for treatment of blood pressure, can have motor side-effects. In mice, clonidine can cause both decreased locomotion and impaired rotarod performance (Capasso et al, 1996; Dogrul and Uzbay, 2004). Intriguingly, mice treated with clonidine were unable to improve their rotarod performance with training (Galeotti et al, 2004), precisely the type of motor learning deficit that would be predicted by cerebellar motor learning theories based on our findings of suppressed instructive signals.…”

Section: Discussionmentioning

confidence: 99%

Noradrenergic Control of Associative Synaptic Plasticity by Selective Modulation of Instructive Signals

Carey

Regehr

2009

Neuron

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Synapses throughout the brain are modified through associative mechanisms in which one input provides an instructive signal for changes in the strength of a second co-activated input. In cerebellar Purkinje cells, climbing fiber synapses provide an instructive signal for plasticity at parallel fiber synapses. Here we show that noradrenaline activates α2-adrenergic receptors to control short-term and long-term associative plasticity of parallel fiber synapses. This regulation of plasticity does not reflect a conventional direct modulation of the postsynaptic Purkinje cell or presynaptic parallel fibers. Instead, noradrenaline reduces associative plasticity by selectively decreasing the probability of release at the climbing fiber synapse, which in turn decreases climbing fiber-evoked dendritic calcium signals. These findings raise the possibility that targeted presynaptic modulation of instructive synapses could provide a general mechanism for dynamic context-dependent modulation of associative plasticity.

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Section: Discussionmentioning

confidence: 99%

Noradrenergic Control of Associative Synaptic Plasticity by Selective Modulation of Instructive Signals

Carey

Regehr

2009

Neuron

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“…Several studies have implicated the noradrenergic system in motor learning (Capasso et al, 1996;Keller and Smith, 1983;Mason and Iverson, 1974;McCormick and Thompson, 1982;Pompeiano, 1998;Watson and McElligott, 1984). High levels of GC activity during behaviour could facilitate plasticity at different locations in the cerebellar cortex (Gao et al, 2012).…”

Section: Implications For Sensorimotor Processing and Learning In Thementioning

confidence: 99%

Norepinephrine controls the gain of the inhibitory circuit in the cerebellar input layer

Lanore¹,

Rothman²,

Coyle³

et al. 2019

Preprint

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Golgi cells (GoCs) are the main inhibitory interneurons in the input layer of the cerebellar cortex and are electrically coupled together, forming syncytia. GoCs control the excitability of granule cells (GCs) through feedforward, feedback and spillovermediated inhibition. The GoC circuit therefore plays a central role in determining how sensory and motor information is transformed as it flows through the cerebellar input layer. Recent work has shown that GCs are activated when animals perform active behaviours, but the underlying mechanisms remain poorly understood. Norepinephrine (NE), also known as noradrenaline, is a powerful modulator of network function during active behavioral states and the axons of NE-releasing neurons in the locus coeruleus innervate the cerebellar cortex. Here we show that NE hyperpolarizes the GoC membrane potential, decreases spontaneous firing and reduces the gain of the spike frequency versus input-current relationship. The GoC membrane hyperpolarization can be mimicked with an α2-noradrenergic agonist, inhibited with a specific α2 antagonist and is abolished when G protein-coupled inwardly-rectifying potassium (GIRK) channels are blocked. Moreover, NE reduces the effective electrical coupling between GoCs through a persistent sodium current (INaP)-dependent mechanism. Our results suggest that NE controls the gain of the GoC inhibitory circuit by modulating membrane conductances that act to reduce membrane excitability and decrease electrical coupling. These mechanisms appear configured to reduce the level of GoC inhibition onto GCs during active behavioural states.

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Effects of indole-3-carbinol on clonidine-induced neurotoxicity in rats: Impact on oxidative stress, inflammation, apoptosis and monoamine levels

2014

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Dexamethasone modifies the behavioral effects induced by clonidine in mice

Cited by 9 publications

References 38 publications

Noradrenergic Control of Associative Synaptic Plasticity by Selective Modulation of Instructive Signals

Noradrenergic Control of Associative Synaptic Plasticity by Selective Modulation of Instructive Signals

Norepinephrine controls the gain of the inhibitory circuit in the cerebellar input layer

Effects of indole-3-carbinol on clonidine-induced neurotoxicity in rats: Impact on oxidative stress, inflammation, apoptosis and monoamine levels

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