Effects of noradrenaline on the firing rate of vestibular neurons

Licata, F.; Volsi, Guido Li; Maugeri, Giuseppe; Ciranna, Lucia; Santangelo, F

doi:10.1016/0306-4522(93)90293-o

Cited by 33 publications

(13 citation statements)

References 44 publications

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“…effects, especially in the lateral geniculate nucleus Aghajanian, 1980, 1982;Holdefer and Jacobs, 1994) or the thalamic reticular nucleus (Pinault and Deschenes, 1992). Nonetheless, inhibitory effects of noradrenaline mediated by a1 receptors have been observed in vivo on vestibular neurons (Licata et al, 1993). In fact, as demonstrated in the hippocampus (Scbziani et al, 1993), the inhibitory effects of a1 receptors are mediated by presynaptic mechanisms.…”

Section: Pharmacology Of the Noradfendine Effectsmentioning

confidence: 99%

Effects of Noradrenaline on Frequency Tuning of Rat Auditory Cortex Neurons

Manunta

Edeline

1997

Eur J of Neuroscience

105

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The selectivity of rat auditory cortex neurons for pure tone frequency was studied during and after ionophoretic application (5-40 nA) of noradrenaline in urethane-anaesthetized rats. The dominant effect induced by noradrenaline was a significant decrease in spontaneous (93/268 cells) and evoked activity (133/268 cells) which outlasted the application. In the whole population of cells (n = 268) the signal-to-noise ratio, computed using as the signal either the mean evoked response or the response at the best frequency, was unchanged during noradrenaline application. It was significantly increased only for cells showing significantly decreased spontaneous activity, and was significantly decreased for cells showing increased spontaneous activity. Frequency selectivity was significantly increased for the whole population during and after noradrenaline application. It was also significantly increased for cells showing significantly decreased evoked activity, and was significantly decreased for cells showing increased evoked activity. The noradrenaline-induced inhibition was not blocked by propranolol (beta antagonist); it was blocked by prazosin (alpha1 antagonist) and partly mimicked by phenylephrine (alpha1 agonist). GABA, which also inhibited spontaneous and evoked activity, slightly increased the signal-to-noise ratio and significant increased frequency selectivity. However, when noradrenaline was ejected in the presence of bicuculline at doses that were able to block GABAergic inhibition, the inhibitory effects of noradrenaline on spontaneous and evoked activity were still observed. The possible function of noradrenaline-induced inhibitions in sensory cortices is briefly discussed.

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Section: Pharmacology Of the Noradfendine Effectsmentioning

confidence: 99%

Effects of Noradrenaline on Frequency Tuning of Rat Auditory Cortex Neurons

Manunta

Edeline

1997

Eur J of Neuroscience

105

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“…However, NAd also has the opposite effect on a small number of neurons (Podda et al, 2001) and dopamine regulates GABAergic synapses contacting vestibular neurons (Vibert et al, 1994). Even more complex loops might be involved in vivo as injection of NAd decreases the activity of medial 2° VN, unlike the direct cellular effect (Kirsten and Sharma, 1976; Tychsen and Sitaram, 1989; Licata et al, 1993). Reciprocal connections between the vestibular neurons and noradrenergic neurons located in the locus coeruleus (Schuerger and Balaban, 1993, 1999; Horowitz et al, 2005) involved in stress responses and in the sleep/wake cycle (Takahashi et al, 2010) make the coeruleo-vestibular network a candidate for therapeutics of neuro-otologic balance disorders.…”

Section: Neuromodulation Of Central Vestibular Neuronsmentioning

confidence: 99%

Reconsidering the Role of Neuronal Intrinsic Properties and Neuromodulation in Vestibular Homeostasis

Beraneck¹,

Idoux²

2012

Front. Neur.

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The sensorimotor transformations performed by central vestibular neurons constantly adapt as the animal faces conflicting sensory information or sustains injuries. To ensure the homeostasis of vestibular-related functions, neural changes could in part rely on the regulation of 2° VN intrinsic properties. Here we review evidence that demonstrates modulation and plasticity of central vestibular neurons’ intrinsic properties. We first present the partition of Rodents’ vestibular neurons into distinct subtypes, namely type A and type B. Then, we focus on the respective properties of each type, their putative roles in vestibular functions, fast control by neuromodulators and persistent modifications following a lesion. The intrinsic properties of central vestibular neurons can be swiftly modulated by a wealth of neuromodulators to adapt rapidly to temporary changes of ecophysiological surroundings. To illustrate how intrinsic excitability can be rapidly modified in physiological conditions and therefore be therapeutic targets, we present the modulation of vestibular reflexes in relation to the variations of the neuromodulatory inputs during the sleep/wake cycle. On the other hand, intrinsic properties can also be slowly, yet permanently, modified in response to major perturbations, e.g., after unilateral labyrinthectomy (UL). We revisit the experimental evidence, which demonstrates that drastic alterations of the central vestibular neurons’ intrinsic properties occur following UL, with a slow time course, more on par with the compensation of dynamic deficits than static ones. Data are interpreted in the framework of distributed processes that progress from global, large-scale coping mechanisms (e.g., changes in behavioral strategies) to local, small-scale ones (e.g., changes in intrinsic properties). Within this framework, the compensation of dynamic deficits improves over time as deeper modifications are engraved within the finer parts of the vestibular-related networks. Finally, we offer perspectives and working hypotheses to pave the way for future research aimed at understanding the modulation and plasticity of central vestibular neurons’ intrinsic properties.

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“…Iontophoretic application of N E to neocortex or hippocampus results in both excitatory and inhibitory responses (Szabadi, 1979;Langmoen et al, 1981;Nishi et al, 1981;Segal, 1981;Madison and Nicoll, 1986;Waterhouse, 1986;Stanton, 1992). The excitatory response of N E appears to be mediated via the ␤-receptors and /or ␣1-ARs, whereas the inhibitory response is mediated via the ␣2-ARs (Curet and deMontigny, 1988;Parfitt et al, 1988;Licata et al, 1993). This dual action of NE on neuronal activity is apparent when synaptic N E content is elevated with N E reuptake blockers; these agents do not alter the animal's susceptibility to convulsant stimuli (K leinrok et al, 1991;Yacobi and Burnham, 1991).…”

Section: Without Dopsmentioning

confidence: 99%

Norepinephrine-Deficient Mice Have Increased Susceptibility to Seizure-Inducing Stimuli

Szot

Weinshenker

White³

et al. 1999

J. Neurosci.

127

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Several lines of evidence suggest that norepinephrine (NE) can modulate seizure activity. However, the experimental methods used in the past cannot exclude the possible role of other neurotransmitters coreleased with NE from noradrenergic terminals. We have assessed the seizure susceptibility of genetically engineered mice that lack NE. Seizure susceptibility was determined in the dopamine ␤-hydroxylase null mutant (Dbh Ϫ/Ϫ) mouse using four different convulsant stimuli: 2,2,2-trifluroethyl ether (flurothyl), pentylenetetrazol (PTZ), kainic acid, and high-decibel sound. Dbh Ϫ/Ϫ mice demonstrated enhanced susceptibility (i.e., lower threshold) compared with littermate heterozygous (Dbh ϩ/Ϫ) controls to flurothyl, PTZ, kainic acid, and audiogenic seizures and enhanced sensitivity (i.e., seizure severity and mortality) to flurothyl, PTZ, and kainic acid. c-Fos mRNA expression in the cortex, hippocampus (CA1 and CA3), and amygdala was increased in Dbh Ϫ/Ϫ mice in association with flurothyl-induced seizures. Enhanced seizure susceptibility to flurothyl and increased seizure-induced c-fos mRNA expression were reversed by pretreatment with L-threo-3,4-dihydroxyphenylserine, which partially restores the NE content in Dbh Ϫ/Ϫ mice. These genetically engineered mice confirm unambiguously the potent effects of the noradrenergic system in modulating epileptogenicity and illustrate the unique opportunity offered by Dbh Ϫ/Ϫ mice for elucidating the pathways through which NE can regulate seizure activity.

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Effects of noradrenaline on the firing rate of vestibular neurons

Cited by 33 publications

References 44 publications

Effects of Noradrenaline on Frequency Tuning of Rat Auditory Cortex Neurons

Effects of Noradrenaline on Frequency Tuning of Rat Auditory Cortex Neurons

Reconsidering the Role of Neuronal Intrinsic Properties and Neuromodulation in Vestibular Homeostasis

Norepinephrine-Deficient Mice Have Increased Susceptibility to Seizure-Inducing Stimuli

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