Behavioral effects of lesions of the central noradrenergic bundles in the rat

Verleye, Marc; Bernet, François

doi:10.1016/0091-3057(83)90110-7

Cited by 7 publications

(3 citation statements)

References 42 publications

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“…As discussed above, the LC sends an excitatory projection to the central and basal nuclei of the amygdala (see Section 4.2.1) and the same nuclei of the amygdala receive an excitatory input from the LC (see Section 5.2). Stimulation of the LC can evoke anxiety (McDougle et al, 1995; Redmond and Huang, 1979) and lesions of the central noradrenergic system lead to attenuation of fear-related responses (Redmond, 1987; Verleye and Bernet, 1983). On the other hand, there is evidence that anxious states lead to the activation of the LC (Charney et al, 1990; Cullinan et al, 1995; Rasmussen and Jacobs, 1986).…”

Section: Pathophysiology Of the Lcmentioning

confidence: 99%

Functional neuroanatomy of the central noradrenergic system

2013

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The central noradrenergic neurone, like the peripheral sympathetic neurone, is characterized by a diffusely arborizing terminal axonal network. The central neurones aggregate in distinct brainstem nuclei, of which the locus coeruleus (LC) is the most prominent. LC neurones project widely to most areas of the neuraxis, where they mediate dual effects: neuronal excitation by α₁-adrenoceptors and inhibition by α₂-adrenoceptors. The LC plays an important role in physiological regulatory networks. In the sleep/arousal network the LC promotes wakefulness, via excitatory projections to the cerebral cortex and other wakefulness-promoting nuclei, and inhibitory projections to sleep-promoting nuclei. The LC, together with other pontine noradrenergic nuclei, modulates autonomic functions by excitatory projections to preganglionic sympathetic, and inhibitory projections to preganglionic parasympathetic neurones. The LC also modulates the acute effects of light on physiological functions ('photomodulation'): stimulation of arousal and sympathetic activity by light via the LC opposes the inhibitory effects of light mediated by the ventrolateral preoptic nucleus on arousal and by the paraventricular nucleus on sympathetic activity. Photostimulation of arousal by light via the LC may enable diurnal animals to function during daytime. LC neurones degenerate early and progressively in Parkinson's disease and Alzheimer's disease, leading to cognitive impairment, depression and sleep disturbance.

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Section: Pathophysiology Of the Lcmentioning

confidence: 99%

Functional neuroanatomy of the central noradrenergic system

2013

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“…Administration of the α 2 -adrenoceptor antagonist yohimbine activates the LC (see section 3.2), which in turn produces an increase in anxiety [141, 282, 300, 453]. Conversely, bilateral lesions of the LC [363] or of the ascending noradrenergic projection arising from it [475], lead to a reduction in fear-related responses.…”

Section: Physiological Manipulation Of Locus Coeruleus Activitymentioning

confidence: 99%

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Samuels

Szabadi²

2008

403

365

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The locus coeruleus (LC), the major noradrenergic nucleus of the brain, gives rise to fibres innervating most structures of the neuraxis. Recent advances in neuroscience have helped to unravel the neuronal circuitry controlling a number of physiological functions in which the LC plays a central role. Two such functions are the regulation of arousal and autonomic activity, which are inseparably linked largely via the involvement of the LC. Alterations in LC activity due to physiological or pharmacological manipulations or pathological processes can lead to distinct patterns of change in arousal and autonomic function. Physiological manipulations considered here include the presentation of noxious or anxiety-provoking stimuli and extremes in ambient temperature. The modification of LC-controlled functions by drug administration is discussed in detail, including drugs which directly modify the activity of LC neurones (e.g., via autoreceptors, storage, reuptake) or have an indirect effect through modulating excitatory or inhibitory inputs. The early vulnerability of the LC to the ageing process and to neurodegenerative disease (Parkinson’s and Alzheimer’s diseases) is of considerable clinical significance. In general, physiological manipulations and the administration of stimulant drugs, α2-adrenoceptor antagonists and noradrenaline uptake inhibitors increase LC activity and thus cause heightened arousal and activation of the sympathetic nervous system. In contrast, the administration of sedative drugs, including α2-adrenoceptor agonists, and pathological changes in LC function in neurodegenerative disorders and ageing reduce LC activity and result in sedation and activation of the parasympathetic nervous system.

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“…The score was the number of squares traversed in 5 minutes. (Kasture et al, 2000;Ray et al, 2003;Verleye and Bernet, 1983) Pentobarbitone sodium (40 mg/kg, i.p., Abott India Ltd.) was used to measure the PB induced hypnosis. After the injection each animal was placed on its back gently.…”

Section: Animal Treatmentmentioning

confidence: 99%

Suppression of penicillin-induced epileptiform activity by Nigella sativa: Possible mediation by neurotransmitters

Guha¹,

Biswas²,

Purkayastha³

2005

Biogenic Amines

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Nigella sativa (NS), an endogenous plant of family Ranunculaceae, exhibits a wide range of biological activity. This report explores the effect of aqueous extract of NS seeds on penicillin-(PCN-100 IU in 100 µl) induced epileptic rat model. Oral pretreatment of NS (250 mg/kg) suppressed PCN-induced seizure considerably, reduced spike-wave discharges and occurrence of generalized tonic-clonic seizures. Electroencephalographic data showed NS pretreatment to experimental animals elicited 85% abolition of high voltage spike discharges. NS pretreatment resulted in elevation of serotonin (5-HT) level and decreased dopamine (DA) level in cerebral cortex (CC), cerebellum (CB), caudate nucleus (CN) and midbrain (MB). A significant decrease in norepinephrine (NE) level was observed only in the CC. The present study suggests that chronic administration of NS protects PCNinduced generalized epilepsy by selectively altering the monoamine level in different brain regions. The seizure abolition observed in the NS pretreated rats was comparable to the anticonvulsive pattern exhibited by diazepam. The results suggest that NS has promising anticonvulsant action.

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Behavioral effects of lesions of the central noradrenergic bundles in the rat

Cited by 7 publications

References 42 publications

Functional neuroanatomy of the central noradrenergic system

Functional neuroanatomy of the central noradrenergic system

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Suppression of penicillin-induced epileptiform activity by Nigella sativa: Possible mediation by neurotransmitters

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