Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons

Borsody, Mark K.; Weiss, Jay M.

doi:10.1016/0006-8993(96)00199-0

Cited by 60 publications

(45 citation statements)

References 58 publications

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“…4). In this group, noradrenergic neurons exhibited three different firing patterns, 52% of the neurons displaying a regular firing pattern, 32% discharging an irregular and 16% having a bursting firing pattern ( All the recorded neurons located in the LC and displayed electrophysiological characteristics of noradrenergic neurons in this study, corresponding to previously reported [11] . The results of the present study showed that the unilateral lesion of the nigrostriatal pathway induced an obvious increase in the firing rate with change in the firing pattern of noradrenergic neurons recorded in the LC of rats.…”

Section: Resultssupporting

confidence: 82%

Firing activity of locus coeruleus noradrenergic neurons increases in a rodent model of Parkinsonism

et al. 2009

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Objective To investigate the changes in the firing activity of noradrenergic neurons in the locus coeruleus (LC) in a rat model of Parkinson disease (PD). Methods 2 and 4 weeks after unilateral lesion of the nigrostriatal pathway in the rat by local injection of 6-hydroxydopamine (6-OHDA) into the right substantia nigra pars compacta (SNc), the firing activity of noradrenergic neurons in LC was recorded by extracellular single unit recording. Results The firing rate of LC noradrenergic neurons increased significantly 2 and 4 weeks after 6-OHDA lesions compared to normal rats, respectively (P < 0.05). The percentage of irregularly firing neurons was obviously higher than that of normal rats during the fourth week after SNc lesion (P < 0.05). Conclusion LC noradrenergic neurons are overactive and more irregular in 6-OHDA-lesioned rats. These changes suggest an implication of the LC in the pathophysiological mechanism of PD.

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Section: Resultssupporting

confidence: 82%

Firing activity of locus coeruleus noradrenergic neurons increases in a rodent model of Parkinsonism

et al. 2009

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“…CRF. For example, CRF affects the tonic electrophysiological activity of the LC (Lejeune and Millan, 2003;Valentino and Foote, 1987;Borsody and Weiss, 1996), which is involved in the tonic descending inhibitory control of spinal cord circuits (Besson and Chaouch, 1987). Taken together, our findings provide evidence that in the tonic pain animal model of FCA hindpaw inflammation low, systemically ineffective doses of i.c.v.…”

Section: Opioid-mediated Inhibition Of Inflammatory Pain Following Isupporting

confidence: 56%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist a-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissueFbut not peripheral sensory neuronsFthat coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dosedependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.

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“…However, a partial agonist effect of D-Phe-CRH in the LC could potentially be masked by a low baseline CRH tone in vivo. Partial agonist effects of ␣-helical CRH have been reported previously in vitro (Rainnie et al, 1992;Yu and Shinnick-Gallagher, 1998;Smart et al, 1999) and in vivo (Menzaghi et al, 1994;Borsody and Weiss, 1996). Nonetheless, the CRH antagonist still reduced the magnitude of the CRH-evoked increase in the LC FR.…”

Section: Antagonists Of Crh Receptorsmentioning

confidence: 53%

Corticotropin-Releasing Hormone Directly Activates Noradrenergic Neurons of the Locus Ceruleus RecordedIn Vitro

Jedema¹,

Grace²

2004

J. Neurosci.

158

126

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The neuropeptide corticotropin-releasing hormone (CRH) activates locus ceruleus (LC) neurons, thereby increasing norepinephrine levels throughout the CNS. Despite anatomical and physiological evidence for CRH innervation of the LC, the mechanism of CRH-evoked activation of LC neurons is unknown. Moreover, given the apparent absence of mRNA for CRH receptors in LC neurons, the exact location of action of CRH within the cerulear region is debated. Using in vitro intracellular recordings from rat brainstem, we examined whether CRH exerts a direct effect on LC neurons and which ionic currents are likely affected by CRH. We demonstrate that CRH dose-dependently increases the firing rate of LC neurons through a direct (TTX-and cadmium-insensitive) mechanism by decreasing a potassium conductance. The CRH-evoked activation of LC neurons is, at least in part, mediated by CRH 1 receptors and a cAMP-dependent second messenger system. These data provide additional support that CRH functions as an excitatory neurotransmitter in the LC and the hypothesis that dysfunction of the CRH peptidergic and noradrenergic systems observed in patients with mood and anxiety disorders are functionally related.

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Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons

Cited by 60 publications

References 58 publications

Firing activity of locus coeruleus noradrenergic neurons increases in a rodent model of Parkinsonism

Firing activity of locus coeruleus noradrenergic neurons increases in a rodent model of Parkinsonism

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Corticotropin-Releasing Hormone Directly Activates Noradrenergic Neurons of the Locus Ceruleus RecordedIn Vitro

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