The role of afferents to the locus coeruleus in the handling stress-induced increase in the release of noradrenaline in the medial prefrontal cortex: a dual-probe microdialysis study in the rat brain

Kawahara, Hiroshi; Kawahara, Yukie; Westerink, Ben H.C.

doi:10.1016/s0014-2999(99)00793-1

Cited by 96 publications

(51 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This study demonstrates the modulatory effects that acute handling stress has on MP-induced DA overflow. Consistent with previous findings (Kawahara et al 2000;Nakane et al 1994), these data demonstrate that acute handling stress increases DA and NE overflow in the mPFC. The DA responsivity to MP was reduced by 30% in animals handled 2 h prior to drug challenge.…”

Section: Discussionsupporting

confidence: 92%

“…manner from the DA system, which might be a function of inputs from several limbic brain regions. For example, infusion of GABA A and GABA B antagonists (bicuculline and CGP 52432, respectively) into the LC did not alter the handling-induced increases of NE in the mPFC (Kawahara et al 2000). In the same study, a non-NMDA glutamate receptor antagonist (DNQX) did not alter stressinduced changes in the mPFC NE overflow, whereas infusion of an NMDA glutamate receptor antagonist (CPP) reduced the stress-induced response of mPFC NE.…”

Section: Noradrenergic Response To Mp Challenge and Stressmentioning

confidence: 87%

“…This augmented response might be due to cross innervation of the mPFC from several brain stem projections, such as the A10 pathway from the ventral tegmental area (VTA) and/or noradrenergic connections from the locus coeruleus (LC). More specifically, systemic stressors such as handling, restraint, or immobilization increase mPFC levels of DA by 150-300% (Enrico et al 1998;Feenstra et al 1995), and NE levels by 160-250% Kawahara et al 2000;Shimizu et al 1994). These responses can be modulated by infusion of pharmacologic agents directly into the LC and the VTA, indicating the influence of these regions on mPFC function.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Marsteller

Gerasimov

Schiffer

et al. 2002

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Noradrenergic Response To Mp Challenge and Stressmentioning

confidence: 87%

mentioning

confidence: 99%

See 1 more Smart Citation

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Marsteller

Gerasimov

Schiffer

et al. 2002

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…These antagonists do not themselves suppress adrenergic activity, and CP154,526 failed to modify FCX levels of NE herein, in line with the lack of influence of local administration of CP154,526 into the LC upon adrenergic transmission (Kawahara et al 2000). However, a mild ‫%51ف(‬ relative to basal values) diminution in frontocortical release of NE upon i.p.…”

Section: Monoaminergic Transmissionmentioning

confidence: 54%

“…administration of CP154,526 (32 mg/kg) was recently documented by Isogawa et al (2000). Further, CP154,526 and peptidergic CRF 1 antagonists abrogate the induction of corticolimbic NE release provoked by stress (Shimizu et al 1994;Smagin et al 1997;Kawahara et al 2000), an action which may contribute to their anxiolytic properties. Although this provides a parallel with BZDs, which also inhibit LC-adrenergic neurones, the significance of modulation of adrenergic transmission to anxious states remains under discussion (Swiergiel et al 1992;Valentino et al 1993;Weiss et al 1994;Millan et al 2000b).…”

Section: Monoaminergic Transmissionmentioning

confidence: 87%

Anxiolytic Properties of the Selective, Non-peptidergic CRF1 Antagonists, CP154,526 and DMP695 A Comparison to Other Classes of Anxiolytic Agent

Millan

2001

Neuropsychopharmacology

View full text Add to dashboard Cite

The selective, non-peptidergic corticotropin-releasing factor (CRF) 1 receptor antagonists, CP154,526 and DMP695, dose-dependently increased punished responses of rats in a Vogel conflict test and enhanced social interaction (SI) of rats in an unfamiliarCorticotropin-releasing factor (CRF) plays a crucial role in modulation of the release of adrenocorticotrophic hormone from the anterior pituitary (De Souza 1995). In addition, CRF is broadly distributed throughout the mammalian central nervous system (CNS), being concentrated in corticolimbic regions such as amygdala, hippocampus, and periaqueductal gray (PAG) and frontal cortex (FCX), as well as the locus coeruleus (LC) and dorsal raphe nucleus (DRN), the origin of ascending adrenergic and serotonergic projections, respectively (Sawchenko et al. 1993;Van Bockstaele et al. 1996;Price et al. 1998;Steckler and Holsboer 1999). In line with this organization, independently of the hypothalamocorticotrophic axis, cerebral CRF-containing neurones fulfill an important role in the control of emotional behavior (Adamec and McKay 1993;De Souza 1995;Mitchell 1998;Steckler and Holsboer 1999;Smagin and Dunn 2000), actions expressed via two principal subtypes of CRF receptor, both of which positively couple to adenyl cyclase (Grigoriadis et al. 1996). CRF 1 receptors bind CRF and a related neuropeptide, urocortin, with high affinity whereas CRF 2 receptors display a NO . 4 distinct preference for the latter (Donaldson et al. 1996;Grigoriadis et al. 1996). Of several splice variants of the latter, the CRF 2 ␣ subtype is found predominantly in the rodent CNS, notably in several corticolimbic regions enriched in CRF itself, such as the hippocampus, medial amygdala, septum, olfactory bulb, and raphe nuclei, although species differences in this regard should be pointed out (Chalmers et al. 1995;Sánchez et al. 1999). Studies of mRNA encoding CRF 1 receptors and of the corresponding peptide have established a contrasting pattern of distribution in rats with a predominance of CRF 1 over CRF 2 ␣ sites in anterior pituitary, FCX and basolateral amygdala, as well as high levels in the hippocampus and PAG (Potter et al. 1994;Chalmers et al. 1995;Sánchez et al. 1999;Chen et al. 2000).These observations provide a neuroanatomical substrate for a potential role of CRF 1 and/or CRF 2 receptors in the control of mood (Coplan et al. 1996;Steckler and Holsboer 1999), and, in this regard, there is a diversity of evidence implicating CRF 1 sites in the modulation of anxious states. First, several studies have reported anxiogenic actions of CRF (and urocortin) upon i.c.v. administration (see Steckler and Holsboer, 1999) and similar effects have been seen upon direct introduction into the dorsal PAG (Martins et al. 1997), basolateral amygdala (Sajdyk et al. 1999), and hippocampus (Radulovic et al. 1999), structures possessing a high density of CRF 1 receptors. Second, direct evidence for participation of CRF 1 receptors in anxiogenic actions is derived from studies of antisense probes for their ...

show abstract

Sensorineural hearing loss in combined modality treatment of nasopharyngeal carcinoma

Chen

Jackson

Budnick

et al. 2006

Cancer

145

View full text Add to dashboard Cite

Objective To explore the prevalence and possible predictors of cognitive impairment in persons with rheumatoid arthritis (RA). Methods Individuals from a longitudinal cohort study of RA participated in a study visit that included a range of physical, psychosocial, and biologic metrics. Cognitive function was assessed using a battery of 12 standardized neuropsychological measures yielding 16 indices. Subjects were classified as “impaired” if they performed 1 SD below age‐based population norms on at least 4 of 16 indices. Logistic regression analyses were conducted to identify which of the following were significant predictors of cognitive impairment: sex, race, income, education, depression, disease duration, disease severity, C‐reactive protein (CRP) level, glucocorticoid use, and cardiovascular disease (CVD) risk factors. Results A total of 115 subjects with a mean ± SD age of 58.6 ± 10.8 years were included; 64% were women and 81% were white. The proportion of persons who were classified as cognitively impaired was 31%. Education, income, glucocorticoid use, and CVD risk factors independently predicted cognitive impairment, controlling for sex, race, disease duration, disease severity, CRP level, and depression. Individuals with cognitive impairment were more likely to have low education (odds ratio [OR] 6.18, 95% confidence interval [95% CI] 1.6–23.87), have low income (OR 7.12, 95% CI 1.35–37.51), use oral glucocorticoids (OR 2.92, 95% CI 1.05–8.12), and have increased CVD risk factors (OR 1.61, 95% CI 1.19–2.17 per risk factor). Conclusion The findings of this study suggest that the burden of cognitive impairment in RA is significant, and future studies identifying specific etiologic contributors to cognitive impairment are warranted.

show abstract

The role of afferents to the locus coeruleus in the handling stress-induced increase in the release of noradrenaline in the medial prefrontal cortex: a dual-probe microdialysis study in the rat brain

Cited by 96 publications

References 37 publications

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

Anxiolytic Properties of the Selective, Non-peptidergic CRF1 Antagonists, CP154,526 and DMP695 A Comparison to Other Classes of Anxiolytic Agent

Sensorineural hearing loss in combined modality treatment of nasopharyngeal carcinoma

Contact Info

Product

Resources

About