Forebrain afferents to the rat dorsal raphe nucleus demonstrated by retrograde and anterograde tracing methods

Peyron, Christelle; Petit, Jean‐Marie; Rampon, Claire; Jouvet, Michel; Luppi, Pierre‐Hervé

doi:10.1016/s0306-4522(97)00268-6

Cited by 459 publications

(398 citation statements)

References 56 publications

Supporting

Mentioning

348

Contrasting

Unclassified

Order By: Relevance

“…On the other hand, the areas around the rhinal sulcus, such as the lateral orbitofrontal cortex (LO) and the dorsal part of the agranular insular cortex (AID), constitute the lateral prefrontal cortex in rats, because they have reciprocal connections to the mediodorsal thalamic nucleus (Zilles and Wree 1995;Fuster 1997) which is a main anatomical criterion for belonging to the PFC. Although LO and AID have projection fibers to the dorsal raphe nucleus in rats (Peyron et al 1998;Beckstead 1979), these fibers, unlike those originating from mPFC, probably have no functional relevance for the serotonergic neurotransmission, because electrical stimulation of AID and LO did not alter hippocampal 5-HT output in the present study. There are two reasons for this functional difference between medial and lateral PFC: first, the medial PFC sends significantly more efferent fibers to the dorsal raphe nucleus than LO and AID; and second, only the medial PFC projects to the whole of the dorsal raphe nucleus (Peyron et al 1998).…”

Section: Discussioncontrasting

confidence: 49%

“…Consistent with this hypothesis, it has been demonstrated that rat medial prefrontal cortex (prelimbic area) has dense efferent projections to both the dorsal and the median raphe nuclei (Aghajanian and Wang 1977;Beckstead 1979;Wyss and Sripanidkulchai 1984;Sesack et al 1989;Behzadi et al 1990;Peyron et al 1998). Thus, it is possible that PFC stimulation activates the raphe nuclei leading to increased -HT levels in terminal areas.…”

Section: Discussionmentioning

confidence: 66%

“…Stimulation of such cortical areas outside the PFC as the medial precentral area Fr2, the primary motor, and the parietal cortex did not affect serotonin output in either hippocampus or amygdala. One possible explanation for this is that the prefrontal cortex is the only cortical area with direct projections to the midbrain raphe nuclei in rats (Aghajanian and Wang 1977;Behzadi et al 1990;Marcinkiewicz et al 1989;Peyron et al 1998), as well as in primates (Arnsten and GoldmanRakic 1984). It is noteworthy that there is still open debate as to whether the medial precentral area Fr2, located in the dorsomedial, or so-called shoulder region of the rat frontal cortex, belongs to the PFC (Uylings and Van Eden 1990;Preuss 1995).…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

View full text Add to dashboard Cite

Decreased activity of the prefrontal cortex (PFC), as well as reduced serotonergic neurotransmission, is considered as a characteristic feature of major depression. The mechanism by which electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS) achieve their antidepressant effects may involve changes in PFC activity. It is, however, still unclear whether these changes are accompanied by increased synaptic availability of serotonin (5-HT). In the present study, 5-HT efflux in the rat ventral hippocampus and amygdala was analyzed using in vivo microdialysis during low-current electrical stimulation of PFC and other cortical regions. Electrical stimulation of the medial PFC produced current-dependent increases in limbic 5-HT output in both urethane-anesthetized and behaving rats. No effects on 5-HT levels were seen after comparable stimulation of either the lateral parts of the PFCAn extensive body of clinical evidence suggests that prefrontal cortex (PFC) abnormalities are involved in the pathophysiology of major depression. Significantly decreased cerebral blood flow as well as reduced rates of glucose metabolism have been consistently found in the PFC of depressed patients (Soares and Mann 1997;Kennedy et al. 1997;George et al. 1993). This reduction seems to be localized predominantly in the left hemisphere (Baxter et al. 1989;Martinot et al. 1990). This is supported by structural neuroimaging studies demonstrating that poststroke depression is more likely to occur following a lesion in the left PFC rather than either in the right PFC or elsewhere in the left hemisphere (Morris et al. 1996;Robinson et al. 1984). Both neuropsychological and oculomotor functioning of prefrontal cortex is impaired in depression (Goodwin 1997;Sweeney et al. 1998). Furthermore, symptom improvement and remission of depressed patients have been associated with increases in cerebral blood flow and glucose metabolism in this region (Goodwin et al. 1993;Bench et al. 1995;Bonne and Krausz 1997;Buchsbaum et al. 1997 NO . 3 This close association between prefrontal cortical dysfunction and depression suggests that enhancement of PFC activity might be beneficial in the treatment of this disorder. Consistent with this idea, electroconvulsive therapy (ECT), as well as transcranial magnetic stimulation (TMS), seems to achieve its antidepressant effects by altering PFC activity. ECT leads to pronounced prefrontal EEG changes, which are directly related to the therapeutic outcome. Hence, the efficacy of ECT seems to be critically linked to prefrontal cortex involvement in ECT-induced seizure activity (Sackeim et al. 1996). This is further supported by studies that have reported changes in cerebral blood flow in prefrontal cortex of ECT responders (Nobler et al. 1994;Bonne et al. 1996;Petracca et al. 1995). In recent years, repetitive TMS of the left dorsolateral prefrontal cortex has emerged as a successful antidepressant treatment (Pascual-Leone et al. 1996;George et al. 1997). Although the exact mechanism underlying the ef...

show abstract

Section: Discussioncontrasting

confidence: 49%

Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

View full text Add to dashboard Cite

show abstract

“…In addition, the evidence below suggests that the σ1R is also involved in the pathogenesis of depressive disorders: (1) compared with hea lthy participants, the plasma level of the σ1R declines in patients with depression and increases after treatment with antidepressants [34] ; (2) σ1R-knockout mice show a prolonged immobility time in the forced swimming test, an animal model of depression, indicating that deletion of σ1Rs exacerbates the severity of depression [35] ; (3) administration of σ1R agonists reduces the immobility time in the forced swimming and tail-suspension tests in a dose-dependent manner, exhibiting a good antidepressant-like effect. In contrast, σ1R ant agonists blocks its antidepressant-like effect [36] ; and (4) the σ1R has a regulatory effect on monoamine neurotransmitters: σ1R agonists in rats up-regulate DA levels in the frontal cortex, increase the discharge of serotonergic neurons in the dorsal raphe nucleus, and enhance 5-HT release [37,38] .…”

mentioning

confidence: 99%

New hypothesis and treatment targets of depression: an integrated view of key findings

2015

View full text Add to dashboard Cite

Major depressive disorder (MDD) is a common and devastating psychiatric disorder characterized by persistent low mood, cognitive disorder, and impaired social function. Despite its complex mechanisms, increasing evidence has identified the involvement of neurotrophic factors, inflammatory cytokines, the hypothalamuspituitary-adrenal axis, and glutamate receptors in the pathophysiology of this illness. The present review synthesizes recent research achievements to defi ne the network between different hypotheses of MDD and to understand which part is most pivotal for its pathogenesis. By integrating MDD-related signal pathways, we highlight brain-derived neurotrophic factor (BDNF) dysfunction and increased apoptosis as the fi nal common cascades, and new therapeutic strategies aiming to enhance BDNF function have been shown to exert a rapid and effective antidepressant action.

show abstract

“…Serotonergic innervation of the striatum is provided by the dorsal raphe nucleus, which also sends serotonergic projections to several other forebrain regions, including the frontal cortex (Vertes, 1991). Animal studies have demonstrated that the raphe nuclei also receive afferent (feedback) projections from widespread forebrain, including prefrontal, regions (Peyron et al, 1998). The ventral medial prefrontal cortex exerts a powerful inhibitory influence on serotonergic neurons in the dorsal raphe nucleus (Hajós et al, 1998;Varga et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Increased striatal serotonin synthesis following cortical resection in children with intractable epilepsy

et al. 2008

View full text Add to dashboard Cite

show abstract

Forebrain afferents to the rat dorsal raphe nucleus demonstrated by retrograde and anterograde tracing methods

Cited by 459 publications

References 56 publications

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

New hypothesis and treatment targets of depression: an integrated view of key findings

Increased striatal serotonin synthesis following cortical resection in children with intractable epilepsy

Contact Info

Product

Resources

About