Afferents to the median raphe nucleus of the rat: Retrograde cholera toxin and wheat germ conjugated horseradish peroxidase tracing, and selectived-[3H]aspartate labelling of possible excitatory amino acid inputs

Behzadi, Gila; Kalén, Peter; Parvopassu, F.; Wiklund, Leif

doi:10.1016/0306-4522(90)90194-9

Cited by 124 publications

(80 citation statements)

References 96 publications

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“…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: 65%

“…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%

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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

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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...

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

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

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“…In many cases, forebrain structures that receive serotonergic innervations from the raphe nuclei send neuronal inputs back to the midbrain serotonergic nuclei [165]. Morphological evidence has been presented for the existence of a glutamatergic pathway arising from the median prefrontal cortex and projecting to the raphe nuclei [16]. Furthermore, it has been shown that GABA interneurons in the raphe nuclei are the primary targets for the cortico-raphe glutamatergic neurons [42] and their stimulation by glutamate release leads to inhibition of 5-HTergic cells [71,165].…”

Section: External Connections Of the Raphe Nuclei With Other Brain Stmentioning

confidence: 99%

The Pharmacology of the Neurochemical Transmission in the Midbrain Raphe Nuclei of the Rat

Hársing

2006

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3 H]5-HT taken up by raphe tissue indicated various pools where the neurotransmitter release may originate from these stores differed both in size and rate constant. 5-HT release originates not only from vesicles but also from cytoplasmic stores via a transporter-dependent exchange process establishing synaptic and non-synaptic neurochemical transmission in the serotonergic somatodendritic area. Manipulation of 5-HT transporter function modulates extracellular 5-HT concentrations in the raphe nuclei: of the SSRIs, fluoxetine was found 5-HT releaser, whereas citalopram did not exhibit this effect. Serotonergic projection neurons in the raphe nuclei possess inhibitory 5-HT 1A and 5-HT 1B/1D receptors and facilitatory 5-HT 3 receptors, which regulate 5-HT release in an opposing fashion. This observation indicates that somatodendritic 5-HT release in the raphe nuclei is under the control of several 5-HT homoreceptors. 5-HT 7 receptors located on glutamatergic axon terminals indirectly inhibit 5-HT release by reducing glutamatergic facilitation of serotonergic projection neurons. An opposite regulation of glutamatergic axon terminals was also found by involvement of the inhibitory 5-HT 7 and the stimulatory 5-HT 2 receptors as these receptors inhibit and stimulate glutamate release in raphe slice preparation, respectively, Furthermore, postsynaptic 5-HT 1B/1D heteroreceptors interact with release of GABA in inhibitory fashion in raphe GABAergic interneurons. Serotonergic projection neurons also possess glutamate and GABA heteroreceptors; NMDA and AMPA receptors release 5-HT, whereas both GABA A and GABA B receptors inhibit somatodendritic 5-HT release. Evidence was found for reciprocal interactions between serotonergic and glutamatergic as well as serotonergic and GABAergic innervations in the raphe nuclei. Serotonergic neurons in the raphe nuclei also receive noradrenergic innervation arising from the locus coeruleus and alpha-1 and alpha-2 adrenoceptors inhibited [3 H]5-HT release in our experimental conditions. The close relation between 5-HT transporter and release-mediating 5-HT autoreceptors was also shown by addition of L-deprenyl, a drug possessing inhibition of type B monoamine oxidase and 5-HT reuptake. L-Deprenyl selectively desensitizes 5-HT 1B but not 5-HT 1A receptors and these effects are not related to inhibition of 5-HT metabolism but rather to inhibition of 5-HT transporter.

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“…For example, there exists an extensive projection from CeA to the posterior lateral hypothalamus (Gonzales and Chesselet, 1990;Krettek and Price, 1978;Price and Amaral, 1981;Zahm et al, 1999;Petrovich et al, 2001), which in turn projects to VTA (Phillipson, 1979;Hosoya and Matsushita, 1981;Berk and Finkelstein, 1982). Similarly, CeA could influence serotonergic neuronal activity via either a direct projection to the dorsal raphe nucleus (Price and Amaral, 1981;Peyron et al, 1998) or a multisynaptic pathway, possibly through the lateral hypothalamus (Behzadi et al, 1990;Peyron et al, 1998;Hosoya and Matsushita, 1981;Berk and Finkelstein, 1982). Finally, a projection from CeA to the paraventricular nucleus of the hypothalamus has been described, through which CeA could influence CORT secretion (Gray et al, 1989;Marcilhac and Siaud, 1997;Prewitt and Herman, 1998).…”

Section: Circuitry Underlying Cea-ampa-induced Activation Of Monoaminmentioning

confidence: 99%

AMPA Receptor Stimulation within the Central Nucleus of the Amygdala Elicits a Differential Activation of Central Dopaminergic Systems

Stalnaker

Berridge

2003

Neuropsychopharmacol

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Appetitive and aversive arousing stimuli increase rates of dopamine (DA) release, particularly within the prefrontal cortex (PFC). Evidence suggests an activating influence of both the central (CeA) and basolateral (BlA) nuclei of the amygdala on DA neurotransmission. For example, lesions of CeA block stressor-induced increases in DA release. Additionally, electrical stimulation of BlA increases DA release in select terminal fields. Previous studies indicate that glutamatergic AMPA receptors modulate CeA and BlA output. However, the extent to which AMPA receptors participate in amygdala-dependent activation of DA neurotransmission is unknown. The current studies examined the effects of bilateral AMPA infusions within CeA or BlA on post-mortem and in vivo microdialysis indices of DA release. Additionally, stress is associated with moderate increases in serotonin (5-HT) neurotransmission that are also blocked by CeA lesions. Thus, the current studies also examined the impact of AMPA infusions on post-mortem indices of 5-HT utilization. AMPA infusion into CeA, but not BlA, increased post-mortem indices of DA and 5-HT release in a pattern comparable to that observed under appetitive/aversive conditions. In vivo microdialysis studies confirmed that AMPA infusions into CeA, but not BlA, increase extracellular PFC DA levels. When infused into sleeping animals, CeA-AMPA infusion also elicited a rapid-onset transition into waking. Thus, CeA-AMPA receptors exert an excitatory influence on DA and 5-HT neurotransmission and on behavioral state. Combined, these results suggest that CeA-AMPA receptors may participate in the coordination of neural systems involved in the regulation of behavioral state under high-arousal conditions.

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Afferents to the median raphe nucleus of the rat: Retrograde cholera toxin and wheat germ conjugated horseradish peroxidase tracing, and selectived-[3H]aspartate labelling of possible excitatory amino acid inputs

Cited by 124 publications

References 96 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

The Pharmacology of the Neurochemical Transmission in the Midbrain Raphe Nuclei of the Rat

AMPA Receptor Stimulation within the Central Nucleus of the Amygdala Elicits a Differential Activation of Central Dopaminergic Systems

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