Control of serotonergic neurons in rat brain by dopaminergic receptors outside the dorsal raphe nucleus

Martı́n-Ruiz, Raúl; Ugedo, Luisa; Honrubia, M.; Mengod, Guadalupe; Artigas, Francesc

doi:10.1046/j.1471-4159.2001.00275.x

Cited by 66 publications

(44 citation statements)

References 61 publications

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“…As dopaminergic innervation of the hippocampus is low, no augmentation of DA levels were detectable. It has been previously shown that DA D 1 -specific compounds had no effect on the turnover of 5-HT (Lappalainen et al, 1991), and that the DA D 2 receptor agonist increased local 5-HT release in RN (Ferre S and Artigas F, 1993), although this effect may be mediated at D 2 receptors localized outside the raphe nuclei (Martin-Ruiz et al, 2001b). However, no effect was observed on extracellular DA levels in the raphe nuclei after a single administration, or the combination of the 5-HT 2C antagonist with citalopram, which renders an interaction with DA neurons less likely.…”

Section: Dopaminementioning

confidence: 97%

Augmentation of SSRI Effects on Serotonin by 5-HT2C Antagonists: Mechanistic Studies

Cremers

Rea

Bosker

et al. 2007

Neuropsychopharmacol

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The treatment of depression may be improved by using an augmentation approach involving selective serotonin reuptake inhibitors (SSRIs) in combination with compounds that focus on antagonism of inhibitory serotonin receptors. Using microdialysis coupled to HPLC, it has recently been shown that the systemic co-administration of 5-HT 2C antagonists with SSRIs augmented the acute effect of SSRIs on extracellular 5-HT. In this paper, we have investigated the mechanism through which this augmentation occurs. The increase in extracellular 5-HT was not observed when both compounds were locally infused. However, varying the route of administration for both compounds differentially revealed that an augmentation took place when the 5-HT 2C antagonist was locally infused into ventral hippocampus and the SSRI given systemically, but not when systemic 5-HT 2C antagonist was co-administered with the local infusion of citalopram. This suggests that the release of extracellular serotonin in ventral hippocampus may be controlled by (an)other brain area(s). As 5-HT 2C receptors are not considered to be autoreceptors, this would implicate that other neurotransmitter systems are involved in this process. To investigate which neurotransmitter systems were involved in the interaction, systemic citalopram was challenged with several glutamatergic, GABA-ergic, noradrenergic, and dopaminergic compounds to determine their effects on serotonin release in ventral hippocampus. It was determined that the involvement of glutamate, norepinephrine, and dopamine in the augmentation did not seem likely, whereas evidence implicated a role for the GABA-ergic system in the augmentation.

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Section: Dopaminementioning

confidence: 97%

Augmentation of SSRI Effects on Serotonin by 5-HT2C Antagonists: Mechanistic Studies

Cremers

Rea

Bosker

et al. 2007

Neuropsychopharmacol

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“…On the other hand, the data suggest that D 2 dopamine receptors (but not D 1 ) within RLi/PAG seem to participate in the rewarding effects of heroin, since their blockade with eticlopride (a very selective D 2 antagonist; Seeman and Van Tol, 1994) reduced CPP to heroin in a dose-dependent manner. D 2 dopamine receptors are known to be expressed by PAG neurons (Bouthenet et al, 1987;Martin-Ruiz et al, 2001), but the presence and distribution of D 1 dopamine receptor in neurons of RLi/PAG has not been described so far. The present study indicates that a population of RLi/ PAG neurons expressing D 2 dopamine receptors are involved in the modulation of heroin's rewarding effects.…”

Section: Thmentioning

confidence: 99%

“…However, these receptors could be also heteroceptors located on nondopaminergic neurons, and D 2 -mediated effects could be indirect through a modification of other neurotransmitter systems such as the midbrain serotonergic one. Thus, it is known that dopamine depolarizes midbrain serotonin neurons by an action on DA D 2 receptors (Haj-Dahmane and Shen, 2000), and systemic quinpirole (D 2 agonist) enhances serotonin release in the DR (Martin-Ruiz et al, 2001), and it has been proposed that DA D 2 receptors outside the DR (likely on PAG GABA neurons) control serotonergic activity in this nucleus (Martin-Ruiz et al, 2001). Furthermore, DR serotonin neurotransmission is involved in CPP, because local infusions of the 5-HT 1 agonist 8-OH-DPAT into the DR produce CPP (Fletcher et al, 1993).…”

Section: Thmentioning

confidence: 99%

Role for Dopamine Neurons of the Rostral Linear Nucleus and Periaqueductal Gray in the Rewarding and Sensitizing Properties of Heroin

Flores

Galan-Rodriguez

Ramiro-Fuentes

et al. 2005

Neuropsychopharmacol

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There is a mesencephalic dopaminergic network outside the ventral tegmental area (VTA), including structures such as the rostral linear nucleus (RLi) and periaqueductal gray (PAG). These nuclei project to neural areas implicated in reinforcing effects of drugs, indicating that they could participate in opiate reward. The objectives were to study the morphological characteristics of the dopamine network of the RLi/PAG region, and to discern its role on rewarding and sensitizing effects of heroin in rats, following dopamine depletion or local injection of dopaminergic antagonists. The findings indicated that this network is composed of small cells in the RLi/ventral PAG, large multipolar dopamine PAG neurons, and periaqueductal PAG neurons. Following repeated heroin, large PAG neurons and small RLi/ ventral PAG cells (not periaqueductal neurons) were activated, since tyrosine-hydroxylase was adaptively induced, without changes in protein kinase Aa. After dopamine depletion, small RLi/ventral PAG neurons and large cells of the PAG (not periaqueductal ones) were selectively affected by the neurotoxin. Dopamine neurons of the nearby VTA and dorsal raphe were not affected, as revealed by cell counting. After lesion, 'anxiety-like' responses and basal locomotion were not altered. However, conditioned place preference to heroin was found to be abolished, as well as heroin-induced motor sensitization. Following infusions of dopaminergic antagonists into RLi/PAG, D 2 (not D 1 ) receptor blocking dose-dependently abolished heroin-induced reward. The present study provides evidence that dopamine neurons of the RLi/PAG region (excluding PAG periaqueductal cells) show adaptive biochemical changes after heroin, and mediate the rewarding and sensitizing effects of this drug. D 2 dopamine receptors within the RLi/PAG region participate in these effects.

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“…The interactions between various types and subtypes of GluR, second messenger molecules, eicosanoid metabolites, reactive oxygen species (ROS), reactive nitrogen species (RNS), lipid peroxidation products (LPP), and phosphorylating enzymes make control of these systems extremely complex. Studies of Martin-Ruiz et al [50] have disclosed that GluR also interact with serotonergic, adrenergic, and cholinergic neural nets as well.…”

Section: +mentioning

confidence: 99%

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

Blaylock

Strunecká

2009

CMC

125

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Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.

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Control of serotonergic neurons in rat brain by dopaminergic receptors outside the dorsal raphe nucleus

Cited by 66 publications

References 61 publications

Augmentation of SSRI Effects on Serotonin by 5-HT2C Antagonists: Mechanistic Studies

Augmentation of SSRI Effects on Serotonin by 5-HT2C Antagonists: Mechanistic Studies

Role for Dopamine Neurons of the Rostral Linear Nucleus and Periaqueductal Gray in the Rewarding and Sensitizing Properties of Heroin

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

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