Modulation of brain stem monoamines and γ-aminobutyric acid by NK1 receptors in rats

Ma, Qing‐Ping; Bleasdale, Catherine

doi:10.1097/00001756-200210070-00024

Cited by 36 publications

(24 citation statements)

References 21 publications

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“…SP receptors are found on GABAergic and glutamatergic neurons in the DRN [36][37][38]. Treatment with SP antagonists increases the firing rates of serotonergic neurons in the DRN [39,40], and stimulation of the Hb inhibits DRN neuronal firing [16].…”

Section: Functional Anatomy Of the Lateral Habenula-dorsal Raphe Nuclmentioning

confidence: 99%

The role of lateral habenula–dorsal raphe nucleus circuits in higher brain functions and psychiatric illness

Zhao

Zhang

Yang

et al. 2015

Behavioural Brain Research

107

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Serotonergic neurons in the dorsal raphe nucleus (DRN) play an important role in regulation of many physiological functions. The lateral nucleus of the habenular complex (LHb) is closely connected to the DRN both morphologically and functionally. The LHb is a key regulator of the activity of DRN serotonergic neurons, and it also receives reciprocal input from the DRN. The LHb is also a major way-station that receives limbic system input via the stria medullaris and provides output to the DRN and thereby indirectly connects a number of other brain regions to the DRN. The complex interactions of the LHb and DRN contribute to the regulation of numerous important behavioral and physiological mechanisms, including those regulating cognition, reward, pain sensitivity and patterns of sleep and waking. Disruption of these functions is characteristic of major psychiatric illnesses, so there has been a great deal of interest in how disturbed LHb-DRN interactions may contribute to the symptoms of these illnesses. This review summarizes recent research related to the roles of the LHb-DRN system in regulation of higher brain functions and the possible role of disturbed LHb-DRN function in the pathogenesis of psychiatric disorders, especially depression.

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Section: Functional Anatomy Of the Lateral Habenula-dorsal Raphe Nuclmentioning

confidence: 99%

The role of lateral habenula–dorsal raphe nucleus circuits in higher brain functions and psychiatric illness

Zhao

Zhang

Yang

et al. 2015

Behavioural Brain Research

107

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“…However, its reduction of the inhibitory influence of citalopram and fluoxetine upon DRN firing mimics the effects of chronic administration of NK 1 antagonists (Haddjeri and Blier, 2001;Guiard et al, 2005), and of genetic elimination of NK 1 receptors in mice (Froger et al, 2001;Santarelli et al, 2001;Gobbi et al, 2007). A subpopulation (some 30%) of 5-HT neurones in the DRN bear NK 1 receptors (Froger et al, 2001;Ma and Bleasdale, 2002;Lacoste et al, 2006), raising the possibility that NK 1 antagonists (via signalling crosstalk) disrupt the inhibitory influence of SSRI-engaged 5-HT 1A autoreceptors upon DRN firing. Indeed, the inhibitory influence of 5-HT 1A agonists on the DRN is blunted by chronic treatment with NK 1 antagonists (Haddjeri and Blier, 2001;Guiard et al, 2005), and by genetic deletion of NK 1 receptors (Froger et al, 2001;Santarelli et al, 2001).…”

Section: Discussion Potentiation By Gr205171 Of the Influence Of Citamentioning

confidence: 97%

“…Possible Involvement of Gabaergic, Glutatamergic, and Adrenergic Mechanisms NK 1 receptors have been identified on GABAergic neurones surrounding 5-HT cell bodies in the DRN, and studies in the septum and cortex suggest that NK 1 receptor antagonists may indirectly excite serotonergic neurones via a reduction of inhibitory GABAergic tone (Sloviter et al, 2001;Ma and Bleasdale, 2002;Stacey et al, 2002;Szeidemann et al, 1995;Ebner et al, 2008). This would enhance their responsiveness to SSRIs, by analogy to GABA B antagonists (Millan, 2006;Cremers et al, 2007).…”

Section: Discussion Potentiation By Gr205171 Of the Influence Of Citamentioning

confidence: 99%

“…First, long-term treatment with various classes of antidepressant modifies central tissue levels of substance P, an effect observed in the absence of an alteration in NK 1 receptor expression (Shirayama et al, 1996;Sartori et al, 2004). Second, NK 1 receptors are localized in: the dorsal raphe nucleus (DRN), the origin of ascending serotonergic projections (Froger et al, 2001;Santarelli et al, 2001;Commons and Valentino, 2002;Ma and Bleasdale, 2002;Lacoste et al, 2006); the locus coeruleus, the source of adrenergic input to corticolimbic regions (Santarelli et al, 2001;Ma and Bleasdale, 2002); and the ventrotegmental area (VTA), from which dopaminergic pathways project to the frontal cortex (FCX) and limbic regions (Lessard and Pickel, 2005). Third, NK 1 receptors are broadly distributed in limbic structures implicated in the control of mood, such as the FCX, hippocampus, lateral septum, nucleus accumbens, basolateral amygdala (BLA), and hypothalamus (Liu et al, 2002;Saffroy et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Neurokinin1 Antagonists Potentiate Antidepressant Properties of Serotonin Reuptake Inhibitors, Yet Blunt Their Anxiogenic Actions: A Neurochemical, Electrophysiological, and Behavioral Characterization

Gobert

Brocco

Dekeyne

et al. 2008

Neuropsychopharmacol

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Though neurokinin 1 (NK 1 ) receptor antagonists are active in experimental models of depression, clinical efficacy has proven disappointing. This encourages interest in association of NK 1 receptor blockade with inhibition of serotonin (5-HT) reuptake. The selective NK 1 antagonist, GR205171, dose-dependently enhanced citalopram-induced elevations of extracellular levels of 5-HT in frontal cortex, an action expressed stereospecifically vs its less active distomer, GR226206. Further, increases in 5-HT levels in dorsal hippocampus, basolateral amygdala, nucleus accumbens, and striatum were likewise potentiated, and GR205171 similarly facilitated the influence of fluoxetine upon levels of 5-HT, as well as dopamine and noradrenaline. In parallel electrophysiological studies, the inhibitory influence of citalopram and fluoxetine upon raphe-localized serotonergic neurones was stereospecifically blunted by GR205171. Antidepressant actions of citalopram in a forced-swim test in mice were stereospecifically potentiated by GR205171, and it also enhanced attenuation by citalopram of stress-related ultrasonic vocalizations in rats. Further, GR205171 and citalopram additively abrogated the advance in circadian rhythms provoked by exposure to light in hamsters. By contrast, GR205171 stereospecifically blocked anxiogenic actions of citalopram in social interaction procedures in rats and gerbils, and stereospecifically abolished facilitation of fearinduced foot tapping by fluoxetine in gerbils. By analogy to GR205171, a further NK 1 antagonist, RP67580, enhanced the influence of citalopram upon frontocortical levels of 5-HT and potentiated its actions in the forced swim test. In conclusion, NK 1 receptor blockade differentially modulates functional actions of SSRIs: antidepressant properties are reinforced, whereas anxiogenic effects are attenuated. Combined NK 1 receptor antagonism/5-HT reuptake inhibition may offer advantages in the management of depressed and anxious states.

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“…NK1R activation generally suppresses the output of the dorsal raphe nucleus (Valentino et al, 2003;Guiard et al, 2007), and inhibition of the NK1R can increase serotonergic activity (Santarelli et al, 2001;Conley et al, 2002;Gobbi et al, 2007). Also, NK1Rs are found on the noradrenergic cell bodies of the locus coeruleus (LC) (Chen et al, 2000;Ma and Bleasdale, 2002) and influence the output of these neurons, although the direction of this influence is unclear. Most studies suggest that SP can increase LC firing and that NK1R antagonists attenuate stress-induced norepinephrine (NE) release (Guyenet and Aghajanian, 1977;Cheeseman et al, 1983;Renoldi and Invernizzi, 2006); however, there has been some suggestion that NK1R antagonists themselves can increase NE in some terminal fields (Millan et al, 2001;Maubach et al, 2002).…”

Section: Sp and Crh: Siblings In Behavioral Neurochemical And Endocmentioning

confidence: 99%

The Neurokinin-1 Receptor in Addictive Processes

Schank

2014

J Pharmacol Exp Ther

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Stress can trigger drug-seeking behavior, increase selfadministration rates, and enhance drug reward. A number of stress-related neuropeptides have been shown to mediate these behavioral processes. The most studied peptide in this category is corticotropin-releasing hormone (CRH), which has been shown to mediate stress-induced reinstatement of drug seeking, escalated self-administration, and drug withdrawal, but it does not seem to be involved in baseline drug self-administration or cue-induced reinstatement. This pattern of effects holds for many classes of drugs, including alcohol, opiates, and psychostimulants. The neurokinin-1 receptor (NK1R) is the preferred receptor for the endogenous stress-related neuropeptide substance P (SP).The SP/NK1R system is a major mediator of stress and anxiety, and over the last several years, it has been demonstrated that the SP/NK1R system can have effects similar to those of CRH on drug taking and drug seeking. Specifically, NK1R inhibition attenuates escalated self-administration of alcohol as well as stress-induced reinstatement of alcohol and cocaine seeking; however, in contrast to other stress systems, the NK1R also appears to have a role in primary reward and reinforcement for opiates. This review outlines the role of NK1R in drug-seeking behaviors and highlights recent results from clinical studies that suggest that the NK1R may be a promising drug target going forward.

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Modulation of brain stem monoamines and γ-aminobutyric acid by NK1 receptors in rats

Cited by 36 publications

References 21 publications

The role of lateral habenula–dorsal raphe nucleus circuits in higher brain functions and psychiatric illness

The role of lateral habenula–dorsal raphe nucleus circuits in higher brain functions and psychiatric illness

Neurokinin1 Antagonists Potentiate Antidepressant Properties of Serotonin Reuptake Inhibitors, Yet Blunt Their Anxiogenic Actions: A Neurochemical, Electrophysiological, and Behavioral Characterization

The Neurokinin-1 Receptor in Addictive Processes

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