Subcellular distribution and plasticity of neurokinin-1 receptors in the rat substantia nigra and ventral tegmental area

Lessard, Andrée; Pickel, Virginia M.

doi:10.1016/j.neuroscience.2005.07.025

Cited by 33 publications

(38 citation statements)

References 80 publications

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“…Correspondingly, GR205171 and RP67580 increased extracellular levels of NA in FCX, as well as in the BLA and hippocampusFstructures likewise innervated by the LC (Millan et al, 2001b). The VTA possess a high density of NK 1 sites (Lessard and Pickel, 2005), and electrical activity of VTAlocalized dopaminergic neurons is accelerated by blockade of NK 1 receptors, an effect accompanied by increases in DA levels in FCX (Lejeune et al, 2002). This finding was confirmed herein for GR205171, reproduced with RP67580 and extended to the BLA.…”

Section: Discussion Potentiation By Gr205171 Of the Influence Of Citasupporting

confidence: 72%

“…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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Section: Discussion Potentiation By Gr205171 Of the Influence Of Citasupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

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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“…Furthermore, high intensity pulses, when presented alone, produce a significant decrease in extracellular dopamine levels in the Acb, but this change is inhibited when a prepulse precedes the pulse (Humby et al, 1996). In parallel studies of neurokinin 1 receptor distributions in the ventral tegmental area also showed that AS-evoked relocation of these receptors was not affected by the presence or absence of prepulses in the acoustic startle testing (Lessard and Pickel, 2005).…”

Section: Methodological Considerationsmentioning

confidence: 94%

“…The immunogold quantification methods used for between-group comparisons were similar to those used in other studies (Glass et al, 2005;Lessard and Pickel, 2005). All the sections from each of the four experimental groups were co-processed, and special care was taken to use identical sampling methods.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Hara

Pickel

2007

Neuroscience

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Prepulse inhibition of the startle response to auditory stimulation (AS) is a measure of sensorimotor gating that is disrupted by the dopamine D1/D2 receptor agonist, apomorphine. The apomorphine effect on prepulse inhibition is ascribed in part to altered synaptic transmission in the limbicassociated shell and motor-associated core subregions of the nucleus accumbens (Acb). We used electron microscopic immunolabeling of dopamine D1 receptors (D1Rs) in the Acb shell and core to test the hypothesis that region-specific redistribution of D1Rs is a short-term consequence of AS and/or apomorphine administration. Thus, comparisons were made in the Acb of rats sacrificed one hour after receiving a single subcutaneous injection of vehicle (VEH) or apomorphine (APO) alone or in combination with startle-evoking AS (VEH+AS, APO+AS). In both regions of all animals, the D1R immunoreactivity was present in somata and large, as well as small, presumably more distal dendrites and dendritic spines. In the Acb shell, compared with the VEH+AS group, the APO+AS group had more spines containing D1R immunogold particles, and these particles were more prevalent on the plasma membranes. This suggests movement of D1Rs from distal dendrites to the plasma membrane of dendritic spines. Small-and medium-sized dendrites also showed a higher plasmalemmal density of D1R in the Acb shell of the APO+AS group compared with the APO group. In the Acb core, the APO+AS group had a higher plasmalemmal density of D1R in medium-sized dendrites compared with the APO or VEH+AS group. Also in the Acb core, D1R-labeled dendrites were significantly smaller in the VEH+AS group compared to all other groups. These results suggest that alerting stimuli and apomorphine synergistically affect distributions of D1R in Acb shell and core. Thus adaptations in D1R distribution may contribute to sensorimotor gating deficits that can be induced acutely by apomorphine or develop over time in schizophrenia.

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“…To test this hypothesis, we examined the electron microscopic immunocytochemical labeling of the NR1 subunit in relation to the D1R in the Acb shell and core of rats receiving a single injection of vehicle (VEH) or apomorphine (APO) alone, or in combination of AS (VEH+AS, APO+AS). The rats in the APO+AS group used in this study were previously reported to have a significant disruption of PPI, whereas rats in the VEH+AS group had normal PPI (Lessard and Pickel, 2005;Hara and Pickel, 2007). The results from the current study provide the first ultrastructural evidence that redistribution of NMDA receptors in D1R-containing neurons occurs following apomorphine-induced disruption of PPI.…”

Section: Introductionmentioning

confidence: 49%

Preferential relocation of the N-methyl-d-aspartate receptor NR1 subunit in nucleus accumbens neurons that contain dopamine D1 receptors in rats showing an apomorphine-induced sensorimotor gating deficit

Hara¹,

Pickel²

2008

Neuroscience

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Sensorimotor gating as measured by prepulse inhibition (PPI) to startle-evoking auditory stimulation (AS) is disrupted in schizophrenia and in rodents receiving systemic administration of apomorphine, a dopamine D1/D2 receptor agonist, or MK-801, an NMDA receptor antagonist. The functional analogies and our prior results showing apomorphine-and AS-induced relocation of the dopamine D1 receptor (D1R) in the nucleus accumbens (Acb) shell suggest that apomorphine and AS may affect the subcellular distribution of the NMDA receptor NR1 subunit, a protein that forms proteinprotein interactions with the D1R. We quantitatively compared the electron microscopic immunogold labeling for NR1 in dendritic profiles distinguished with respect to presence of D1R immunoreactivity and location in the Acb shell or core of rats receiving a single subcutaneous injection of vehicle (VEH) or apomorphine (APO) alone, or combined with AS (VEH+AS, APO +AS). The rats in the APO+AS group were previously shown to have PPI deficits, whereas the rats in the VEH+AS group had normal PPI. A significantly higher percentage of plasmalemmal and a lower percentage of cytoplasmic NR1 immunogold particles were seen in D1R-labeled dendritic spines in the Acb shell of the APO+AS group compared with all other groups. D1R-containing small dendrites in the Acb shell of the APO+AS group also showed a significantly higher density of plasmalemmal and a lower density of cytoplasmic NR1 immunogold particles compared with VEH or APO groups. In the Acb core, the APO+AS group had significantly fewer dendritic spines coexpressing NR1 and D1R compared with VEH or VEH+AS groups. These results, together with our earlier findings, suggest that NMDA receptors are preferentially mobilized in D1R-containing Acb neurons of rats showing apomorphine-induced disruption of PPI in a paradigm using acoustic stimulation.

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Subcellular distribution and plasticity of neurokinin-1 receptors in the rat substantia nigra and ventral tegmental area

Cited by 33 publications

References 80 publications

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

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

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Preferential relocation of the N-methyl-d-aspartate receptor NR1 subunit in nucleus accumbens neurons that contain dopamine D1 receptors in rats showing an apomorphine-induced sensorimotor gating deficit

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