The effect of the acute and chronic administration of CP 96,345, a selective neurokinin1 receptor antagonist, on midbrain dopamine neurons in the rat: A single unit, extracellular recording study

Minabe, Yoshio; Emori, Kenji; Toor, Alon; Stutzmann, Grace E.; Ashby, Charles R.

doi:10.1002/(sici)1098-2396(199601)22:1<35::aid-syn4>3.0.co;2-j

Cited by 27 publications

(5 citation statements)

References 42 publications

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“…Peripheral administration of SP increased dopamine in the NAc (Boix et al, 1992) and microinjection of SP analogs into the VTA indicate that this effect is mediated by NK1R activation in the VTA (Figure 5A) (Elliott et al, 1986, 1991; Barnes et al, 1990). Conversely, an NK1R antagonist was shown to reduce the number of spontaneously active dopaminergic neurons in the VTA, further supporting that NK1R antagonists may reduce the intake of rewarding substances by suppressing activation of the mesolimbic pathway (Minabe et al, 1996). SP or an SP analog in the VTA has also increased dopamine or its metabolites in other postsynaptic targets (e.g., PFC, amygdala) (Deutch et al, 1985; Elliott et al, 1986; Barnes et al, 1990).…”

Section: Substance Pmentioning

confidence: 87%

“…SP or an SP analog in the VTA has also increased dopamine or its metabolites in other postsynaptic targets (e.g., PFC, amygdala) (Deutch et al, 1985; Elliott et al, 1986; Barnes et al, 1990). Furthermore, an NK1R antagonist reduced the number of active dopaminergic neurons in the SN, which indicates that NK1R inhibition may also suppress the nigrostriatal pathway (Minabe et al, 1996). Therefore, NK1R modulation of dopamine signaling in corticostriatal-limbic circuitry could mechanistically explain the effects of the SP/NK1R system on behaviors related to AUD.…”

Section: Substance Pmentioning

confidence: 99%

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Gut-brain peptides in corticostriatal-limbic circuitry and alcohol use disorders

et al. 2014

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Peptides synthesized in endocrine cells in the gastrointestinal tract and neurons are traditionally considered regulators of metabolism, energy intake, and appetite. However, recent work has demonstrated that many of these peptides act on corticostriatal-limbic circuitry and, in turn, regulate addictive behaviors. Given that alcohol is a source of energy and an addictive substance, it is not surprising that increasing evidence supports a role for gut-brain peptides specifically in alcohol use disorders (AUD). In this review, we discuss the effects of several gut-brain peptides on alcohol-related behaviors and the potential mechanisms by which these gut-brain peptides may interfere with alcohol-induced changes in corticostriatal-limbic circuitry. This review provides a summary of current knowledge on gut-brain peptides focusing on five peptides: neurotensin, glucagon-like peptide 1, ghrelin, substance P, and neuropeptide Y. Our review will be helpful to develop novel therapeutic targets for AUD.

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Section: Substance Pmentioning

confidence: 87%

Section: Substance Pmentioning

confidence: 99%

Gut-brain peptides in corticostriatal-limbic circuitry and alcohol use disorders

et al. 2014

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“…In the striatum, DA can induce the expression of preprotachykinin-A (PPT-A) mRNA coding for SP, as has been shown in slice cultures (Campbell and Walker 2001). In addition, SP originating from the striatum can stimulate midbrain neurones to produce DA, as shown by the fact that the administration of a SP receptor antagonist can decrease the activity of VTA and SN neurones (Minabe et al 1996). Evidently, modulation of such a positive feedback loop can play an important role in addiction, because DA release has been associated with reward and reward prediction (Schultz 1998).…”

mentioning

confidence: 94%

“…It should be noted that autoradiographic localization (Quirion et al 1983) and immunohistochemistry (Nakaya et al 1994) have revealed that dopaminergic neurones of the rat brain express very low levels of NK-1 receptors. However, a selective NK-1 agonist increases the activity of VTA and SN cells (Overton et al 1992), whereas a selective NK-1 antagonist decreases it (Minabe et al 1996). This apparent discrepancy may be due to an inefficient way of detecting NK-1 receptors, because a more recent study using single-cell RT-PCR demonstrated that SN dopaminergic neurones of the rat express considerable amounts of NK-1 receptor mRNA (Futami et al 1998).…”

mentioning

confidence: 99%

C/EBPβ couples dopamine signalling to substance P precursor gene expression in striatal neurones

Kovács

Steinmann

Magistretti

et al. 2006

Journal of Neurochemistry

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Dopamine-induced changes in striatal gene expression are thought to play an important role in drug addiction and compulsive behaviour. In this study we report that dopamine induces the expression of the transcription factor CCAAT/ Enhancer Binding Protein b (C/EBP)-b in primary cultures of striatal neurones. We identifed the preprotachykinin-A (PPT-A) gene coding for substance P and neurokinin-A as a potential target gene of C/EBPb. We demonstrated that C/EBPb physically interacts with an element of the PPT-A promoter, thereby facilitating substance P precursor gene transcription. The regulation of PPT-A gene by C/EBPb could subserve many important physiological processes involving substance P, such as nociception, neurogenic inflammation and addiction. Given that substance P is known to increase dopamine signalling in the striatum and, in turn, dopamine increases substance P expression in medium spiny neurones, our results implicate C/EBPb in a positive feedback loop, changes of which might contribute to the development of drug addiction.

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“…Experimental and preclinical evidence suggested that substance P is involved in several neurological diseases, including degeneration of human motoneurons (Vacca-Galloway and Steinberger, 1986; Tang et al, 1990; Yung et al, 1992), depression (Santarelli and Saxe, 2003; Czeh et al, 2005), Alzheimer's disease (Rioux and Joyce, 1993; Rosler et al, 2001), Parkinson's disease (Pezzoli et al, 1984; Rioux and Joyce, 1993) and Huntington's disease (Lastres-Becker et al, 2002). In terms of cellular actions, previous electrophysiological studies have demonstrated that substance P can enhance firing rate and depolarized neurons in several brain areas (Stanfield et al, 1985; Norris et al, 1993; Shirakawa and Moore, 1994; Napier et al, 1995; Minabe et al, 1996; Li and Guyenet, 1997; Wang and Robertson, 1997, 1998; Mitrovic and Napier, 1998; Preston et al, 2000; Bailey et al, 2004). It is therefore generally regarded as an excitatory neurotransmitter or neuromodulator.…”

Section: Introductionmentioning

confidence: 99%

Neurokinin-1 receptor activation in globus pallidus

2009

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The undecapeptide substance P has been demonstrated to modulate neuronal activity in a number of brain regions by acting on neurokinin-1 receptors. Anatomical studies revealed a moderate level of neurokinin-1 receptor in rat globus pallidus. To determine the electrophysiological effects of neurokinin-1 receptor activation in globus pallidus, whole-cell patch-clamp recordings were performed in the present study. Under current-clamp recordings, neurokinin-1 receptor agonist, [Sar9, Met(O2)11] substance P (SM-SP) at 1 μM, depolarized globus pallidus neurons and increased their firing rate. Consistently, SM-SP induced an inward current under voltage-clamp recording. The depolarization evoked by SM-SP persisted in the presence of tetrodotoxin, glutamate and GABA receptor antagonists, indicating its direct postsynaptic effects. The neurokinin-1 receptor antagonist, SR140333B, could block SM-SP-induced depolarization. Further experiments showed that suppression of potassium conductance was the predominant ionic mechanism of SM-SP-induced depolarization. To determine if neurokinin-1 receptor activation exerts any effects on GABAergic and glutamatergic neurotransmission, the action of SM-SP on synaptic currents was studied. SM-SP significantly increased the frequency of spontaneous inhibitory postsynaptic currents, but only induced a transient increase in the frequency of miniature inhibitory postsynaptic currents. No change was observed in both spontaneous and miniature excitatory postsynaptic currents. Based on the direct excitatory effects of SM-SP on pallidal neurons, we hypothesize that neurokinin-1 receptor activation in globus pallidus may be involved in the beneficial effect of substance P in Parkinson's disease.

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The effect of the acute and chronic administration of CP 96,345, a selective neurokinin1 receptor antagonist, on midbrain dopamine neurons in the rat: A single unit, extracellular recording study

Cited by 27 publications

References 42 publications

Gut-brain peptides in corticostriatal-limbic circuitry and alcohol use disorders

Gut-brain peptides in corticostriatal-limbic circuitry and alcohol use disorders

C/EBPβ couples dopamine signalling to substance P precursor gene expression in striatal neurones

Neurokinin-1 receptor activation in globus pallidus

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