The new neurokinin 1‐sensitive receptor mediates the facilitation by endogenous tachykinins of the NMDA‐evoked release of acetylcholine after suppression of dopaminergic transmission in the matrix of the rat striatum

Kemel, M.L.; Pérez, Sylvie; Beaujouan, Jean‐Claude; Jabourian, Maritza; Soubrié, Philippe; Głowiński, J.

doi:10.1046/j.1471-4159.2003.02010.x

Cited by 14 publications

(10 citation statements)

References 61 publications

(149 reference statements)

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“…In recent studies, it has been found that tachykinins acting via NK 1 receptors facilitate NMDA evoked release of acetylcholine which is apparent after suppression of dopaminergic transmission [202]. Since increased acetylcholine release would be expected to exacerbate movement disorders, it has been suggested that selective tachykinin antagonists could be used as indirect anti-cholinergic agents in Parkinson's disease [202].…”

Section: Tachykinins In Parkinson's Diseasementioning

confidence: 99%

“…Since increased acetylcholine release would be expected to exacerbate movement disorders, it has been suggested that selective tachykinin antagonists could be used as indirect anti-cholinergic agents in Parkinson's disease [202]. However, striatal PPT gene expression has been shown to reflect Parkinsonian signs in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease [203], and it has been suggested that tachykinin peptides might have a therapeutic role in Parkinson's disease [204].…”

Section: Tachykinins In Parkinson's Diseasementioning

confidence: 99%

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Tachykinins and Neuropsychiatric Disorders

Chahl

2006

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The classical tachykinins, substance P, neurokinin A and neurokinin B are predominantly found in the nervous system where they act as neurotransmitters and neuromodulators. Their respective preferred receptors are NK1, NK2, and NK3 receptors. The presence of substance P in nociceptive primary afferent neurons, electrophysiological studies showing that it activated neurons in the dorsal horn of the spinal cord, and behavioral studies in animals, supported the concept that substance P was an important transmitter in the nociceptive pathway. It was therefore surprising that non-peptide NK1 receptor antagonists were ineffective as analgesics in clinical pain conditions. Nevertheless, the discovery that NK1 receptor antagonists had antidepressant activity led to renewed interest in these antagonists. It is disappointing that clinical trials of MK869 (aprepitant) for depression were suspended. The future of NK1 receptor antagonists as antidepressant drugs will depend on the outcome of clinical trials with other NK1 receptor antagonists. NK1 receptor antagonists were also found to be effective antiemetics, and aprepitant has recently become available for the treatment of chemotherapy induced emesis. Although less is known of the potential of NK2 and NK3 receptor antagonists, recent trials of NK3 receptor antagonists have shown efficacy in schizophrenia. The discovery of a new family of tachykinins, the hemokinins and endokinins, which acts on NK1 receptors and has potent effects on immune cells, has implications for the clinical use of NK1 receptor antagonists. Thus specific therapeutic strategies may be required to enable NK1 receptor antagonists to be introduced for treatment of neuropsychiatric disorders.

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Section: Tachykinins In Parkinson's Diseasementioning

confidence: 99%

Section: Tachykinins In Parkinson's Diseasementioning

confidence: 99%

Tachykinins and Neuropsychiatric Disorders

Chahl

2006

CDT

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“…2000). The concentration of NKA and SP(6–11) leading to 50% reversal of the SSR240600 response were from Kemel et al. 2003 in the sensorimotor and calculated from experiments shown in Fig 4 in the limbic/PF territory of the dorsal striatum.…”

Section: Resultsmentioning

confidence: 99%

“…2000). In the striatal sensorimotor territory, the direct tachykinin/NK 1 control of ACh release is mediated by the new NK 1 ‐sensitive subtype of NK 1 R binding site (Kemel et al. 2003).…”

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confidence: 99%

Tachykinin regulation of cholinergic transmission in the limbic/prefrontal territory of the rat dorsal striatum: implication of new neurokinine 1‐sensitive receptor binding site and interaction with enkephalin/mu opioid receptor transmission

Pérez

Tierney

Deniau

et al. 2007

Journal of Neurochemistry

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The tachykinin neurokinin 1 receptors (NK 1 Rs) regulation of acetylcholine release and its interaction with the enkephalin/ mu opioid receptors (MORs) transmission was investigated in the limbic/prefrontal (PF) territory of the dorsal striatum. Using double immunohistochemistry, we first showed that in this territory, cholinergic interneurons contain tachykinin NK 1 Rs and co-express MORs in the last part of the light period (afternoon). In slices of the striatal limbic/PF territory, following suppression of the dopaminergic inhibitory control of acetylcholine release, application of the tachykinin NK 1 R antagonist, SSR240600, markedly reduced the NMDA-induced acetylcholine release in the morning but not in the afternoon when the enkephalin/MOR regulation is operational. In the afternoon, the NK 1 R antagonist response required the suppression of the enkephalin/MOR inhibitory control of acetylcholine release by bfunaltrexamine. The pharmacological profile of the tachykinin NK 1 R regulation tested by application of the receptor agonists [[Pro 9 ]substance P, neurokinin A, neuropeptide K, and substance P(6-11)] and antagonists (SSR240600, GR205171, GR82334, and RP67580) indicated that the subtype of tachykinin NK 1 R implicated are the new NK 1 -sensitive receptor binding site. Therefore, in the limbic/ PF territory of the dorsal striatum, endogenous tachykinin facilitates acetylcholine release via a tachykinin NK 1 R subtype. In the afternoon, the tachykinin/NK 1 R and the enkephalin/MOR transmissions interact to control cholinergic transmission.

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“…There is functional evidence for interaction between these two transmitter pathways in the striatum where substance P facilitates NMDA evoked acetylcholine release (Kemel et al, 2003). Whilst electrophysiological evidence shows that NK1 receptors are on medium spiney neurons (Gabaergic) that also respond to glutamatergic drive (Blomeley and Bracci, 2008) implying neuronal colocalisation of some glutamate receptors with NK1 receptors.…”

Section: Introductionmentioning

confidence: 99%