Localization of striatal and nigral tachykinin receptors in the rat
Reference (31)
- et al.
Substance P and neurokinin A regulate by different mechanisms dopamine release from dendrites and nerve terminals of the nigrostriatal dopaminergic neurons
Neuroscience
(1988) - et al.
The GABA and substance P inputs to dopaminergic neurones in the substantia nigra of the rat
Brain Res.
(1990) Substance P-dopamine relationship in the rat substantia nigra: a light and electron microscopy study of double immunocytochemically labeled materials
Brain Res.
(1988)- et al.
Visualization of neurokinin-3 receptor sites in rat brain using the highly selective ligand [3H]senktide
Brain Res.
(1990) - et al.
Autoradiographic distribution of brain neurokinin-1/substance P receptors using a highly selective ligand [3H]-[Sar9, Met(O2)11]-substance P
Brain Res.
(1990) - et al.
Substance P in the substantia nigra
Brain Res.
(1976) - et al.
Tachykinin receptor types: classification and membrane signalling mechanisms
Neurochem. Int.
(1991) Mismatches between neurotransmitter and receptor localizations in brain: observations and implications
Neuroscience
(1987)- et al.
Substance K excites dopaminergic and non-dopaminergic neurons in rat substantia nigra
Brain Res.
(1985) - et al.
Evidence for the existence of substance P-containing fibres in striato-nigral and pallido-nigral pathways in rat brain
Brain Res.
(1977)
Substance P infusion into substantia nigra of the rat: behavioural analysis and involvement of striatal dopamine
Eur. J. Pharmacol.
The localization and characterization of substance P and substance K in striatonigral neurons
Brain Res.
Substance P receptors: localization by light microscopic autoradiography in rat brain using [3H]SP as the radioligand
Brain Res.
Localization of neurokinin B in the central nervous system of the rat
Peptides
Stimulatory effect of substance P on the spontaneous release of newly synthesized [3H]dopamine from rat striatal slices: a tetrodotoxin-sensitive process
Neuropharmacology
Cited by (44)
A Second Wave for the Neurokinin Tac2 Pathway in Brain Research
2021, Biological PsychiatryCitation Excerpt :Moreover, NKB infusion in the nucleus basalis magnocellularis prevents choline acetyltransferase decline in the cortex (48) and stimulates acetylcholine esterase activity in aging (49). It is worth noting that part of the above-described effects involve the dopaminergic system because the NK3R is located on dopamine nerve terminals within the striatum (8). Furthermore, the influence of Tac2 on the cholinergic system in aging and Alzheimer’s disease could represent a therapeutic target for other disorders such as anxiety (40,50).
Mapping the binding pocket of a novel, high-affinity, slow dissociating tachykinin NK<inf>3</inf> receptor antagonist: Biochemical and electrophysiological characterization
2014, NeuropharmacologyCitation Excerpt :It is prominently expressed in limbic areas of the brain, many of which have been implicated in schizophrenia (Harrison, 1999). Importantly, the NK3 receptor is also located on dopaminergic neurons in the midbrain regions such as substantia nigra (A9), ventral tegmental area and nucleus raphe linealis (A10) (Chen et al., 1998; Langlois et al., 2001; Stoessl, 1994). Activation of the midbrain NK3 receptor with the endogenous ligand NKB or the highly specific agonist succinyl-DFMe-FGLM-NH2 (senktide) increased the firing frequency of dopaminergic neurons and as a consequence the dopamine (DA) release in the nucleus accumbens (Alonso et al., 1996; Marco et al., 1998; Nalivaiko et al., 1997).
3D-Quantitative structure-activity relationship and docking studies of the tachykinin NK<inf>3</inf> receptor
2011, Bioorganic and Medicinal Chemistry LettersCharacterization of nuclear neurokinin 3 receptor expression in rat brain
2011, NeuroscienceCitation Excerpt :Reducing the AB concentration was necessary to detect this increase because the higher concentration of AB that was used in Fig. 3B resulted in a maximal signal in nuclear fractions from normotensive control animals that obscured the hydralazine-induced increase. NK3-Rs are widely distributed in the brain (Stoessl and Hill, 1990; Stoessl, 1994; Ding et al., 1996; Shughrue et al., 1996; Yip and Chahl, 2000; Harrison et al., 2004), and intraventricular injection of senktide has been shown to induce fos expression in many of these areas (Smith and Flynn, 2000). As shown in Figs. 6 and 7, we confirmed the expression of NK3-R in whole tissue and nuclear fractions obtained from punches of Caud/putamen, LS, BNST, amygdala, MPOA, PVN, SN, and VTA using both the N-terminal and 2nd extracellular loop ABs.
Predominant surface distribution of neurokinin-3 receptors in non-dopaminergic dendrites in the rat substantia nigra and ventral tegmental area
2007, NeuroscienceCitation Excerpt :The differential subcellular distributions of NK1 and NK3 receptors in the SN and VTA suggest different functional sites for activation of distinct subtypes of neurokinin receptors. The presence of NK3 gold particles in midbrain TH-labeled dendrites is consistent with the known involvement of NK3 receptors in the modulation of the nigrostriatal and mesocorticolimbic DA pathways in the respective SN and VTA (Elliott et al., 1991; Humpel et al., 1991; Humpel and Saria, 1993; Stoessl, 1994; Bannon and Whitty, 1995; Chen et al., 1998; Marco et al., 1998; Friedman et al., 2002; Bishop and Walker, 2004). In DA neurons, the NK3 gold particles were however largely cytoplasmic, suggesting that they are not locally activated.