Presence of NK<sub>2</sub> binding sites in the rat brain

Saffroy, M.; Torrens, Y.; Głowiński, J.; Beaujouan, Jean‐Claude

doi:10.1046/j.1471-4159.2001.00633.x

Cited by 32 publications

(7 citation statements)

References 72 publications

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“…On the basis of identified NK 2 ‐ and NK 3 ‐R in the medial septum (Shughrue et al, 1996; Saffroy et al, 2001) and on Steinberg et al's (1998) results, we hypothesized that injection of the endogenous NK 2 ‐ and NK 3 ‐R agonists, respectively, NKA and NKB, into the medial septum would increase extracellular ACh in the hippocampus, as assessed by in vivo microdialysis and HPLC. In fact, we found that both neurokinins enhanced ACh release, not only in the hippocampus, but also in the amygdale, but not in the frontal cortex.…”

Section: Discussionmentioning

confidence: 94%

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Schäble¹,

Huston²,

Silva³

2010

Hippocampus

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The neurokinin receptors (NK-R), NK(2)- and NK(3)-R, have been implicated in behavioral processes, but apparently in opposite ways: while NK(2)-R agonism disrupts memory and has anxiogenic-like action, NK(3) -R agonists facilitate memory and display anxiolytic-like effects. Systemic application of NK(2)-R antagonists block the release of acetylcholine (ACh) in the hippocampus, which is induced by intraseptal administration of the NK(2)-R ligand, neurokinin A (NKA). We investigated the effects of medial septal injection of NKA and a preferred ligand of NK(3)-R, neurokinin B (NKB), on the activity of cholinergic neurons of the basal forebrain and assessed the role of the medial septal NK(2)-R in the control of extracellular ACh levels in cholinergic projection areas. ACh was dialysed in the frontal cortex, amygdala and hippocampus of anesthetized animals and was analysed by HPLC-EC. ACh levels in hippocampus and amygdala, but not in frontal cortex were increased after intraseptal injection of either NKA or NKB (0.1, 1, 10 μM). Application of the nonpeptidic NK(2)-R antagonist, saredutant SR48968 (1, 10, 100 pM), followed by NKA (1 μM) or NKB (10 μM) injection into the medial septum, blocked the ACh increase in hippocampus and amygdala. These results indicate that medial septal NK(2)-R have an important role in mediating ACh release, for one, via the septal-hippocampal cholinergic projection and, secondly, via direct or indirect route to the amygdala, but not frontal cortex. They also support the hypothesis that hippocampal cholinergic neurotransmission controls amygdala function suggesting that this interaction is regulated via NK(2)-R in the medial septum.

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Section: Discussionmentioning

confidence: 94%

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Schäble¹,

Huston²,

Silva³

2010

Hippocampus

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“…Apparently, blockade of NK 2 receptors does not inhibit the initial magnitude of the HR increase induced by pain, but reduces the duration of the response. NK2 binding sites were detected in few brain structures, including the hippocampus, the septum the thalamus and the prefrontal cortex (19–21). Pharmacological studies also support the presence of NK 2 receptors in the brain (22).…”

Section: Discussionmentioning

confidence: 99%

Blockade of Tachykinin NK₁/NK₂ Receptors in the Brain Attenuates the Activation of Corticotrophin‐Releasing Hormone Neurones in the Hypothalamic Paraventricular Nucleus and the Sympathoadrenal and Pituitary‐Adrenal Responses to Formalin‐Induced Pain in the Rat

Čulman

Das

Ohlendorf

et al. 2010

J Neuroendocrinology

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Evidence from pharmacological studies has implicated substance P (SP), a natural ligand of tachykinin NK(1) receptors which can also interact with NK(2) receptors, in the generation of pressor and tachycardic responses to stress. Using selective blockade of brain NK(1) and NK(2) receptors, we tested in conscious rats the hypothesis that SP initiates, within the neuronal brain circuits, the sympathoadrenal, hypothalamic-pituitary-adrenal (HPA) and behavioural responses to noxious stimuli. Formalin injected s.c. through a chronically implanted catheter in the area of the lower leg was used as a pain stimulus. Rats were pretreated i.c.v. with vehicle or the selective, nonpeptide antagonists of tachykinin NK(1) and NK(2) receptors, RP 67580 and SR 48968, respectively. Ten minutes thereafter, formalin was injected s.c. and the cardiovascular responses were recorded, plasma concentrations of catecholamines, adrenocorticotrophic hormone (ACTH) and corticosterone were determined and the expression of the inducible transcription factor c-Fos in the paraventricular (PVN) and supraoptic nuclei was detected to identify neurones which were activated during pain stimulation. Blockade of NK(1) and NK(2) receptors attenuated the formalin-induced increases in mean arterial pressure and heart rate, adrenaline and ACTH concentrations in plasma, and completely abolished the pain-induced c-Fos expression in corticotrophin-releasing hormone neurones localised in the parvocellular division of the PVN. The results obtained provide pharmacological evidence that tachykinins, most probably SP, act as mediators within the neuronal circuits linked to the initiation and control of the cardiovascular, sympathoadrenal, HPA and behavioural responses to pain stimuli and provide an excitatory input to corticotrophin-releasing hormone neurones in the PVN to activate the HPA axis. Our data demonstrating the inhibition of the complex response pattern to noxious stimuli and stress are consistent with the proposed anxiolytic and antidepressant activity of NK(1) and NK(2) receptor antagonists.

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“…NK1 receptors have been identified in the brains of gerbils and humans with a content up to 607 and 432 fmoles/mg, respectively [44], whereas NK2 and NK3 receptors achieve only 7.3 (rat) [117] and 31.2 fmoles/mg [59] [118], respectively. For the NK1 receptor the sequence of affinities of the preferred neurokinins is SP = HK-1 > NPG > NKA = NPK > NKB [184] [197].…”

Section: Mammalian Neurokinins and Their Receptorsmentioning

confidence: 99%

Neuropeptide Receptors in Pain Circuitries: Useful Targets for CNS Imaging with Non-Peptide Ligands Suitable for PET?

Pissarek¹

2014

WJNS

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Presence of NK₂ binding sites in the rat brain

Cited by 32 publications

References 72 publications

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Blockade of Tachykinin NK₁/NK₂ Receptors in the Brain Attenuates the Activation of Corticotrophin‐Releasing Hormone Neurones in the Hypothalamic Paraventricular Nucleus and the Sympathoadrenal and Pituitary‐Adrenal Responses to Formalin‐Induced Pain in the Rat

Neuropeptide Receptors in Pain Circuitries: Useful Targets for CNS Imaging with Non-Peptide Ligands Suitable for PET?

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Presence of NK2 binding sites in the rat brain

Cited by 32 publications

References 72 publications

Neurokinin2‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Neurokinin2‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Blockade of Tachykinin NK1/NK2 Receptors in the Brain Attenuates the Activation of Corticotrophin‐Releasing Hormone Neurones in the Hypothalamic Paraventricular Nucleus and the Sympathoadrenal and Pituitary‐Adrenal Responses to Formalin‐Induced Pain in the Rat

Neuropeptide Receptors in Pain Circuitries: Useful Targets for CNS Imaging with Non-Peptide Ligands Suitable for PET?

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Product

Resources

About

Presence of NK₂ binding sites in the rat brain

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Neurokinin₂‐R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B

Blockade of Tachykinin NK₁/NK₂ Receptors in the Brain Attenuates the Activation of Corticotrophin‐Releasing Hormone Neurones in the Hypothalamic Paraventricular Nucleus and the Sympathoadrenal and Pituitary‐Adrenal Responses to Formalin‐Induced Pain in the Rat