Control by tachykinin NK2 receptors of CRF1 receptor-mediated activation of hippocampal acetylcholine release in the rat and guinea-pig

Desvignes, Christophe; Rouquier, L.; Souilhac, J.; Mons, G.; Rodier, Daniel; Soubrié, Philippe; Steinberg, R.

doi:10.1016/s0143-4179(03)00019-2

Cited by 20 publications

(15 citation statements)

References 29 publications

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“…injection of CRF also induced hippocampal ACh release. Since this effect, as well as the stroking‐induced release of hippocampal ACh were attenuated by antagonism of NK 2 ‐R and CRF 1 ‐R, it was suggested that stress‐induced hippocampal ACh release is controlled by the NK 2 ‐R agonist NKA (Desvignes et al, 2003). Systemic NK 2 ‐R antagonism by SR48968 reduced anxiety‐like behavior associated to stress and to a threatening stimulus (Griebel et al, 2001a, b; Salome et al, 2006; Louis et al, 2008; Micale et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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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: 99%

“…administration of corticotrophin releasing factor stimulated release of ACh in the hippocampus, and pretreatment with the NK 2 ‐R antagonist SR48968 (i.p. 1 mg/kg), but not by NK 1 ‐ or NK 3 ‐R antagonists, counteracted this effect (Desvignes et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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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“…In contrast, long-day exposure produced the opposite effects: rats explored the open arms less and exhibited increased immobility time. Interestingly, CRF expression can induce elevations in hippocampal acetylcholine (Desvignes et al, 2003). Such an increase is consistent with physostigmine-induced increases in immobility in the FST in mice that is hippocampal-mediated (Mineur et al, 2013).…”

Section: Key Studies Investigating Cycling/switching Into Other Stmentioning

confidence: 99%

Investigating the mechanism(s) underlying switching between states in bipolar disorder

Young

Dulcis

2015

European Journal of Pharmacology

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Bipolar Disorder (BD) is a unique disorder that transcends domains of function since the same patient can exhibit depression or mania, states with polar opposite mood symptoms. During depression, people feel helplessness, reduced energy, and risk aversion, while with mania behaviors include grandiosity, increased energy, less sleep, and risk preference. The neural mechanism(s) underlying each state are gaining clarity, with catecholaminergic disruption seen during mania, and cholinergic dysfunction during depression. The fact that the same patient cycles/switches between these states is the defining characteristic of BD however. Of greater importance therefore, is the mechanism(s) underlying cycling from one state - and its associated neural changes - to another, considered the ‘holy grail’ of BD research. Herein, we review studies investigating triggers that induce switching to these states. By identifying such triggers, researchers can study neural mechanisms underlying each state and importantly how such mechanistic changes can occur in the same subject. Current animal models of this switch are also discussed, from submissive- and dominant-behaviors to kindling effects. Focus however, is placed on how seasonal changes can induce manic and depressive states in BD sufferers. Importantly, changing photoperiod lengths can induce local switches in neurotransmitter expression in normal animals, from increased catecholaminergic expression during periods of high activity, to increased somatostatin and corticotrophin releasing factor during periods of low activity. Identifying susceptibilities to this switch would enable the development of targeted animal models. From animal models, targeted treatments could be developed and tested that would minimize the likelihood of switching.

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“…Furthermore, the possibility of NK2 receptor‐mediated modulation of sympathetic nerves cannot be excluded (Shinkai & Takayanagi, 1993). Finally, supraspinal NK2 receptors located in hippocampal and hypothalamic areas might modulate the gastrointestinal responses that follow emotional stimuli ( Desvignes et al , 2003 ). In this context, however, it should be pointed out that most of the preclinical evidence for the possible involvement of NK2 receptors in IBS symptoms has been obtained through the use of nepadutant (MEN11420), a cyclic peptide‐selective NK2 receptor antagonist that does not cross the blood–brain barrier to any pharmacologically significant extent ( Catalioto et al , 1998 ).…”

Section: Distribution Of Tks and Nk2 Receptors In The Gastrointestinamentioning

confidence: 99%

Tachykinin NK2 receptor antagonists for the treatment of irritable bowel syndrome

Lecci

Capriati

Maggi

2004

British J Pharmacology

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Tachykinin NK2 receptors are expressed in the gastrointestinal tract of both laboratory animals and humans. Experimental data indicate a role for these receptors in the regulation of intestinal motor functions (both excitatory and inhibitory), secretions, inflammation and visceral sensitivity. In particular, NK2 receptor stimulation inhibits intestinal motility by activating sympathetic extrinsic pathways or NANC intramural inhibitory components, whereas a modulatory effect on cholinergic nerves or a direct effect on smooth muscle account for the NK2 receptor-mediated increase in intestinal motility. Accordingly, selective NK2 receptor antagonists can reactivate inhibited motility or decrease inflammation-or stress-associated hypermotility. Intraluminal secretion of water is increased by NK2 receptor agonists via a direct effect on epithelial cells, and this mechanism is active in models of diarrhoea since selective antagonists reverse the increase in faecal water content in these models. Hyperalgesia in response to intraluminal volume signals is possibly mediated through the stimulation of NK2 receptors located on peripheral branches of primary afferent neurones. NK2 receptor antagonists reduce the hyper-responsiveness that occurs following intestinal inflammation or application of stressful stimuli to animals. Likewise, NK2 receptor antagonists reduce intestinal tissue damage induced by chemical irritation of the intestinal wall or lumen. In healthy volunteers, the selective NK2 antagonist nepadutant reduced the motility-stimulating effects and irritable bowel syndrome-like symptoms triggered by intravenous infusion of neurokinin A, and displayed other characteristics that could support its use in patients. It is concluded that blockade of peripheral tachykinin NK2 receptors should be considered as a viable mechanism for decreasing the painful symptoms and altered bowel habits of irritable bowel syndrome patients.

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Control by tachykinin NK2 receptors of CRF1 receptor-mediated activation of hippocampal acetylcholine release in the rat and guinea-pig

Cited by 20 publications

References 29 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

Investigating the mechanism(s) underlying switching between states in bipolar disorder

Tachykinin NK2 receptor antagonists for the treatment of irritable bowel syndrome

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Control by tachykinin NK2 receptors of CRF1 receptor-mediated activation of hippocampal acetylcholine release in the rat and guinea-pig

Cited by 20 publications

References 29 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

Investigating the mechanism(s) underlying switching between states in bipolar disorder

Tachykinin NK2 receptor antagonists for the treatment of irritable bowel syndrome

Contact Info

Product

Resources

About

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