Activation of trace amine-associated receptor 1 attenuates schedule-induced polydipsia in rats

Sukhanov, I.; Dorotenko, Artem; Dolgorukova, Antonina; Hoener, Marius C.; Gainetdinov, Raul R.; Bespalov, Anton

doi:10.1016/j.neuropharm.2018.10.034

Cited by 13 publications

(8 citation statements)

References 35 publications

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“…The TAAR1 activation‐induced increased time spent on the open arm, reduced withdrawal symptoms and increased paw withdrawal threshold in LA rats during withdrawal cannot be explained by the possible sedative effect of TAAR1 partial agonist RO5263397. Although RO5263397 was shown to attenuate the hyperlocomotion induced by dopamine transporter inhibitor and NMDA receptor blockers (PCP and L‐687,414), 63 the dose used here (5.6 mg/kg) was shown not to affect the locomotor activity in naïve rats in previous studies 64–66 . Meanwhile, the effect of TAAR1 activation on withdrawal might be nicotine‐specific as we have shown that RO5263397 did not affect the naltrexone‐induced jumping behaviour and conditioned place aversion (CPA) in morphine‐dependent mice 60 .…”

Section: Discussionmentioning

confidence: 70%

Activation of trace amine‐associated receptor 1 attenuates nicotine withdrawal‐related effects

et al. 2021

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Nicotine addiction is a leading avoidable brain disorder globally. Although nicotine induces a modest reinforcing effect, which is important for the initial drug use, the transition from nicotine use to nicotine addiction involves the mechanisms responsible for the negative consequences of drug abstinence. Recent study suggested that trace amine-associated receptor 1 (TAAR1) is a promising pharmacological target for the modulation of positive reinforcing effects of nicotine. However, whether TAAR1 plays a part in the negative reinforcement of nicotine withdrawal remains to be determined. Here, using a long-access (LA) self-administration model, we investigated whether LA rats show increased nicotine intake and withdrawal symptoms in comparison with saline and ShA rats and then tested the effect of TAAR1 partial agonist RO5263397 on nicotine withdrawal effects. We found that rats from long-access group showed significant abstinence-induced anxiety-like behaviour, mechanic hypersensitivity, increased number of precipitated withdrawal signs and higher motivation for the drug, while rats from short-access did not differ from saline group. TAAR1 partial agonist RO5263397 significantly reduced the physical and motivational withdrawal effects of nicotine in LA rats, as reflected by increased time spent on the open arm in the elevated plus maze (EPM) test, normalized paw withdrawal threshold, decreased withdrawal signs and motivation to self-administer nicotine.This study indicates that activation of TAAR1 attenuates the negative-reinforcing effects of nicotine withdrawal and further suggests TAAR1 as a promising target to treat nicotine addiction.

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Section: Discussionmentioning

confidence: 70%

Activation of trace amine‐associated receptor 1 attenuates nicotine withdrawal‐related effects

et al. 2021

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“…In SIP-prone rats, differences in the binding affinity of DA D1-like/D2-like receptors exist in limbic and cortical circuits (amygdala, VTA, NAc, and medial prefrontal cortex [mPFC]) (Pellón et al, 2011). Furthermore, pharmacological pretreatment with either DA agonists/antagonists, serotonergic or monoamine modulators, reduce SIP behaviors (i.e., drinking and licking; see Table 2) (Moreno and Flores, 2012; Navarro et al, 2015; Rodriguez et al, 2017; Sukhanov et al, 2019). High drinking rats also show elevated serotonergic activity in the amygdala (Moreno et al, 2012) and reduced 5-HT 2A receptor binding in the mPFC (Mora et al, 2018) with additional evidence for changes in DA activity in the PFC, NAc, and amygdala (Moreno et al, 2012).…”

Section: Schedule-induced Polydipsia As a Model Of Obsessive Compulsimentioning

confidence: 99%

The Bed Nucleus of the Stria Terminalis, Homeostatic Satiety, and Compulsions: What Can We Learn From Polydipsia?

Banasikowski

Hawken

2019

Front. Behav. Neurosci.

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A compulsive phenotype characterizes several neuropsychiatric illnesses – including but not limited to – schizophrenia and obsessive compulsive disorder. Because of its perceived etiological heterogeneity, it is challenging to disentangle the specific neurophysiology that precipitates compulsive behaving. Using polydipsia (or non-regulatory water drinking), we describe candidate neural substrates of compulsivity. We further postulate that aberrant neuroplasticity within cortically projecting structures [i.e., the bed nucleus of the stria terminalis (BNST)] and circuits that encode homeostatic emotions (thirst, hunger, satiety, etc.) underlie compulsive drinking. By transducing an inaccurate signal that fails to represent true homeostatic state, cortical structures cannot select appropriate and adaptive actions. Additionally, augmented dopamine (DA) reactivity in striatal projections to and from the frontal cortex contribute to aberrant homeostatic signal propagation that ultimately biases cortex-dependent behavioral selection. Responding becomes rigid and corresponds with both erroneous, inflexible encoding in both bottom-up structures and in top-down pathways. How aberrant neuroplasticity in circuits that encode homeostatic emotion result in the genesis and maintenance of compulsive behaviors needs further investigation.

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“…Äëÿ åãî îöåíêè â äîêëèíè÷åñêèõ èññëåäîâàíèÿõ èñïîëüçóþò ìåòîäèêó "ïîëèäèïñèÿ, îáóñëîâëåííàÿ ðåaeèìîì ïèùåâîãî ïîäêðåïëåíèÿ", êîòîðàÿ îáëàäàåò âíåøíåé, êîíñòðóêòíîé è ïðåäèêòèâíîé âàëèäíîñòüþ [32]. Â ýêñïåðèìåíòàõ íà êðûñàõ ïîêàçàíî, ÷òî ââåäåíèå Ro5263397 äîçîçàâèñèìî ñíèaeàëî êîìïóëüñèâíîå ïèòü¸, âûçâàííîå ðåaeèìàìè ïèùåâîãî ïîäêðåïëåíèÿ "ôèêñèðîâàííîå âðåìÿ 1 ìèíóòà" è "ôèêñèðîâàííûé èíòåðâàë 1 ìèíóòà" â äîçàõ, êîòîðûå íå îêàçûâàëè âëèÿíèå íà äâèãàòåëüíóþ àêòèâíîñòü aeèâîòíûõ è ïèòüåâîå ïîâåäåíèå [55]. Êðîìå òîãî, äîêàçàíî, ÷òî ïîâòîðíîå ââåäåíèå Ro5263397 íå ñíèaeàëî îáíàðóaeåííîå ïðîòèâîêîìïóëüñèâíîå äåéñòâèå ïðåïàðàòà [55], òî åñòü ê ïðåïàðàòó íå ðàçâèâàëàñü òîëåðàíòíîñòü, ôàêòîð êîòîðûé ñíèaeàåò òåðàïåâòè÷åñêóþ öåííîñòü ìíîãèõ ïñèõîòðîïíûõ ïðåïàðàòîâ [5].…”

Section: Taar1 è îêðunclassified

Рецепторы, Ассоциированные Со Следовыми Аминами, 1-Го Подтипа Как Новая Терапевтическая Мишень В Нейропсихофармакологии

Sukhanov¹,

Звартау²,

Gainetdinov³

2019

Эксп. и клин. фармакол.

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Психоневрологические расстройства — одна из главных проблем современного здравоохранения. Данные клинических исследований свидетельствуют о том, что в группе риска возникновения психических расстройств находится каждый третий человек в мире. Поэтому поиск новых потенциальных мишеней для лекарственных средств — актуальная и важная задача современной экспериментальной психофармакологии. Одной из таких мишеней могут быть описанные в начале XXI века рецепторы, ассоциированные со следовыми аминами, 1-го подтипа (Trace Amine Associated Receptors 1, TAAR1). TAAR1 принадлежат к большому семейству рецепторов, сопряжённых с G-белком. Результаты недавних исследований доказали, что этот подтип рецепторов способен регулировать активность дофаминергической системы. В настоящем обзоре подробно рассмотрены эффекты TAAR1 лигандов в различных доклинических моделях психоневрологических расстройств.

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Activation of trace amine-associated receptor 1 attenuates schedule-induced polydipsia in rats

Cited by 13 publications

References 35 publications

Activation of trace amine‐associated receptor 1 attenuates nicotine withdrawal‐related effects

Activation of trace amine‐associated receptor 1 attenuates nicotine withdrawal‐related effects

The Bed Nucleus of the Stria Terminalis, Homeostatic Satiety, and Compulsions: What Can We Learn From Polydipsia?

Рецепторы, Ассоциированные Со Следовыми Аминами, 1-Го Подтипа Как Новая Терапевтическая Мишень В Нейропсихофармакологии

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