Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats

Abstract Excessive alcohol consumption is a known risk factor for stroke, but the effect of stroke on alcohol intake is unknown. The dorsomedial striatum (DMS) and midbrain areas of the nigrostriatal circuit are critically associated to stroke and alcohol addiction. Here we sought to explore the inf...

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Autores principales:	Cathy C. Y. Huang, Tengfei Ma, Emily A. Roltsch Hellard, Xuehua Wang, Amutha Selvamani, Jiayi Lu, Farida Sohrabji, Jun Wang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/be8a2e2935c647aeacf438e8fd4610b1
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spelling	oai:doaj.org-article:be8a2e2935c647aeacf438e8fd4610b12021-12-02T12:30:37ZStroke triggers nigrostriatal plasticity and increases alcohol consumption in rats10.1038/s41598-017-02714-z2045-2322https://doaj.org/article/be8a2e2935c647aeacf438e8fd4610b12017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02714-zhttps://doaj.org/toc/2045-2322Abstract Excessive alcohol consumption is a known risk factor for stroke, but the effect of stroke on alcohol intake is unknown. The dorsomedial striatum (DMS) and midbrain areas of the nigrostriatal circuit are critically associated to stroke and alcohol addiction. Here we sought to explore the influence of stroke on alcohol consumption and to uncover the underlying nigrostriatal mechanism. Rats were trained to consume alcohol using a two-bottle choice or operant self-administration procedure. Retrograde beads were infused into the DMS or midbrain to label specific neuronal types, and ischemic stroke was induced in the dorsolateral striatum (DLS). Slice electrophysiology was employed to measure excitability and synaptic transmission in DMS and midbrain neurons. We found that ischemic stroke-induced DLS infarction produced significant increases in alcohol preference, operant self-administration, and relapse. These increases were accompanied by enhanced excitability of DMS and midbrain neurons. In addition, glutamatergic inputs onto DMS D1-neurons was potentiated, whereas GABAergic inputs onto DMS-projecting midbrain dopaminergic neurons was suppressed. Importantly, systemic inhibition of dopamine D1 receptors attenuated the stroke-induced increase in operant alcohol self-administration. Our results suggest that the stroke-induced DLS infarction evoked abnormal plasticity in nigrostriatal dopaminergic neurons and DMS D1-neurons, contributing to increased post-stroke alcohol-seeking and relapse.Cathy C. Y. HuangTengfei MaEmily A. Roltsch HellardXuehua WangAmutha SelvamaniJiayi LuFarida SohrabjiJun WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Cathy C. Y. Huang Tengfei Ma Emily A. Roltsch Hellard Xuehua Wang Amutha Selvamani Jiayi Lu Farida Sohrabji Jun Wang Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
description	Abstract Excessive alcohol consumption is a known risk factor for stroke, but the effect of stroke on alcohol intake is unknown. The dorsomedial striatum (DMS) and midbrain areas of the nigrostriatal circuit are critically associated to stroke and alcohol addiction. Here we sought to explore the influence of stroke on alcohol consumption and to uncover the underlying nigrostriatal mechanism. Rats were trained to consume alcohol using a two-bottle choice or operant self-administration procedure. Retrograde beads were infused into the DMS or midbrain to label specific neuronal types, and ischemic stroke was induced in the dorsolateral striatum (DLS). Slice electrophysiology was employed to measure excitability and synaptic transmission in DMS and midbrain neurons. We found that ischemic stroke-induced DLS infarction produced significant increases in alcohol preference, operant self-administration, and relapse. These increases were accompanied by enhanced excitability of DMS and midbrain neurons. In addition, glutamatergic inputs onto DMS D1-neurons was potentiated, whereas GABAergic inputs onto DMS-projecting midbrain dopaminergic neurons was suppressed. Importantly, systemic inhibition of dopamine D1 receptors attenuated the stroke-induced increase in operant alcohol self-administration. Our results suggest that the stroke-induced DLS infarction evoked abnormal plasticity in nigrostriatal dopaminergic neurons and DMS D1-neurons, contributing to increased post-stroke alcohol-seeking and relapse.
format	article
author	Cathy C. Y. Huang Tengfei Ma Emily A. Roltsch Hellard Xuehua Wang Amutha Selvamani Jiayi Lu Farida Sohrabji Jun Wang
author_facet	Cathy C. Y. Huang Tengfei Ma Emily A. Roltsch Hellard Xuehua Wang Amutha Selvamani Jiayi Lu Farida Sohrabji Jun Wang
author_sort	Cathy C. Y. Huang
title	Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
title_short	Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
title_full	Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
title_fullStr	Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
title_full_unstemmed	Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
title_sort	stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/be8a2e2935c647aeacf438e8fd4610b1
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Stroke triggers nigrostriatal plasticity and increases alcohol consumption in rats

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