Abstract
The habenula is a complex nucleus composed of lateral and medial subnuclei, which connect between the limbic forebrain and midbrain. Over the past few years, the lateral habenula has received considerable attention because of its potential roles in cognition and in the pathogenesis of various psychiatric disorders. Unlike extensively studied lateral habenula, anatomically and histologically distinct medial habenula remains largely understudied. The medial habenula can be further subdivided into a dorsal region containing excitatory neurons that express the tachykinin neuropeptide substance P and a ventral region containing dense cholinergic neurons. Although the medial habenula is the source of one of the major cholinergic pathways in the brain, relatively few studies have been conducted to understand its roles. Recently, however, the medial habenula cholinergic system has attracted more attention because of its potential to provide therapeutic targets for the treatment of nicotine withdrawal symptoms, drug addiction, and various mood disorders. Here, we discuss the role of the medial habenula cholinergic system in brain function.
Highlights
The habenula is part of the epithalamus and is divided into medial and lateral subregions, each with a unique gene-expression profile [1]
Over the last few years, studies have shown that neuronal activity in the lateral habenula (LHb) is regulated by factors in the external environment, such as rewards or aversive stimuli, and this altered LHb neuronal activity is associated with the onset of depression [2,3,4]
The lower hedonic state induced by chronic unpredictable mild stress (CUMS) was restored there is no change in the nicotine-induced firing rate in habenula cholinergic neurons in mice chronically treated with nicotine, re-exposure to nicotine during withdrawal increases the rate of spontaneous firing
Summary
The habenula is part of the epithalamus and is divided into medial and lateral subregions, each with a unique gene-expression profile [1]. Optogenetic stimulation of GAD2-expressing GABAergic neurons in the IPN induces physical withdrawal symptoms in both nicotine-naïve and chronic nicotine-exposed mice, and the affective symptoms are ameliorated by IPN-selective infusion of a NMDA receptor antagonist [10].
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