ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2024
Basal forebrain-lateral habenula inputs and control of impulsive behavior.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Genetic and pharmacological evidence linking CB1R signaling to hippocampal GABAergic dysfunction in ASD mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Increased encoding of aversive stimuli by lateral habenula neurons during ΔNature communications · 2026Article
- Neuroanatomical and behavioral characterization of corticotropin-releasing factor-expressing lateral Habenula neurons in mice.Communications biology · 2026Article
- Neuroanatomical and behavioral characterization of corticotropin releasing factor-expressing lateral Habenula neurons in mice.bioRxiv : the preprint server for biology · 2026Article
- Phenome-wide analysis of genetically imputed neuroimaging phenotypes reveals associations with psychiatric traits in a multi-ancestry cohort.medRxiv : the preprint server for health sciences · 2025Article
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8 authors.
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Abstract
Deficits in impulse control are observed in several neurocognitive disorders, including attention deficit hyperactivity (ADHD), substance use disorders (SUDs), and those following traumatic brain injury (TBI). Understanding brain circuits and mechanisms contributing to impulsive behavior may aid in identifying therapeutic interventions. We previously reported that intact lateral habenula (LHb) function is necessary to limit impulsivity defined by impaired response inhibition in rats. Here, we examine the involvement of a synaptic input to the LHb on response inhibition using cellular, circuit, and behavioral approaches. Retrograde fluorogold tracing identified basal forebrain (BF) inputs to LHb, primarily arising from ventral pallidum and nucleus accumbens shell (VP/NAcs). Glutamic acid decarboxylase and cannabinoid CB1 receptor (CB1R) mRNAs colocalized with fluorogold, suggesting a cannabinoid modulated GABAergic pathway. Optogenetic activation of these axons strongly inhibited LHb neuron action potentials and GABA release was tonically suppressed by an endogenous cannabinoid in vitro. Behavioral experiments showed that response inhibition during signaled reward omission was impaired when VP/NAcs inputs to LHb were optogenetically stimulated, whereas inhibition of this pathway did not alter LHb control of impulsivity. Systemic injection with the psychotropic phytocannabinoid, Δ
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