title: GABA neurons of the VTA drive conditioned place aversion.
abstract: Salient but aversive stimuli inhibit the majority of dopamine (DA) neurons in the ventral tegmental area (VTA) and cause conditioned place aversion (CPA). The cellular mechanism underlying DA neuron inhibition has not been investigated and the causal link to behavior remains elusive. Here, we show that GABA neurons of the VTA inhibit DA neurons through neurotransmission at GABA(A) receptors. We also observe that GABA neurons increase their firing in response to a footshock and provide evidence that driving GABA neurons with optogenetic effectors is sufficient to affect behavior. Taken together, our data demonstrate that synaptic inhibition of DA neurons drives place aversion.
authors.affiliation: Department of Basic Neurosciences, University of Geneva, 1211 Geneva, Switzerland.
authors.forename: Kelly R
authors.initials: KR
authors.lastname: Tan
authors.forename: Cédric
authors.initials: C
authors.lastname: Yvon
authors.forename: Marc
authors.initials: M
authors.lastname: Turiault
authors.forename: Julie J
authors.initials: JJ
authors.lastname: Mirzabekov
authors.forename: Jana
authors.initials: J
authors.lastname: Doehner
authors.forename: Gwenaël
authors.initials: G
authors.lastname: Labouèbe
authors.forename: Karl
authors.initials: K
authors.lastname: Deisseroth
authors.forename: Kay M
authors.initials: KM
authors.lastname: Tye
authors.forename: Christian
authors.initials: C
authors.lastname: Lüscher
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000235:genetics; D000701:Analgesics, Opioid / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D000075402:Channelrhodopsins; D003216:Conditioning, Operant / Q000187:drug effects / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000502:physiology*; D004597:Electroshock / Q000009:adverse effects; D004924:Escape Reaction / Q000187:drug effects / Q000502:physiology*; D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels / Q000172:deficiency / Q000235:genetics; D059330:GABAergic Neurons / Q000187:drug effects / Q000502:physiology*; D005968:Glutamate Decarboxylase / Q000235:genetics; D006220:Haloperidol / Q000494:pharmacology; D066298:In Vitro Techniques; D008164:Luminescent Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009020:Morphine / Q000494:pharmacology; D055095:Optics and Photonics; D013997:Time Factors; D014446:Tyrosine 3-Monooxygenase / Q000235:genetics / Q000378:metabolism; D017557:Ventral Tegmental Area / Q000166:cytology* / Q000187:drug effects
chemical_list: D000701:Analgesics, Opioid; D001426:Bacterial Proteins; D000075402:Channelrhodopsins; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels; C497069:Kcnj6 protein, mouse; D008164:Luminescent Proteins; C054562:yellow fluorescent protein, Bacteria; D009020:Morphine; D014446:Tyrosine 3-Monooxygenase; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2; D006220:Haloperidol; D001058:Apomorphine