Neuron (Cambridge, Mass.), 2012-03, Vol.73 (6), p.1173-1183
2012
Details
- Autor(en) / Beteiligte
- Titel
- GABA Neurons of the VTA Drive Conditioned Place Aversion
- Ist Teil von
- Neuron (Cambridge, Mass.), 2012-03, Vol.73 (6), p.1173-1183
- Ort / Verlag
- United States: Elsevier Inc
- Erscheinungsjahr
- 2012
- Link zum Volltext
- Quelle
- ScienceDirect Journals (5 years ago - present)
- Beschreibungen/Notizen
- 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 GABAA 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. ► In the VTA, optogenetic activation of GABA neurons in vivo inhibits DA neurons ► A footshock excites GABA neurons and inhibits of a large majority of DA neurons ► The inhibition of DA neurons by a footshock is GABAA receptor dependent ► Activation of GABA neurons is sufficient to elicit conditioned place aversion Tan et al. show that footshock induces GABA neuron excitation, leading to GABAA receptor-mediated inhibition of DA neurons. Optogenetic manipulation shows that VTA GABA neurons activation or direct inhibition of DA neurons is sufficient to drive behavioral aversion.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0896-6273eISSN: 1097-4199DOI: 10.1016/j.neuron.2012.02.015Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6690362
- Format
- –
- Schlagworte
- Action Potentials - drug effects, Action Potentials - genetics, Addictive behaviors, Analgesics, Opioid - pharmacology, Analysis of Variance, Animals, Apomorphine - pharmacology, Aversion, Bacterial Proteins - genetics, Bacterial Proteins - metabolism, Behavior, Channelrhodopsins, Charitable foundations, Conditioning, Operant - drug effects, Conditioning, Operant - physiology, Data processing, Dopamine, Dopamine Agonists - pharmacology, Dopamine Antagonists - pharmacology, Dopaminergic Neurons - drug effects, Dopaminergic Neurons - physiology, Electroshock - adverse effects, Escape Reaction - drug effects, Escape Reaction - physiology, Experiments, Footshock, G Protein-Coupled Inwardly-Rectifying Potassium Channels - deficiency, G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics, GABAergic Neurons - drug effects, GABAergic Neurons - physiology, gamma -Aminobutyric acid A receptors, Genetics, Glutamate Decarboxylase - genetics, Haloperidol - pharmacology, In Vitro Techniques, Information processing, Lasers, Light, Luminescent Proteins - genetics, Luminescent Proteins - metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Morphine - pharmacology, Neurons, Neurotransmission, Optics, Optics and Photonics, Rodents, Time Factors, Tyrosine 3-Monooxygenase - genetics, Tyrosine 3-Monooxygenase - metabolism, Ventral Tegmental Area - cytology, Ventral Tegmental Area - drug effects, Ventral tegmentum