| First Author | Busquets-Garcia A | Year | 2018 |
| Journal | Neuron | Volume | 99 |
| Issue | 6 | Pages | 1247-1259.e7 |
| PubMed ID | 30174119 | Mgi Jnum | J:274604 |
| Mgi Id | MGI:6269323 | Doi | 10.1016/j.neuron.2018.08.014 |
| Citation | Busquets-Garcia A, et al. (2018) Hippocampal CB1 Receptors Control Incidental Associations. Neuron 99(6):1247-1259.e7 |
| abstractText | By priming brain circuits, associations between low-salience stimuli often guide future behavioral choices through a process known as mediated or inferred learning. However, the precise neurobiological mechanisms of these incidental associations are largely unknown. Using sensory preconditioning procedures, we show that type 1 cannabinoid receptors (CB1R) in hippocampal GABAergic neurons are necessary and sufficient for mediated but not direct learning. Deletion and re-expression of CB1R in hippocampal GABAergic neurons abolishes and rescues mediated learning, respectively. Interestingly, paired presentations of low-salience sensory cues induce a specific protein synthesis-dependent enhancement of hippocampal CB1R expression and facilitate long-term synaptic plasticity at inhibitory synapses. CB1R blockade or chemogenetic manipulations of hippocampal GABAergic neurons upon preconditioning affect incidental associations, as revealed by impaired mediated learning. Thus, CB1R-dependent control of inhibitory hippocampal neurotransmission mediates incidental associations, allowing future associative inference, a fundamental process for everyday life, which is altered in major neuropsychiatric diseases. VIDEO ABSTRACT. |
