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• W1524953668 abstract "Fear conditioning, one of the most powerful and widely used methods to investigate themechanisms of associative learning in animals, involves the pairing of an aversivestimulus such as a foot-shock (the unconditioned stimulus; US) with a neutral stimulussuch as a tone (the conditioned stimulus; CS). The tone acquires aversive properties and,on subsequent exposure, will elicit a fear response. Behavioral and in vivoelectrophysiological experiments indicate that NMDA receptor-mediated long-termpotentiation (LTP) in the lateral amygdala (LA), a key structure for emotional learning,underlies the acquisition of Pavlovian fear conditioning.Neuronal activity in the LA is tightly controlled by local inhibitory interneurons.Interneurons exert their inhibitory effect by releasing the neurotransmitter GABA actingon ionotropic GABAA and metabotropic GABAB receptors. There is accumulatingevidence suggesting a role for GABAA and GABAB receptors in regulating amygdaladependentfear and anxiety behavior. However, whereas the role of GABAA receptors forpostsynaptic integration and gating of LTP induction is well documented, nothing isknown about the role of GABAB receptors in the LA.GABABRs are G-protein-coupled receptors that are localized both pre- andpostsynaptically. Postsynaptic GABABRs are coupled to inwardly rectifying K+ channels.Presynaptic GABABRs inhibit neurotransmitter release by decreasing Ca2+ influx at bothGABAergic terminals and glutamatergic terminals. Functional GABAB receptors aregenerally thought to be heterodimers containing GABAB(1) and GABAB(2) subunits. TheGABAB(1) subunit exists in two differentially expressed isoforms, GABAB(1a) andGABAB(1b), differing by the presence of two N-terminal “sushi” domains in theGABAB(1a) isoform.In the main study of the present thesis, using a combined electrophysiological and geneticapproach in mice, I found that presynaptic GABAB heteroreceptors on glutamatergiccortical afferents are predominantly comprised of GABAB(1a) subunits, and criticallydetermine associative properties of presynaptic cortical LTP. In the absence of functionalpresynaptic GABAB heteroreceptors, an NMDA receptor-independent, non-associativeform of presynaptic LTP is unmasked. Strikingly, the loss of associativity of corticoamygdalaLTP is accompanied by a generalization of conditioned fear at the behaviorallevel. This indicates that the specificity of information processing in the LA can be set byactivity-dependent presynaptic inhibition mediated by specific GABAB receptors.In contrast to synaptic plasticity at cortico-amygdala afferents, I found that at thalamicafferents, GABAB receptors facilitate LTP induction by a postsynaptic mechanism.Moreover, this effect could be attributed to GABAB(1b) containing receptors. Thus, in theLA specific subtypes of pre- and postsynaptic GABAB receptors control induction pre- orpostsynaptic LTP in an afferent-specific manner.Taken together, the present findings indicate that GABAB receptors are playing a key rolein controlling associative plasticity in the LA, and suggest that GABAB receptors couldbe a pharmacological target for treatment of psychiatric conditions like anxiety and posttraumatic stress disorder." @default.
• W1524953668 created "2016-06-24" @default.
• W1524953668 creator A5005887968 @default.
• W1524953668 date "2005-01-01" @default.
• W1524953668 modified "2023-09-24" @default.
• W1524953668 title "GABA(B) receptor-mediated modulation of synaptic plasticity in the lateral amygdala" @default.
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