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• W2114218568 endingPage "4409" @default.
• W2114218568 startingPage "4387" @default.
• W2114218568 abstract "Throughout life, fear learning is indispensable for survival and neural plasticity in the lateral amygdala underlies this learning and storage of fear memories. During development, properties of fear learning continue to change into adulthood, but currently little is known about changes in amygdala circuits that enable these behavioural transitions. In recordings from neurons in lateral amygdala brain slices from infant up to adult mice, we show that spontaneous and evoked excitatory and inhibitory synaptic transmissions mature into adolescence. At this time, increased inhibitory activity and signalling has the ability to restrict the function of excitation by presynaptic modulation, and may thus enable precise stimulus associations to limit fear generalization from adolescence onward. Our results provide a basis for addressing plasticity mechanisms that underlie altered fear behaviour in young animals.Convergent evidence suggests that plasticity in the lateral amygdala (LA) participates in acquisition and storage of fear memory. Sensory inputs from thalamic and cortical areas activate principal neurons and local GABAergic interneurons, which provide feed-forward inhibition that tightly controls LA activity and plasticity via pre- and postsynaptic GABAA and GABAB receptors. GABAergic control is also critical during fear expression, generalization and extinction in adult animals. During rodent development, properties of fear and extinction learning continue to change into early adulthood. Currently, few studies have assessed physiological changes in amygdala circuits that may enable these behavioural transitions. To obtain first insights, we investigated changes in spontaneous and sensory input-evoked inhibition onto LA principal neurons and then focused on GABAB receptor-mediated modulation of excitatory sensory inputs in infant, juvenile, adolescent and young adult mice. We found that spontaneous and sensory-evoked inhibition increased during development. Physiological changes were accompanied by changes in dendritic morphology. While GABAB heteroreceptors were functionally expressed on sensory afferents already early in development, they could only be physiologically recruited by sensory-evoked GABA release to mediate heterosynaptic inhibition from adolescence onward. Furthermore, we found GABAB -mediated tonic inhibition of sensory inputs by ambient GABA that also emerged in adolescence. The observed increase in GABAergic drive may be a substrate for providing modulatory GABA. Our data suggest that GABAB -mediated tonic and evoked presynaptic inhibition can suppress sensory input-driven excitation in the LA to enable precise stimulus associations and limit generalization of conditioned fear from adolescence onward." @default.
• W2114218568 created "2016-06-24" @default.
• W2114218568 creator A5042039868 @default.
• W2114218568 creator A5075138621 @default.
• W2114218568 date "2015-08-30" @default.
• W2114218568 modified "2023-10-12" @default.
• W2114218568 title "Postnatal maturation of GABAergic modulation of sensory inputs onto lateral amygdala principal neurons" @default.
• W2114218568 cites W1481077857 @default.
• W2114218568 cites W1481379109 @default.
• W2114218568 cites W149922089 @default.
• W2114218568 cites W1501153304 @default.
• W2114218568 cites W1628708546 @default.
• W2114218568 cites W1703928766 @default.
• W2114218568 cites W1869876350 @default.
• W2114218568 cites W1881927119 @default.
• W2114218568 cites W1916138143 @default.
• W2114218568 cites W1959821071 @default.
• W2114218568 cites W1963556856 @default.
• W2114218568 cites W1969258026 @default.
• W2114218568 cites W1970946379 @default.
• W2114218568 cites W1973380388 @default.
• W2114218568 cites W1975084599 @default.
• W2114218568 cites W1980304996 @default.
• W2114218568 cites W1986283937 @default.
• W2114218568 cites W1993532580 @default.
• W2114218568 cites W2003612326 @default.
• W2114218568 cites W2009000833 @default.
• W2114218568 cites W2009666469 @default.
• W2114218568 cites W2014352371 @default.
• W2114218568 cites W2014438459 @default.
• W2114218568 cites W2015148582 @default.
• W2114218568 cites W2016321438 @default.
• W2114218568 cites W2017171790 @default.
• W2114218568 cites W2019196616 @default.
• W2114218568 cites W2020284109 @default.
• W2114218568 cites W2024036805 @default.
• W2114218568 cites W2024654563 @default.
• W2114218568 cites W2028202495 @default.
• W2114218568 cites W2028299419 @default.
• W2114218568 cites W2032352281 @default.
• W2114218568 cites W2033211327 @default.
• W2114218568 cites W2034283645 @default.
• W2114218568 cites W2034643262 @default.
• W2114218568 cites W2039539900 @default.
• W2114218568 cites W2043327214 @default.
• W2114218568 cites W2047175607 @default.
• W2114218568 cites W2050500053 @default.
• W2114218568 cites W2052987076 @default.
• W2114218568 cites W2057771009 @default.
• W2114218568 cites W2058022492 @default.
• W2114218568 cites W2070893697 @default.
• W2114218568 cites W2073083846 @default.
• W2114218568 cites W2075312117 @default.
• W2114218568 cites W2075561611 @default.
• W2114218568 cites W2075578451 @default.
• W2114218568 cites W2075665234 @default.
• W2114218568 cites W2076445235 @default.
• W2114218568 cites W2077512390 @default.
• W2114218568 cites W2081857442 @default.
• W2114218568 cites W2084176631 @default.
• W2114218568 cites W2084236159 @default.
• W2114218568 cites W2086387632 @default.
• W2114218568 cites W2092568693 @default.
• W2114218568 cites W2092602308 @default.
• W2114218568 cites W2094930366 @default.
• W2114218568 cites W2095939155 @default.
• W2114218568 cites W2097119941 @default.
• W2114218568 cites W2102291779 @default.
• W2114218568 cites W2110627545 @default.
• W2114218568 cites W2112927743 @default.
• W2114218568 cites W2114219594 @default.
• W2114218568 cites W2123483502 @default.
• W2114218568 cites W2125252313 @default.
• W2114218568 cites W2125553341 @default.
• W2114218568 cites W2133743587 @default.
• W2114218568 cites W2137852374 @default.
• W2114218568 cites W2138184969 @default.
• W2114218568 cites W2140404484 @default.
• W2114218568 cites W2143252382 @default.
• W2114218568 cites W2144571934 @default.
• W2114218568 cites W2144813464 @default.
• W2114218568 cites W2149776064 @default.
• W2114218568 cites W2150718243 @default.
• W2114218568 cites W2153404961 @default.
• W2114218568 cites W2154768538 @default.
• W2114218568 cites W2158553737 @default.
• W2114218568 cites W2163634461 @default.
• W2114218568 cites W2167514554 @default.
• W2114218568 cites W2340454904 @default.
• W2114218568 cites W2412056671 @default.
• W2114218568 cites W2415829945 @default.
• W2114218568 cites W2419191705 @default.
• W2114218568 cites W4247763225 @default.
• W2114218568 cites W4250700650 @default.
• W2114218568 doi "https://doi.org/10.1113/jp270645" @default.
• W2114218568 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4594245" @default.
• W2114218568 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26227545" @default.
• W2114218568 hasPublicationYear "2015" @default.

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