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Szonyi, A.

Publications and source records attributed to Szonyi, A..

2 recordsLinked to original sources

Neural mechanisms of adaptive value coding in the amygdala

To address their needs, animals must optimize behavior by integrating external cues with internal state signals, such as hunger or thirst, environmental conditions, and past experiences. Accordingly, the perceived value of a reward varies depending on an animals current needs. Updating the specific value of rewards predicted by external cues depends on the basolateral amygdala (BLA). However, neurophysiological investigations have centered around the assumption of stimulus-invariant value representations and have not been able to account for behavioral findings that support the BLAs ability to represent stimulus-specific value of distinct appetitive or aversive outcomes. To address how the BLA encodes and updates stimulus-specific value representations, we exposed head-fixed mice to distinct sets of gustatory rewards while tracking perceived value using lick microstructural analysis. Two-photon calcium imaging of BLA principal neurons revealed that the magnitude of the BLA population response scaled with perceived reward value and that the values of different rewards were encoded by distinct neuronal subpopulations. Moreover, reward representations rapidly re-scaled when mice were exposed to a reward that was larger than all previous rewards. Finally, value representations depended on an animals internal state as thirst selectively increased the responses to water rewards whereas aversive experiences strongly attenuated responses to sucrose. Our findings demonstrate that value representations in the BLA are stimulus-specific and highly adaptive to account for changes in relative reward value and to reflect an animals current affective and homeostatic state. This mechanism enables sensory-specific value updates necessary for state-adapted decision making and learning.

neuroscience↗

Synaptic co-transmission of acetylcholine and GABA regulates hippocampal states

The basal forebrain cholinergic system is widely assumed to control cortical functions via non-synaptic transmission of a single neurotransmitter, acetylcholine. Yet, using immune-electron tomographic, molecular anatomical, optogenetic and physiological techniques, we find that mouse hippocampal cholinergic terminals invariably establish synapses and their vesicles dock at synapses only. We demonstrate that these synapses do not co-release but co-transmit GABA and acetylcholine via different vesicles, whose release is triggered by distinct calcium channels. This co-transmission evokes fast composite postsynaptic potentials, which are mutually cross-regulated by presynaptic auto-receptors and display different short-term plasticity. The GABAergic component alone effectively suppresses hippocampal sharp wave-ripples and epileptiform activity. The synaptic nature of the forebrain cholinergic system with differentially regulated, fast, GABAergic and cholinergic co-transmission suggests a hitherto unrecognized level of synaptic control over cortical states. This novel model of hippocampal cholinergic neurotransmission could form the basis for alternative pharmacotherapies after cholinergic deinnervation seen in neurodegenerative disorders.\n\nSupplementary materials are attached after the main text.

neuroscience↗