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Cohen-Kashi Malina, K.

Publications and source records attributed to Cohen-Kashi Malina, K..

2 recordsLinked to original sources

Thalamo-insular basis for updating physiological needs

Physiological needs, such as thirst and hunger, produce powerful motivation for behaviors that are essential for survival. Yet, how the brain estimates these needs remains unknown. It is unclear whether the brain continuously monitors bodily signals to create real-time representations, or if existing internal representations are only updated when meaningful changes occur. To address this question, we manipulated thalamic internal sensory inputs to the interoceptive insular cortex. We found that inhibiting internal sensory inputs prevents the updating of insular cortex representations of thirst and hunger, thereby keeping its activity closer to its initial physiological need state. Consequently, cued feeding and drinking, as well as free consumption of food and water, persist beyond the current physiological need. We further show that insular cortex activity normally represents both predictions and sensory information. However, violating learned expectations evokes widespread need-specific prediction error signals. Our results thus reveal a thalamo-cortical basis for updating physiological needs in the brain.

neuroscience↗

High-efficiency optogenetic silencing with soma-targeted anion-conducting channelrhodopsins

Optogenetic silencing allows time-resolved functional interrogation of defined neuronal populations. However, the limitations of inhibitory optogenetic tools impose stringent constraints on experimental paradigms. The high light power requirement of light-driven ion pumps and their effects on intracellular ion homeostasis pose unique challenges, particularly in experiments that demand inhibition of a widespread neuronal population in vivo. Guillardia theta anion-conducting channelrhodopsins (GtACRs) are promising in this regard, due to their high single-channel conductance and favorable photon-ion stoichiometry. However, GtACRs show poor membrane targeting in mammalian cells, and the activity of such channels can cause transient excitation in the axon due to an excitatory chloride reversal potential in this compartment. Here we address both problems by enhancing membrane targeting and subcellular compartmentalization of GtACRs. The resulting GtACR-based optogenetic tools show improved photocurrents, greatly reduced axonal excitation, high light sensitivity and rapid kinetics, allowing highly efficient inhibition of neuronal activity in the mammalian brain.

neuroscience↗