Phasic activation of dorsal raphe serotonin neurons transiently inhibits locomotion without influencing anxiety or producing reinforcement, but when repeated over many days a long-term facilitation of locomotion is produced.
A high axonal chloride concentration explains why activation of light-gated chloride channels causes neurotransmitter release, and a novel hybrid somatodendritic targeting motif ameliorates this phenomenon and improves their inhibitory function.
Sensory deprivation suppresses cortical responsiveness through a selective remodeling of excitatory and inhibitory microcircuit motifs, by simultaneously amplifying feedforward and suppressing feedback excitation.
Activation of the subthalamic nucleus (STN) pauses or disrupts behavior, while STN inhibition reduces the disruptive effects of surprise, indicating that STN activation is both sufficient and necessary for behavioral inhibition.
Electrophysiology measurements characterized eight optogenetic methods, including a new reporter mouse expressing soma-localized light-activated chloride channels, for inactivating small regions of mouse neocortex.