An evolutionarily conserved mechanism involving translational control by p-eIF2α underlies vulnerability to nicotine addiction.

Neuronal activity triggers the dispersal of the Golgi into dendritic Golgi satellites, leading to reshaping of the neuronal surface glycoproteome through processing of glycans to mature, sialic acid-containing forms.

Vulnerability to cocaine addiction during adolescence depends on translational control.

Local elimination of acetylcholine synthesis in habenular neurons demonstrates a key role for vesicular synergy and neurotransmitter co-release in nicotine dependence.

Acetylcholine, released from cholinergic fibers originating from the medial septum, shapes social memory, and controls the CA2 hippocampal circuit via nicotinic receptors localized on GABAergic interneurons.

Glutamatergic projection neurons downstream of cholinergic cells in the basal forebrain potently affect feeding behavior by modulating downstream reward and aversion circuits.

Non-invasive transcutaneous electrical stimulation of the greater occipital nerve using direct current promotes strengthening of memories using late-phase synaptic activity.

Δ⁹-Tetrahydrocannabinol impairs motor coordination in mice by inhibiting autophagy in the striatonigral pathway, thus defining a new conceptual view of how cannabis acts in the brain.