By facilitating glutamate and BDNF release, presynaptic NMDA receptors may control information transfer from the dentate gyrus to the CA3 area of the hippocampus.

In cerebellar interneurons, somatodendritic subthreshold synaptic activity travels down the axon and augments AP-dependent GABA release by a modulation of the intermediate states of voltage-dependent Ca⁺⁺ channels in the presynaptic boutons.

The canonical hippocampal NMDA memory receptor also controls the release of the transmitter glutamate and the growth factor BDNF.

Haloperidol comparably affects learning from social and non-social sources when they are the primary source of information but does not affect learning from (social or non-social) secondary sources, providing evidence in support of domain-general neurochemical mechanisms underpinning social learning.

An anion-selective ligand gated channel acts as a presynaptic auto-receptor to modulate vesicle release and neuronal excitation.

LRRK2 G2019S knock-in mice are a genetically faithful model that recapitulates the slow disease progression of familial PD, with initial alterations to behaviour and neurotransmission providing early pathophysiological targets for neuroprotective interventions.

Presynaptic GABAB receptors are highly expressed and strongly suppress synaptic transmission at the input and output of hippocampal somatostatin interneurons.

In addition to modulating firing rates, the neurotransmitter dopamine exerts a strong influence on the overall number of neurons in striatum that are recruited during behavior.

Midbrain dopamine neurons use sophisticated secretory machinery to establish specialized sites for action potential-evoked release of dopamine from their cell bodies and dendrites.