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

A critical regulator of inhibitory neurotransmitter signaling in the hippocampus has been identified in experiments on mice and been shown to play essential role in synaptic plasticity and memory.

Functional analysis reveals a distinct mode of action of the allosteric modulators in the GABA_B receptor in a pocket that is formed only in the active state and identifies a region in the GABA_B2 subunit important for allosteric agonism.

Soluble amyloid-β precursor peptide has no functional effects at recombinant and native GABA_B receptors.

Summation of metabotropic GABAergic responses remain linear even if most superficial layer interneurons specialized to recruit GABA_B receptors are simultaneously active.

Astrocytes decode temporal interneuron activity and transform inhibitory into excitatory signals that impact excitatory synaptic strength and neuronal circuit function.

A circuit within the nucleus accumbens that exists during a specific developmental window through early adolescence male rats may serve as a substrate that underlies heightened reward seeking in this population.

Rats exposed to a single stressful event experience days-long constitutive activation of the kappa opioid receptor at inhibitory synapses in part of the brain’s reward system, which increases their drug-seeking behavior.

Experiments examining the actions of morphine on single neurons from one of the brain's reward centers, the VTA, reveal the mechanism by which the drug exerts its hedonic effects.

Noradrenergic receptors can control the spontaneous electrical firing of neurons by inhibiting a Na⁺ channel known as NALCN using a pathway shared by metabotropic GABA receptors.