The cyclic neuropeptide somatostatin binds to human Aβ1-42 through an interface that critically relies on a specific tryptophan, thereby blocking the propensity of Aβ to aggregate, a critical step in the pathobiology of Alzheimer's disease.
The midbrain area for salience, reward and aversion in mouse brain harbours among the dopamine cells three subtypes somatostatin-expressing neurons that show combinatorial neurotransmitter phenotypes and interneuron properties.
Somatostatin-expressing interneurons of the rodent dentate gyrus fall into at least two functionally distinct interneuron types with different synaptic integrations into the local dentate gyrus and the more distant medial septum neuronal network.
Presynaptic GABAB receptors are highly expressed and strongly suppress synaptic transmission at the input and output of hippocampal somatostatin interneurons.
Subtypes of dendrite-targeting somatostatin cells segregate into separate networks by specifically connecting with neurons in different layers, forming circuits that could independently control different input pathways to the neocortex.
The discovery of somatostatin-positive inhibitory neurons projecting from mouse cortex to striatum shows that corticostriatal pathways are not exclusively excitatory.
Our work demonstrated that eye opening differentially modulates inhibitory synaptic transmission from Sst-INs and FS-INs to excitatory neurons in the mammalian cortex.
Two distinct types of inhibitory neurons increase the brain's sensitivity to unexpected acoustic signals by amplifying selective suppression of cortical responses to frequent, but not rare sounds.
A neural circuit between layer 2/3 pyramidal cells and somatostatin-expressing inhibitory neurons synchronizes spatially separated regions of the visual cortex to gamma rhythms.
