Somatostatin interneurons are novel mediators of serotonergic modulation in entorhinal cortex via activation of 5-HT2A receptors, a receptor involved in the etiology of different psychiatric disorders.
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.
Gamma rhythms and representation of visual information in the primary visual cortex are specifically modulated by somatostatin+ but not parvalbumin+ neurons in reticular thalamic nucleus.
Cellular and chemogenetic approaches identify a novel mode of chemotransduction involving regulation of basal breathing by CO2/H+-dependent disinhibition.
The discovery of somatostatin-positive inhibitory neurons projecting from mouse cortex to striatum shows that corticostriatal pathways are not exclusively excitatory.
