Abstract
Since its discovery over four decades ago, somatostatin (SOM) receives growing scientific and clinical interest. Being localized in the nervous system in a subset of interneurons somatostatin acts as a neurotransmitter or neuromodulator and its role in the fine-tuning of neuronal activity and involvement in synaptic plasticity and memory formation are widely recognized in the recent literature. Combining transgenic animals with electrophysiological, anatomical and molecular methods allowed to characterize several subpopulations of somatostatin-containing interneurons possessing specific anatomical and physiological features engaged in controlling the output of cortical excitatory neurons. Special characteristic and connectivity of somatostatin-containing neurons set them up as significant players in shaping activity and plasticity of the nervous system. However, somatostatin is not just a marker of particular interneuronal subpopulation. Somatostatin itself acts pre- and postsynaptically, modulating excitability and neuronal responses. In the present review, we combine the knowledge regarding somatostatin and somatostatin-containing interneurons, trying to incorporate it into the current view concerning the role of the somatostatinergic system in cortical plasticity.
Highlights
Over forty years ago, scientists discovered a small 14 amino-acid-long peptide that was able to inhibit the release of growth hormone from the hypothalamus
Using [14C]-2-deoxyglucose autoradiography, we found that classical conditioning, in which the stimulation of a row of vibrissae (CS) was paired with a tail shock (UCS), resulted in an increase in the area of the barrel cortex activated by the vibrissae stimulated during conditioning (Siucinska and Kossut, 1996)
We showed that the GAD upregulation was specific to mice that were conditioned and not seen in the group that received only conditioned stimulus (CS), only UCS, or pseudoconditoning, so the crucial factor is the simultaneous action of CS and UCS (Siucinska and Kossut, 2006)
Summary
Over forty years ago, scientists discovered a small 14 amino-acid-long peptide that was able to inhibit the release of growth hormone from the hypothalamus. The function of SOM is to inhibit the release of several biologically active substances, like: growth hormone, insulin, glucagon, gastrin, secretin, cholecystokinin The localization and distribution of SOM receptors in the CNS and periphery depend on tissue and species They are widely distributed in many tissues, with distinct but overlapping expression pattern, often as multiple subtypes coexisting in the same cell (Kossut et al, 1989). Some biological responses display a selectivity for particular receptor subtype: growth hormone secretion regulation (SSTR2 and 5), insulin secretion (SSTR5), glucagon secretion (SSTR2), and immune responses (SSTR2; Patel, 1999; Table 1). Acetylcholine can regulate the activity of SOM neurons indirectly, through basal forebrain cholinergic activation of VIP-containing interneurons, which contact and inhibit SOM interneurons (Letzkus et al, 2011; Jackson et al, 2016)
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