Somatostatin and Somatostatin-Containing Neurons in Shaping Neuronal Activity and Plasticity

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.

Keywords: GABA; SOM; inhibition; interneurons; plasticity; somatostatin.

Figure 1

During conditioning somatostatin (SOM) interneurons of layer 4 (L4) regulate thalamocortical input gate operated by parvalbumin (PV) interneurons. (A) Before conditioning. During tactile stimulation of vibrissae the input from ventrobasal nucleus of thalamus targets principal cells and PV interneurons. PV interneurons by feedback inhibition control output of principal cells. Principal cells activate SOM interneurons, which inhibit PV interneurons. The input from nucleus basalis to SOM and PV neurons is weak. (B) Cholinergic effects during conditioning. Pairing tactile stimulus with a tail shock stimulate acetylcholine release from nucleus basalis afferents, which inhibits PV—principal cell synapse by M2 receptors, and activates SOM interneurons by nicotinic receptors. Strong activation of SOM interneurons (by principal cell and Ach) results in increased inhibition of PV interneurons and facilitates opening the thalamocortical input gate so that signal from vibrissae stimulated in conditioning achieves stronger excitation of the barrel cortex. Abbreviations: Ach, acetylcholine; CS, conditional stimulus; PC, principal cell; PV, parvalbumin-containing interneuron; PYR, pyramidal neuron; SOM, somatostatin-containing interneuron; UCS, unconditional stimulus.