Reconciling Homeostatic and Use-Dependent Plasticity in the Context of Somatosensory Deprivation

Abstract

The concept of homeostatic plasticity postulates that neurons maintain relatively stable rates of firing despite changing inputs. Homeostatic and use-dependent plasticity mechanisms operate concurrently, although they have different requirements for induction. Depriving central somatosensory neurons of their primary activating inputs reduces activity and results in compensatory changes that favor excitation. Both a reduction of GABAergic inhibition and increase in glutamatergic excitatory transmission are observed in input-deprived cortex. Topographic reorganization of the adult somatosensory cortex is likely driven by both homeostatic and use-dependent mechanisms. Plasticity is induced by changes in the strengths of synaptic inputs, as well as changes in temporal correlation of neuronal activity. However, there is less certainty regarding the in vivo contribution of homeostatic mechanisms as in vitro experiments rely on manipulations that create states that do not normally occur in the living nervous system. Homeostatic plasticity seems to occur, but more in vivo research is needed to determine mechanisms. In vitro research is also needed but should better conform to conditions that might occur naturally in vivo.

Early movement restriction leads to maladaptive plasticity in the sensorimotor cortex and to movement disorders

“…In addition, neurotransmission appeared correlated primarily with somatosensory map features and secondarily with musculoskeletal pathologies, but not with motor map features or locomotion. Taken together, our results emphasize the key role of the functional degradation of the somatosensory hind limb representation, which appears to mainly depend on abnormal patterns (quality) of somatosensory inputs resulting from both postnatal SMR and enduring degraded reafference resulting from disturbed locomotion rather than decreased levels (quantity) of inputs, which likely seems involved in the excitation/inhibition imbalance 47 , 48 . These results proceed from dynamic selection, competition and collaboration of primary neuronal groups on the basis of afferent inputs resulting from behaviors and experience that induce changes in the strength of synaptic connections, thus governing the topographic organization of cortical maps and the corresponding tuning of neurons, and leading to diverse repertoires of movements 49 – 51 .…”

Early movement restriction leads to enduring disorders in muscle and locomotion

“…In addition, neurotransmission appeared correlated primarily with somatosensory map features and secondarily with musculoskeletal pathologies, but not with motor map features or locomotion. Taken together, our results emphasize the key role of the functional degradation of the somatosensory hind limb representation, which appears to mainly depend on abnormal patterns (quality) of somatosensory inputs resulting from both postnatal SMR and enduring degraded reafference resulting from disturbed locomotion rather than decreased levels (quantity) of inputs, which likely seems involved in the excitation/inhibition imbalance 47,48 . These results proceed from dynamic selection, competition and collaboration of primary neuronal groups on the basis of afferent inputs resulting from behaviors and experience that induce changes in the strength of synaptic connections, thus governing the topographic organization of cortical maps and the corresponding tuning of neurons, and leading to diverse repertoires of movements [49][50][51] .…”

Electrophysiological responses to sugars and amino acids in the nucleus of the solitary tract of type 1 taste receptor double-knockout mice

“…The knockout models we studied present an opportunity to assess the possibility of plasticity in the first-order gustatory relay resulting from long-term reduced afferent activity. Most sensory systems exhibit changes in central organization when deprived of such activity, especially when deprivation takes place during early life (Hubel and Wiesel 1962;Orczyk and Garraghty 2015). In the gustatory system, such alterations have been studied after dietary Na ϩ deprivation and following genetic deletion of functional ENaC channels in taste buds.…”