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The Impact of Perineuronal Net Digestion Using Chondroitinase ABC on the Intrinsic Physiology of Cortical Neurons.

TitleThe Impact of Perineuronal Net Digestion Using Chondroitinase ABC on the Intrinsic Physiology of Cortical Neurons.
Publication TypeJournal Article
Year of Publication2018
AuthorsChu P, Abraham R, Budhu K, Khan U, Garcia NDe Marco, Brumberg JC
Date Published2018 09 15
KeywordsAnimals, Chondroitin ABC Lyase, Extracellular Matrix, Female, Male, Membrane Potentials, Mice, Neurons, Somatosensory Cortex, Synaptic Transmission, Tissue Culture Techniques

Perineuronal nets (PNNs) are a form of aggregate Extracellular Matrix (ECM) in the brain. Recent evidence suggests that the postnatal deposition of PNNs may play an active role in regulating neuroplasticity and, potentially, neurological disorders. Observations of high levels of PNN expression around somas, proximal dendrites, and axon initial segments of a subtype of neurons have also led to proposals that PNNs may modulate the intrinsic properties of the neurons they ensheathe. While high levels of PNNs are postnatally expressed throughout the neocortex, it is still unclear how they impact the neuronal physiology of the many classes and subtypes of neurons that exist. In this study, we demonstrate that Chondroitinase ABC digestion of PNNs from acute cortical slices from juvenile mice (P28-35) resulted in neuron-specific impacts on intrinsic physiology. Fast spiking (FS) interneurons showed decreased input resistance, resting membrane potential (RMP), reduced action potential (AP) peaks and altered spontaneous synaptic inputs. Low-Threshold Spiking interneurons showed altered rebound depolarizations and decreased frequency of spontaneous synaptic inputs. Putative excitatory neurons; regular spiking, bursting, and doublet phenotypes did not demonstrate any alterations. Our data indicate that chABC-sensitive PNNs may specifically regulate the intrinsic and synaptic physiology of inhibitory interneurons.

Alternate JournalNeuroscience
PubMed ID30004010
PubMed Central IDPMC6338339
Grant ListR01 MH110553 / MH / NIMH NIH HHS / United States
SC3 GM122657 / GM / NIGMS NIH HHS / United States