1. Bidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo
- Author
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MacKenzie A. Howard, John L.R. Rubenstein, and Scott C. Baraban
- Subjects
Male ,Interneuron ,Ganglionic eminence ,Cell Transplantation ,Green Fluorescent Proteins ,Long-Term Potentiation ,Nonsynaptic plasticity ,Biology ,Hippocampus ,Synaptic Transmission ,Mice ,Neural Stem Cells ,Interneurons ,Oscillometry ,Homeostatic plasticity ,medicine ,Animals ,Homeostasis ,Gene Silencing ,GABAergic Neurons ,gamma-Aminobutyric Acid ,Homeodomain Proteins ,Neurons ,Transplantation ,Neuronal Plasticity ,Multidisciplinary ,Synaptic scaling ,Cell Death ,musculoskeletal, neural, and ocular physiology ,Neurosciences ,Excitatory Postsynaptic Potentials ,Long-term potentiation ,Biological Sciences ,Immunohistochemistry ,Electrophysiology ,medicine.anatomical_structure ,nervous system ,gamma frequency oscillations ,Neurological ,Synapses ,neural transplantation ,Excitatory postsynaptic potential ,GABAergic ,excitatory/inhibitory balance ,LTP ,Neuroscience ,Transcription Factors - Abstract
Significance We describe homeostatic plasticity of both excitatory synaptic transmission and intrinsic properties of CA1 pyramidal neurons in distal-less homeobox 1 ( Dlx1 −/− ) mice, a genetic model of postdevelopment interneuron cell death. Loss of synaptic inhibition and compensation by excitation led to enhanced potential for long-term potentiation (LTP) and altered neural oscillations. This shows that homeostatic compensation may rebalance inhibition and excitation but cannot fully normalize neural function. Transplantation of interneuron progenitor cells restored inhibitory synaptic transmission to WT levels and induced a reversal of homeostatic changes to excitation and excitability. LTP and gamma oscillations were also normalized after integration of transplanted interneurons. These data indicate that homeostatic plasticity functions in vivo to balance activity based on inhibitory tone.
- Published
- 2013
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