Suppression of enriched environment-induced neurogenesis in a rodent model of neuropathic pain

• Published in: Neuroscience letters Vol. 440; no. 3; pp. 314 - 318
• Main Authors: Terada, Mioko, Kuzumaki, Naoko, Hareyama, Nana, Imai, Satoshi, Niikura, Keiich, Narita, Michiko, Yamazaki, Mitsuaki, Suzuki, Tsutomu, Narita, Minoru
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 08.08.2008; Elsevier
• Subjects: Animals; Basic Helix-Loop-Helix Transcription Factors - metabolism; Behavior, Animal; Biological and medical sciences; Cell Count - methods; Cell Proliferation; Disease Models, Animal; Environment; Environmental enrichment; Fundamental and applied biological sciences. Psychology; Hippocampus; Hippocampus - pathology; Hippocampus - physiopathology; Male; Mice; Mice, Inbred C57BL; Microtubule-Associated Proteins - metabolism; Nerve Tissue Proteins - metabolism; Neurogenesis; Neurons - physiology; Neuropeptides - metabolism; Pain; Pain Measurement - methods; Reaction Time - physiology; Sciatica - pathology; Sciatica - therapy; Time Factors; Vertebrates: nervous system and sense organs; Pain; Neurogenesis; Environmental enrichment; Hippocampus; Vertebrata; Mammalia; Rodentia; Environmental enrichment;Pain;Hippocampus;Neurogenesis; Models; Stimulating environment
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2008.05.078

Exposure to an enriched environment (EE) enhances neurogenesis and regulates emotionality. Previous reports have revealed that the rate of neurogenesis can be influenced by various environmental, endocrine, and pharmacologic stimuli. Chronic pain is a debilitating disease state characterized by complex alterations in both peripheral and central nociceptive pathways. In the present study, we evaluated the effect of chronic pain on environmental enrichment-induced hippocampal neurogenesis. Nerve-ligated mice were housed either in a standard environment or in the EE for 4 weeks. EE increased the immunoreactivity for doublecortin (DCX), a marker for immature neuron-positive cells, in the dentate gyrus (DG). Furthermore, the number of NeuroD (a neurogenic basic helix–loop–helix factor)-positive cells, in the DG was clearly increased by EE. Under these conditions, chronic pain suppressed enriched environment-mediated induction of both DCX- and NeuroD-labeled cells. These results suggest that chronic pain has stress-like damaging modulatory effects on hippocampal neurogenesis.