Abstract
In this study, we examined chemokine receptor expression and function in rat cerebellar neurons. Calcium imaging experiments demonstrated that a wide variety of chemokines elicited [Ca(2+)](i) transients in acutely isolated and cultured cerebellar Purkinje and granule neurons. In many cases, these chemokine responses were pertussis toxin (PTX) insensitive. In addition, chemokines activated the Ca(2+) and cAMP-dependent transcription factor CREB and the extracellular response kinases ERK1/ERK2. Chemokines increased the survival of Purkinje neurons deprived of their trophic support. Thus, the presence of chemokine receptors and the signaling pathways they activate suggest that chemokines play a role in the control of cerebellar neuron survival and development and may mediate communication between the CNS and the immune system.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Biological Transport / drug effects
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Biological Transport / physiology
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Calcium / metabolism
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Cells, Cultured
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Cellular Senescence / physiology
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Cerebellum / cytology
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Cerebellum / metabolism*
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Cerebellum / physiology
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Chemokines / pharmacology
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Chemokines / physiology
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Chemokines, CC / pharmacology
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Electrophysiology
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Immunohistochemistry
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In Vitro Techniques
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Macrophage Inflammatory Proteins / pharmacology
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Neurons / metabolism*
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Pertussis Toxin
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Purkinje Cells / physiology
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Rats
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Rats, Inbred Strains
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Receptors, Chemokine / metabolism*
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Signal Transduction / drug effects
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Tissue Distribution
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Viral Proteins*
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Virulence Factors, Bordetella / pharmacology
Substances
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Chemokines
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Chemokines, CC
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Macrophage Inflammatory Proteins
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Receptors, Chemokine
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Viral Proteins
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Virulence Factors, Bordetella
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vMIP-1 protein, Human herpesvirus 8
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vMIP-II
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Pertussis Toxin
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Calcium