These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: A glutamatergic component of lead toxicity in adult brain: the role of astrocytic glutamate transporters.
    Author: Struzyńska L.
    Journal: Neurochem Int; 2009; 55(1-3):151-6. PubMed ID: 19428820.
    Abstract:
    Astroglial cells have a variety of roles in the central nervous system (CNS), providing a homeostasis for the proper functioning of neuronal cells. The classical view concerning the supportive role of astroglia towards associated neurons has to be extended. A great number of new evidences suggest that astrocytes interact closely with neurons being involved in the active control of neuronal activity and metabolism, forming with pre- and postsynaptic nerve terminals a tripartite synapse. Astrocytes control many aspects of brain function. Regulation of extracellular glutamate concentration, potentially neurotoxic neurotransmitter, is fundamental. Glial glutamate transporters system is of importance in protection against glutamate excitotoxicity and antioxidant defence system which is glutathione. When astrocytes fail to function properly, they influence the degree of neuronal damage. Thus, astrocytes are involved to a very great extent into numerous brain pathologies, including toxicity of heavy metals, like lead (Pb). Under pathological conditions they appear to express two opposite features: they are neuroprotective (until they can) or deleterious for neurons and may participate in neuronal damage. The very well known affinity of Pb to astroglia and the changes in glutamatergic transmission upon Pb toxicity, led us to discuss the role of astroglia and astrocytic glutamate transporters in the neurotoxicity of this metal. Our observations are viewed against a background of other results.
    [Abstract] [Full Text] [Related] [New Search]