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Glutamate pretreatment affects Ca2+ signaling in processes of astrocyte pairs.
J Neurochem 2007; 100(1):105-17JN

Abstract

Simultaneous somatic patch-pipette recording of a single astrocyte to evoke voltage-gated calcium currents, and Ca(2+) imaging, were used to study the spatial and temporal profiles of depolarization-induced changes in intracellular Ca(2+) ([Ca(2+)](i)) in the processes of cultured rat cortical astrocytes existing as pairs. Transient Ca(2+) changes locked to depolarization were observed as microdomains in the processes of the astrocyte pairs, and the responses were more pronounced in the adjoining astrocyte. Considering the functional significance of higher concentrations of glutamate observed in certain pathological conditions, Ca(2+) transients were recorded following pretreatment of cells with glutamate (500 microM for 20 min). This showed distance-dependent incremental scaling and attenuation in the presence of the metabotropic glutamate receptor (mGluR) antagonist, alpha-methyl(4-carboxy-phenyl) glycine (MCPG). Estimation of local Ca(2+) diffusion coefficients in the astrocytic processes indicated higher values in the adjoining astrocyte of the glutamate pretreated group. Intracellular heparin introduced into the depolarized astrocyte did not affect the Ca(2+) transients in the heparin-loaded astrocyte but attenuated the [Ca(2+)](i) responses in the adjoining astrocyte, suggesting that inositol 1,4,5 triphosphate (IP(3)) may be the transfer signal. The uncoupling agent, 1-octanol, attenuated the [Ca(2+)](i) responses in both the control and glutamate pretreated astrocytes, indicating the role of gap junctional communication. Our studies indicate that individual astrocytes have distinct functional domains, and that the glutamate-induced alterations in Ca(2+) signaling involve a sequence of intra- and intercellular steps in which phospholipase C (PLC), IP(3), internal Ca(2+) stores, VGCC and gap junction channels appear to play an important role.

Authors+Show Affiliations

Molecular Biophysics Unit, Indian Institute of Science, Bangalore, India.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17059561

Citation

Padmashri, Ragunathan, and Sujit Kumar Sikdar. "Glutamate Pretreatment Affects Ca2+ Signaling in Processes of Astrocyte Pairs." Journal of Neurochemistry, vol. 100, no. 1, 2007, pp. 105-17.
Padmashri R, Sikdar SK. Glutamate pretreatment affects Ca2+ signaling in processes of astrocyte pairs. J Neurochem. 2007;100(1):105-17.
Padmashri, R., & Sikdar, S. K. (2007). Glutamate pretreatment affects Ca2+ signaling in processes of astrocyte pairs. Journal of Neurochemistry, 100(1), pp. 105-17.
Padmashri R, Sikdar SK. Glutamate Pretreatment Affects Ca2+ Signaling in Processes of Astrocyte Pairs. J Neurochem. 2007;100(1):105-17. PubMed PMID: 17059561.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glutamate pretreatment affects Ca2+ signaling in processes of astrocyte pairs. AU - Padmashri,Ragunathan, AU - Sikdar,Sujit Kumar, Y1 - 2006/10/24/ PY - 2006/10/25/pubmed PY - 2007/2/23/medline PY - 2006/10/25/entrez SP - 105 EP - 17 JF - Journal of neurochemistry JO - J. Neurochem. VL - 100 IS - 1 N2 - Simultaneous somatic patch-pipette recording of a single astrocyte to evoke voltage-gated calcium currents, and Ca(2+) imaging, were used to study the spatial and temporal profiles of depolarization-induced changes in intracellular Ca(2+) ([Ca(2+)](i)) in the processes of cultured rat cortical astrocytes existing as pairs. Transient Ca(2+) changes locked to depolarization were observed as microdomains in the processes of the astrocyte pairs, and the responses were more pronounced in the adjoining astrocyte. Considering the functional significance of higher concentrations of glutamate observed in certain pathological conditions, Ca(2+) transients were recorded following pretreatment of cells with glutamate (500 microM for 20 min). This showed distance-dependent incremental scaling and attenuation in the presence of the metabotropic glutamate receptor (mGluR) antagonist, alpha-methyl(4-carboxy-phenyl) glycine (MCPG). Estimation of local Ca(2+) diffusion coefficients in the astrocytic processes indicated higher values in the adjoining astrocyte of the glutamate pretreated group. Intracellular heparin introduced into the depolarized astrocyte did not affect the Ca(2+) transients in the heparin-loaded astrocyte but attenuated the [Ca(2+)](i) responses in the adjoining astrocyte, suggesting that inositol 1,4,5 triphosphate (IP(3)) may be the transfer signal. The uncoupling agent, 1-octanol, attenuated the [Ca(2+)](i) responses in both the control and glutamate pretreated astrocytes, indicating the role of gap junctional communication. Our studies indicate that individual astrocytes have distinct functional domains, and that the glutamate-induced alterations in Ca(2+) signaling involve a sequence of intra- and intercellular steps in which phospholipase C (PLC), IP(3), internal Ca(2+) stores, VGCC and gap junction channels appear to play an important role. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/17059561/Glutamate_pretreatment_affects_Ca2+_signaling_in_processes_of_astrocyte_pairs_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04166.x DB - PRIME DP - Unbound Medicine ER -