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Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gamma-aminobutyric acid release onto cerebellum Purkinje neurons.
J Pharmacol Exp Ther. 2007 Oct; 323(1):356-64.JP

Abstract

Recent data have demonstrated that ethanol increases gamma-aminobutyric acid (GABA) release in many brain regions, but little is known about the mechanism responsible for this action. Consistent with previous results, ethanol increased miniature inhibitory postsynaptic current (mIPSC) frequency at the interneuron-Purkinje cell synapse in the slice and in mechanically dissociated neurons. These data suggest that ethanol is increasing spontaneous GABA release at this synapse. It is generally accepted that ethanol increases levels of intracellular calcium and that changes in intracellular calcium can alter neurotransmitter release. Therefore, we examined the contribution of calcium-dependent pathways to the effect of ethanol on spontaneous GABA release at the interneuron-Purkinje cell synapse. Ethanol continued to increase mIPSC frequency in a nominally calcium-free extracellular solution and in the presence of a voltage-dependent calcium channel inhibitor, cadmium chloride. These data suggest that influx of extracellular calcium does not play a critical role in the mechanism of ethanol-enhanced spontaneous GABA release. However, a sarco/endoplasmic-reticulum calcium ATPase pump inhibitor (thapsigargin), an inositol 1,4,5-trisphosphate receptor antagonist (2-aminoethoxydiphenylborate) and a ryanodine receptor antagonist (ryanodine) significantly reduced the ability of ethanol to increase mIPSC frequency. In addition, ethanol was still able to increase mIPSC frequency in the presence of intracellular 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and a cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251); thus, retrograde messengers are not involved in ethanol-enhanced spontaneous GABA release. Overall, these data suggest that calcium release from presynaptic internal stores plays a vital role in the mechanism of ethanol-enhanced spontaneous GABA release at the interneuron-Purkinje cell synapse.

Authors+Show Affiliations

Bowles Center for Alcohol Studies, CB 7178, Thurston-Bowles Building, Chapel Hill, NC 27599-7178, USA. katie_kelm@med.unc.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17652632

Citation

Kelm, M Katherine, et al. "Calcium Release From Presynaptic Internal Stores Is Required for Ethanol to Increase Spontaneous Gamma-aminobutyric Acid Release Onto Cerebellum Purkinje Neurons." The Journal of Pharmacology and Experimental Therapeutics, vol. 323, no. 1, 2007, pp. 356-64.
Kelm MK, Criswell HE, Breese GR. Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gamma-aminobutyric acid release onto cerebellum Purkinje neurons. J Pharmacol Exp Ther. 2007;323(1):356-64.
Kelm, M. K., Criswell, H. E., & Breese, G. R. (2007). Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gamma-aminobutyric acid release onto cerebellum Purkinje neurons. The Journal of Pharmacology and Experimental Therapeutics, 323(1), 356-64.
Kelm MK, Criswell HE, Breese GR. Calcium Release From Presynaptic Internal Stores Is Required for Ethanol to Increase Spontaneous Gamma-aminobutyric Acid Release Onto Cerebellum Purkinje Neurons. J Pharmacol Exp Ther. 2007;323(1):356-64. PubMed PMID: 17652632.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gamma-aminobutyric acid release onto cerebellum Purkinje neurons. AU - Kelm,M Katherine, AU - Criswell,Hugh E, AU - Breese,George R, Y1 - 2007/07/25/ PY - 2007/7/27/pubmed PY - 2007/11/6/medline PY - 2007/7/27/entrez SP - 356 EP - 64 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 323 IS - 1 N2 - Recent data have demonstrated that ethanol increases gamma-aminobutyric acid (GABA) release in many brain regions, but little is known about the mechanism responsible for this action. Consistent with previous results, ethanol increased miniature inhibitory postsynaptic current (mIPSC) frequency at the interneuron-Purkinje cell synapse in the slice and in mechanically dissociated neurons. These data suggest that ethanol is increasing spontaneous GABA release at this synapse. It is generally accepted that ethanol increases levels of intracellular calcium and that changes in intracellular calcium can alter neurotransmitter release. Therefore, we examined the contribution of calcium-dependent pathways to the effect of ethanol on spontaneous GABA release at the interneuron-Purkinje cell synapse. Ethanol continued to increase mIPSC frequency in a nominally calcium-free extracellular solution and in the presence of a voltage-dependent calcium channel inhibitor, cadmium chloride. These data suggest that influx of extracellular calcium does not play a critical role in the mechanism of ethanol-enhanced spontaneous GABA release. However, a sarco/endoplasmic-reticulum calcium ATPase pump inhibitor (thapsigargin), an inositol 1,4,5-trisphosphate receptor antagonist (2-aminoethoxydiphenylborate) and a ryanodine receptor antagonist (ryanodine) significantly reduced the ability of ethanol to increase mIPSC frequency. In addition, ethanol was still able to increase mIPSC frequency in the presence of intracellular 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and a cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251); thus, retrograde messengers are not involved in ethanol-enhanced spontaneous GABA release. Overall, these data suggest that calcium release from presynaptic internal stores plays a vital role in the mechanism of ethanol-enhanced spontaneous GABA release at the interneuron-Purkinje cell synapse. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/17652632/Calcium_release_from_presynaptic_internal_stores_is_required_for_ethanol_to_increase_spontaneous_gamma_aminobutyric_acid_release_onto_cerebellum_Purkinje_neurons_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=17652632 DB - PRIME DP - Unbound Medicine ER -