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Brain-derived neurotrophic factor modulates GABAergic synaptic transmission by enhancing presynaptic glutamic acid decarboxylase 65 levels, promoting asynchronous release and reducing the number of activated postsynaptic receptors.
Neuroscience 2005; 135(3):749-63N

Abstract

Brain-derived neurotrophic factor is known to modulate the function of GABAergic synapses, but the site of brain-derived neurotrophic factor action is still a matter of controversy. This study was aimed at further dissecting the functional alterations produced by brain-derived neurotrophic factor treatment of GABAergic synaptic connections in cultures of the murine superior colliculus. The functional consequences of long-term brain-derived neurotrophic factor treatment were assessed by analysis of unitary evoked and delayed inhibitory postsynaptic currents in response to high frequency stimulation of single axons. It was found that brain-derived neurotrophic factor facilitated the asynchronous release, but had no effect on the probability of evoked release, the size of the readily releasable pool, and the paired-pulse behavior of evoked inhibitory postsynaptic currents. However, the amplitudes of evoked inhibitory postsynaptic currents, delayed inhibitory postsynaptic currents and miniature inhibitory postsynaptic currents were significantly reduced. Non-stationary fluctuation analysis revealed a decrease in the open channel number at the miniature/evoked inhibitory postsynaptic current peak, but no effect on the mean GABA(A) receptor single channel conductance. Quantitative immunocytochemistry uncovered a significant elevation of presynaptic levels of glutamic acid decarboxylase 65. Together, these findings indicate that brain-derived neurotrophic factor treatment induces pre- as well as postsynaptic changes. What effect predominates will depend on the presynaptic activity pattern: at low activation rates brain-derived neurotrophic factor-treated synapses display a pronounced postsynaptic depression, but at high frequencies this depression is fully compensated by an enhancement of asynchronous release.

Authors+Show Affiliations

Sensory and Developmental Physiology Group, Institute of Neurophysiology, Johannes-Mueller-Center of Physiology, Charité-University Medicine Berlin, Tucholskystr. 2, D-10117 Berlin, Germany.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16154289

Citation

Henneberger, C, et al. "Brain-derived Neurotrophic Factor Modulates GABAergic Synaptic Transmission By Enhancing Presynaptic Glutamic Acid Decarboxylase 65 Levels, Promoting Asynchronous Release and Reducing the Number of Activated Postsynaptic Receptors." Neuroscience, vol. 135, no. 3, 2005, pp. 749-63.
Henneberger C, Kirischuk S, Grantyn R. Brain-derived neurotrophic factor modulates GABAergic synaptic transmission by enhancing presynaptic glutamic acid decarboxylase 65 levels, promoting asynchronous release and reducing the number of activated postsynaptic receptors. Neuroscience. 2005;135(3):749-63.
Henneberger, C., Kirischuk, S., & Grantyn, R. (2005). Brain-derived neurotrophic factor modulates GABAergic synaptic transmission by enhancing presynaptic glutamic acid decarboxylase 65 levels, promoting asynchronous release and reducing the number of activated postsynaptic receptors. Neuroscience, 135(3), pp. 749-63.
Henneberger C, Kirischuk S, Grantyn R. Brain-derived Neurotrophic Factor Modulates GABAergic Synaptic Transmission By Enhancing Presynaptic Glutamic Acid Decarboxylase 65 Levels, Promoting Asynchronous Release and Reducing the Number of Activated Postsynaptic Receptors. Neuroscience. 2005;135(3):749-63. PubMed PMID: 16154289.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brain-derived neurotrophic factor modulates GABAergic synaptic transmission by enhancing presynaptic glutamic acid decarboxylase 65 levels, promoting asynchronous release and reducing the number of activated postsynaptic receptors. AU - Henneberger,C, AU - Kirischuk,S, AU - Grantyn,R, Y1 - 2005/09/08/ PY - 2005/03/01/received PY - 2005/06/10/revised PY - 2005/06/14/accepted PY - 2005/9/13/pubmed PY - 2005/12/24/medline PY - 2005/9/13/entrez SP - 749 EP - 63 JF - Neuroscience JO - Neuroscience VL - 135 IS - 3 N2 - Brain-derived neurotrophic factor is known to modulate the function of GABAergic synapses, but the site of brain-derived neurotrophic factor action is still a matter of controversy. This study was aimed at further dissecting the functional alterations produced by brain-derived neurotrophic factor treatment of GABAergic synaptic connections in cultures of the murine superior colliculus. The functional consequences of long-term brain-derived neurotrophic factor treatment were assessed by analysis of unitary evoked and delayed inhibitory postsynaptic currents in response to high frequency stimulation of single axons. It was found that brain-derived neurotrophic factor facilitated the asynchronous release, but had no effect on the probability of evoked release, the size of the readily releasable pool, and the paired-pulse behavior of evoked inhibitory postsynaptic currents. However, the amplitudes of evoked inhibitory postsynaptic currents, delayed inhibitory postsynaptic currents and miniature inhibitory postsynaptic currents were significantly reduced. Non-stationary fluctuation analysis revealed a decrease in the open channel number at the miniature/evoked inhibitory postsynaptic current peak, but no effect on the mean GABA(A) receptor single channel conductance. Quantitative immunocytochemistry uncovered a significant elevation of presynaptic levels of glutamic acid decarboxylase 65. Together, these findings indicate that brain-derived neurotrophic factor treatment induces pre- as well as postsynaptic changes. What effect predominates will depend on the presynaptic activity pattern: at low activation rates brain-derived neurotrophic factor-treated synapses display a pronounced postsynaptic depression, but at high frequencies this depression is fully compensated by an enhancement of asynchronous release. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/16154289/Brain_derived_neurotrophic_factor_modulates_GABAergic_synaptic_transmission_by_enhancing_presynaptic_glutamic_acid_decarboxylase_65_levels_promoting_asynchronous_release_and_reducing_the_number_of_activated_postsynaptic_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(05)00694-9 DB - PRIME DP - Unbound Medicine ER -