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Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex.
Neuroscience 2004; 126(4):955-66N

Abstract

To elucidate chronic actions of brain-derived neurotrophic factor (BDNF) on GABAergic synapses, we examined effects of a long-term application of BDNF for 10-15 days on autapses (synapses) of solitary GABAergic neurons cultured from rat visual cortex. Solitary neuron preparations were used to exclude a possible contamination of BDNF actions on excitatory neurons in dissociated neuron culture or slice preparations. Neurons were confirmed to be GABAergic pharmacologically with bicuculline, a selective antagonist for GABAA receptors and immunocytochemically with antibody against glutamic acid decarboxylase 65, a GABA synthesizing enzyme. To evaluate GABAergic synaptic function, evoked and/or miniature inhibitory postsynaptic currents (IPSCs) were recorded in the whole-cell voltage-clamp mode. The treatment with BDNF at a concentration of 100 ng/ml enhanced the amplitude of evoked IPSCs and the frequency of miniature IPSCs. In contrast, BDNF did not have a detectable effect on the amplitude of miniature IPSCs and the paired pulse ratio of IPSCs evoked by two, successive activations. To evaluate morphological changes, neurons were immunocytochemically stained with antibodies against microtubule-associated protein 2, to visualize somatodendritic region and synapsin I, to visualize presynaptic sites. The quantitative analysis indicated that BDNF increased the area of soma, the numbers of primary dendrites and dendritic branching points, the total length of dendrites and the number of synaptic sites. Such an action of BDNF was seen in both subgroups of GABAergic neurons, parvalbumin-positive and -negative neurons. To visualize functionally active presynaptic sites, neurons were stained with a styryl dye, FM1-43. BDNF increased the number of stained sites that was correlated with the frequency of miniature IPSCs. These results suggest that the chronic treatment with BDNF promotes dendritic and synaptic development of GABAergic neurons in visual cortex.

Authors+Show Affiliations

Division of Neurophysiology, Osaka University Graduate School of Medicine (D-14), Suita, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15207329

Citation

Palizvan, M R., et al. "Brain-derived Neurotrophic Factor Increases Inhibitory Synapses, Revealed in Solitary Neurons Cultured From Rat Visual Cortex." Neuroscience, vol. 126, no. 4, 2004, pp. 955-66.
Palizvan MR, Sohya K, Kohara K, et al. Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex. Neuroscience. 2004;126(4):955-66.
Palizvan, M. R., Sohya, K., Kohara, K., Maruyama, A., Yasuda, H., Kimura, F., & Tsumoto, T. (2004). Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex. Neuroscience, 126(4), pp. 955-66.
Palizvan MR, et al. Brain-derived Neurotrophic Factor Increases Inhibitory Synapses, Revealed in Solitary Neurons Cultured From Rat Visual Cortex. Neuroscience. 2004;126(4):955-66. PubMed PMID: 15207329.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brain-derived neurotrophic factor increases inhibitory synapses, revealed in solitary neurons cultured from rat visual cortex. AU - Palizvan,M R, AU - Sohya,K, AU - Kohara,K, AU - Maruyama,A, AU - Yasuda,H, AU - Kimura,F, AU - Tsumoto,T, PY - 2004/03/03/accepted PY - 2004/6/23/pubmed PY - 2004/10/9/medline PY - 2004/6/23/entrez SP - 955 EP - 66 JF - Neuroscience JO - Neuroscience VL - 126 IS - 4 N2 - To elucidate chronic actions of brain-derived neurotrophic factor (BDNF) on GABAergic synapses, we examined effects of a long-term application of BDNF for 10-15 days on autapses (synapses) of solitary GABAergic neurons cultured from rat visual cortex. Solitary neuron preparations were used to exclude a possible contamination of BDNF actions on excitatory neurons in dissociated neuron culture or slice preparations. Neurons were confirmed to be GABAergic pharmacologically with bicuculline, a selective antagonist for GABAA receptors and immunocytochemically with antibody against glutamic acid decarboxylase 65, a GABA synthesizing enzyme. To evaluate GABAergic synaptic function, evoked and/or miniature inhibitory postsynaptic currents (IPSCs) were recorded in the whole-cell voltage-clamp mode. The treatment with BDNF at a concentration of 100 ng/ml enhanced the amplitude of evoked IPSCs and the frequency of miniature IPSCs. In contrast, BDNF did not have a detectable effect on the amplitude of miniature IPSCs and the paired pulse ratio of IPSCs evoked by two, successive activations. To evaluate morphological changes, neurons were immunocytochemically stained with antibodies against microtubule-associated protein 2, to visualize somatodendritic region and synapsin I, to visualize presynaptic sites. The quantitative analysis indicated that BDNF increased the area of soma, the numbers of primary dendrites and dendritic branching points, the total length of dendrites and the number of synaptic sites. Such an action of BDNF was seen in both subgroups of GABAergic neurons, parvalbumin-positive and -negative neurons. To visualize functionally active presynaptic sites, neurons were stained with a styryl dye, FM1-43. BDNF increased the number of stained sites that was correlated with the frequency of miniature IPSCs. These results suggest that the chronic treatment with BDNF promotes dendritic and synaptic development of GABAergic neurons in visual cortex. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15207329/Brain_derived_neurotrophic_factor_increases_inhibitory_synapses_revealed_in_solitary_neurons_cultured_from_rat_visual_cortex_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306452204001770 DB - PRIME DP - Unbound Medicine ER -