期刊
JOURNAL OF NEUROPHYSIOLOGY
卷 98, 期 2, 页码 1052-1056出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.01214.2006
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资金
- NCRR NIH HHS [P20 RR020146, RR-020146] Funding Source: Medline
- NIDCD NIH HHS [R01 DC007123-04, DC-03195, R03 DC006356-04, DC-07123, R01 DC003195, R03 DC006356-03, R01 DC008702, R03 DC006356-01A1, R03 DC006356-02, R01 DC007123-02, DC-008702, DC-06356, R01 DC007123, R01 DC007123-01A1, R01 DC007123-03, R03 DC006356] Funding Source: Medline
In rat olfactory bulb slices, external tufted ( ET) cells spontaneously generate spike bursts. Although ET cell bursting is intrinsically generated, its strength and precise timing may be regulated by synaptic input. We tested this hypothesis by analyzing whether the burst properties are modulated by activation of ionotropic gamma-aminobutyric acid (GABA) and glutamate receptors. Blocking GABA(A) receptors increased-whereas blocking ionotropic glutamate receptors decreased-the number of spikes/burst without changing the interburst frequency. The GABA(A) agonist (isoguvacine, 10 mu M) completely inhibited bursting or reduced the number of spikes/burst, suggesting a shunting effect. These findings indicate that the properties of ET cell spontaneous bursting are differentially controlled by GABAergic and glutamatergic fast synaptic transmission. We suggest that ET cell excitatory and inhibitory inputs may be encoded as a change in the pattern of spike bursting in ET cells, which together with mitral/tufted cells constitute the output circuit of the olfactory bulb.
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