Nicotine-Induced Enhancement of Glutamatergic and GABAergic Synaptic Transmission in the Mouse Amygdala

Journal of Neurophysiology - Tập 86 Số 1 - Trang 463-474 - 2001
Nobl Barazangi1, Lorna W. Role2,1
1The Center for Neurobiology and Behavior and
2Department of Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York, 10032

Tóm tắt

Presynaptic nicotinic acetylcholine receptors (nAChRs) are thought to mediate some of the cognitive and behavioral effects of nicotine. The olfactory projection to the amygdala, and intra-amygdaloid projections, are limbic relays involved in behavioral reinforcement, a property influenced by nicotine. Co-cultures consisting of murine olfactory bulb (OB) explants and dispersed amygdala neurons were developed to reconstruct this pathway in vitro. Whole cell patch-clamp recordings were obtained from amygdala neurons contacted by OB explant neurites, and spontaneous and evoked synaptic currents were characterized. The majority of the 108 innervated amygdala neurons exhibited glutamatergic spontaneous postsynaptic currents (PSCs), 20% exhibited GABAergic spontaneous PSCs, and 17% exhibited both. Direct extracellular stimulation of OB explants elicited glutamatergic synaptic currents in amygdala neurons. Antibodies to nAChR subunits co-localized with an antibody to synapsin I, a presynaptic marker, along OB explant processes, consistent with the targeting of nAChR protein to presynaptic sites of the mitral cell projections. Hence, we examined the role of presynaptic nAChRs in modulating synaptic transmission in the OB–amygdala co-cultures. Focal application of 500 nM to 1 μM nicotine for 5–60 s markedly increased the frequency of spontaneous PSCs, without a change in the amplitude, in 39% of neurons that exhibited glutamatergic spontaneous PSCs (average peak fold increase = 125.2 ± 33.3). Nicotine also enhanced evoked glutamatergic currents elicited by direct stimulation of OB explant fibers. Nicotine increased the frequency of spontaneous PSCs, without a change in the amplitude, in 35% of neurons that exhibited GABAergic spontaneous PSCs (average peak fold increase = 63.9 ± 34.3). Thus activation of presynaptic nAChRs can modulate glutamatergic as well as GABAergic synaptic transmission in the amygdala. These results suggest that behaviors mediated by olfactory projections may be modulated by presynaptic nAChRs in the amygdala, where integration of olfactory and pheromonal input is thought to occur.

Từ khóa


Tài liệu tham khảo

10.1523/JNEUROSCI.19-07-02693.1999

Alkondon M, 1996, J Pharmacol Exp Ther, 278, 1460

10.1523/JNEUROSCI.18-20-08485.1998

10.1016/0168-0102(85)90001-X

10.1016/0006-8993(78)90782-5

10.1002/(SICI)1096-9861(19970224)378:4<454::AID-CNE2>3.0.CO;2-1

10.1523/JNEUROSCI.19-21-09180.1999

10.1016/S0165-0173(97)00040-4

10.1007/BF02245149

10.1016/0896-6273(90)90344-F

10.1016/0143-4179(94)90102-3

10.1016/S0896-6273(00)80112-9

10.1016/S0736-5748(98)00087-2

10.1016/S0306-4522(99)00169-4

10.1111/j.1749-6632.1999.tb09280.x

10.1016/S0896-6273(00)80775-8

10.1016/S0959-4388(96)80076-6

10.1016/0959-4388(91)90080-Q

10.1038/383713a0

10.1523/JNEUROSCI.18-06-01963.1998

10.1146/annurev.ne.10.030187.001545

10.1007/BF00656997

10.1002/cne.902080207

10.1523/JNEUROSCI.13-04-01551.1993

10.1085/jgp.92.2.145

10.1016/0006-8993(78)90025-2

10.1016/S0959-4388(99)80031-2

10.1016/S0301-0082(97)00028-2

10.1210/endo.138.11.5543

10.1016/S0006-2952(99)00326-3

10.1016/0959-4388(95)80009-3

10.1126/science.286.5440.716

10.1016/0304-3940(91)90765-L

10.1523/JNEUROSCI.17-02-00576.1997

10.1523/JNEUROSCI.13-06-02680.1993

10.1007/s002130050667

10.1002/jnr.490330308

10.1523/JNEUROSCI.18-21-08571.1998

10.1146/annurev.neuro.22.1.443

10.1016/S0166-2236(99)01465-4

10.1126/science.7569895

10.1016/S0959-4388(96)80118-8

Miyata H, 1998, Nihon Arukoru Yakubutsu Igakkai Zasshi, 33, 557

10.1126/science.286.5440.711

10.1007/s004410050616

10.1111/j.1749-6632.1999.tb09271.x

10.1002/cne.902290308

10.1016/S0959-4388(99)00034-3

10.1038/34413

10.1038/37120

10.1002/(SICI)1096-9861(19990524)408:1<61::AID-CNE5>3.0.CO;2-F

10.1523/JNEUROSCI.18-18-07075.1998

10.1073/pnas.85.8.2825

10.1016/S0306-4522(97)00516-2

10.1523/JNEUROSCI.13-02-00596.1993

10.1037/0735-7044.107.2.254

10.1016/S0166-2236(98)01265-X

10.1002/cne.902840212

10.1016/S0166-2236(96)10073-4

10.1016/0361-9230(84)90236-3

Thông tin
Thông tin xuất bản

Journal of Neurophysiology

Tập 86 Số 1

463-474

Thông tin tác giả