Abstract
We investigated the functions of nicotinic receptor activation on area postrema neurons by making whole-cell recordings in rat brainstem slices. Excitatory responses to nicotine application were found in approximately 78% (35/45) of all cells tested. Responsive cells included both the cells that display the hyperpolarization-activated cation current (Ih) and cells that do not display Ih. An inhibitory effect of nicotine was never seen. Current-clamp recordings showed the nicotine-induced depolarization of a cell's membrane potential that could be sufficient to cause spontaneous firing. In voltage-clamp recordings, many cells showed nicotine-induced inward currents (18.3±3.2 pA, n=6) that persisted during pharmacological blockade of synaptic transmission (e.g., zero [Ca2+]out and 5 mM [Mg2+]out, n=6/8). Other two cells, however, showed increases in the frequency of excitatory postsynaptic currents (EPSCs), which were blocked by CNQX (n=2/8). We analyzed miniature EPSCs (mEPSCs) recorded from cells that showed no inward currents but marked increases in the frequency of mEPSCs (0.8±0.2 to 4.8±1.7 Hz, n=4) during nicotine application. Nicotine augmented mEPSC amplitude (n=4); however, amplitude distribution was not significantly changed in two of four cells tested. We conclude that nicotinic receptors in the rat area postrema can excite cells via (1) a direct post- and/or extrasynaptic mechanism; and (2) an indirect enhancement of glutamate release.
| Original language | English |
|---|---|
| Pages (from-to) | 227-233 |
| Number of pages | 7 |
| Journal | Brain Research |
| Volume | 1017 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Aug 13 2004 |
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Keywords
- Acetylcholine receptors: nicotinic
- Area postrema
- Neurotransmitters, modulators, transporters, and receptors
- Nicotinic ACh receptor
- Rat
- Slice
- Whole-cell patch-clamp
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Nicotinic modulation of area postrema neuronal excitability in rat brain slices. / Funahashi, Makoto; Mitoh, Yoshihiro; Matsuo, Ryuji.
In: Brain Research, Vol. 1017, No. 1-2, 13.08.2004, p. 227-233.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nicotinic modulation of area postrema neuronal excitability in rat brain slices
AU - Funahashi, Makoto
AU - Mitoh, Yoshihiro
AU - Matsuo, Ryuji
PY - 2004/8/13
Y1 - 2004/8/13
N2 - We investigated the functions of nicotinic receptor activation on area postrema neurons by making whole-cell recordings in rat brainstem slices. Excitatory responses to nicotine application were found in approximately 78% (35/45) of all cells tested. Responsive cells included both the cells that display the hyperpolarization-activated cation current (Ih) and cells that do not display Ih. An inhibitory effect of nicotine was never seen. Current-clamp recordings showed the nicotine-induced depolarization of a cell's membrane potential that could be sufficient to cause spontaneous firing. In voltage-clamp recordings, many cells showed nicotine-induced inward currents (18.3±3.2 pA, n=6) that persisted during pharmacological blockade of synaptic transmission (e.g., zero [Ca2+]out and 5 mM [Mg2+]out, n=6/8). Other two cells, however, showed increases in the frequency of excitatory postsynaptic currents (EPSCs), which were blocked by CNQX (n=2/8). We analyzed miniature EPSCs (mEPSCs) recorded from cells that showed no inward currents but marked increases in the frequency of mEPSCs (0.8±0.2 to 4.8±1.7 Hz, n=4) during nicotine application. Nicotine augmented mEPSC amplitude (n=4); however, amplitude distribution was not significantly changed in two of four cells tested. We conclude that nicotinic receptors in the rat area postrema can excite cells via (1) a direct post- and/or extrasynaptic mechanism; and (2) an indirect enhancement of glutamate release.
AB - We investigated the functions of nicotinic receptor activation on area postrema neurons by making whole-cell recordings in rat brainstem slices. Excitatory responses to nicotine application were found in approximately 78% (35/45) of all cells tested. Responsive cells included both the cells that display the hyperpolarization-activated cation current (Ih) and cells that do not display Ih. An inhibitory effect of nicotine was never seen. Current-clamp recordings showed the nicotine-induced depolarization of a cell's membrane potential that could be sufficient to cause spontaneous firing. In voltage-clamp recordings, many cells showed nicotine-induced inward currents (18.3±3.2 pA, n=6) that persisted during pharmacological blockade of synaptic transmission (e.g., zero [Ca2+]out and 5 mM [Mg2+]out, n=6/8). Other two cells, however, showed increases in the frequency of excitatory postsynaptic currents (EPSCs), which were blocked by CNQX (n=2/8). We analyzed miniature EPSCs (mEPSCs) recorded from cells that showed no inward currents but marked increases in the frequency of mEPSCs (0.8±0.2 to 4.8±1.7 Hz, n=4) during nicotine application. Nicotine augmented mEPSC amplitude (n=4); however, amplitude distribution was not significantly changed in two of four cells tested. We conclude that nicotinic receptors in the rat area postrema can excite cells via (1) a direct post- and/or extrasynaptic mechanism; and (2) an indirect enhancement of glutamate release.
KW - Acetylcholine receptors: nicotinic
KW - Area postrema
KW - Neurotransmitters, modulators, transporters, and receptors
KW - Nicotinic ACh receptor
KW - Rat
KW - Slice
KW - Whole-cell patch-clamp
UR - http://www.scopus.com/inward/record.url?scp=3142661701&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3142661701&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2004.05.028
DO - 10.1016/j.brainres.2004.05.028
M3 - Article
C2 - 15261119
AN - SCOPUS:3142661701
VL - 1017
SP - 227
EP - 233
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -