Substance P hyperpolarizes vagal sensory neurones of the ferret
Substance P hyperpolarizes vagal sensory neurones of the ferret
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DOI：
10.1113/jphysiol.1996.sp021371
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发表时间：
1996-05-15
影响因子：
5.5
通讯作者：
Weinreich, D
中科院分区：
文献类型：
--
作者：
Jafri, MS;Weinreich, D
1. Intracellular recordings were made in intact and in acutely dissociated vagal afferent neurones (nodose ganglion cells) of the ferret to investigate the effects of substance P (SP).2. In current-clamp recordings, SP (100 nM) applied by superfusion hyperpolarized the membrane potential (7 +/- 0.7 mV; mean +/- S.E.M; n = 105) and decreased the input resistance in 80 % of the neurones. With voltage-clamp recording, XP produced an outward current of 3 +/- 0.2 nA (n = 10).3. The SP current was concentration dependent with an estimated EC(50) of 68 nM. The XP-induced hyperpolarization or current was mimicked by the tachykinin receptor NK1 agonist Ac-[Arg(6), Sar(9), Met(O-2)(11)]SP(6-11) (ASM-SP; 100 nM; n = 10) and blocked by the NK1 antagonist CP-96,345 (10 nar; n = 6), but not by the NK2 antagonist SR48968 (100 nar; n = 4). No measurable change in membrane potential or input resistance was observed with application of either [beta-Ala(8)]neurokinin A or senktide, selective NK2 and NK, receptor agonists, respectively (100 nM; n = 3 for each agonist).4. The reversal potential (E(rev)) for the SP outward current was -85 +/- 2.5 mV (n = 4). The E(rev) for the SP response shifted in a Nernstian manner with changes in extracellular potassium concentration. Alterations in extracellular sodium or chloride concentrations had no significant effect on the E(rev) for the SP response (n = 3 for each ion).5. Nominally Ca2+-free external solution abolished the XP response. Removal of magnesinm from the extracellular solution had no effect on the response.6. Caesium (100 mu M), barium (1 mM), tetraethylammonium (TEA; 5 mM), apamin (10 nM) and 4-aminopyridine (4-AP; 4 mM) each completely prevented the XP response (n greater than or equal to 3 for each).7. These results indicate that SP, via an NK1 receptor, can induce a Ca2+-dependent outward potassium current which hyperpolarizes the resting membrane potential of vagal afferent somata.
