Aylwin M L, Horowitz J M, Bonham A C
Division of Cardiovascular Medicine, Department of Pharmacology, University of California, Davis, California 95616, USA.
Am J Physiol. 1998 Oct;275(4):H1236-46. doi: 10.1152/ajpheart.1998.275.4.H1236.
Area postrema (AP) modulates cardiovascular function through excitatory projections to neurons in nucleus tractus solitarius (NTS), which also process primary sensory (including cardiovascular-related) input via the solitary tract (TS). The neurotransmitter(s) and their receptors in the AP-NTS pathway have not been fully characterized. We used whole cell recordings in voltage- and current-clamp modes in the rat brain stem slice to examine the role of ionotropic glutamatergic receptors and alpha2-adrenergic receptors in the pathway from AP to NTS neurons receiving visceral afferent information via the TS. In neurons voltage clamped at potentials from -100 to +80 mV, AP stimulation (0. 2 Hz) evoked excitatory postsynaptic currents having a fast component blocked by the non-N-methyl-D-aspartate (NMDA) receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxobenzoquinoxaline-7-sulfonamide (NBQX; 3 microM, n = 7) and a slow component blocked by the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV; 50 microM, n = 8). Although NBQX (3 microM, n = 14) abolished AP-evoked action potentials, APV (50 microM, n = 9 or 500 microM, n = 6) or yohimbine, (200 nM, n = 5 or 2 microM, n = 10) did not. Thus, although AP stimulation activates both non-NMDA and NMDA receptors on NTS neurons receiving TS input, only non-NMDA receptors are required for synaptic transmission.
最后区(AP)通过向孤束核(NTS)中的神经元发出兴奋性投射来调节心血管功能,孤束核还通过孤束(TS)处理初级感觉(包括与心血管相关的)输入。AP-NTS通路中的神经递质及其受体尚未完全明确。我们在大鼠脑干切片中采用电压钳和电流钳模式下的全细胞记录,以研究离子型谷氨酸能受体和α2-肾上腺素能受体在从AP到通过TS接收内脏传入信息的NTS神经元的通路中的作用。在钳制电压为-100至+80 mV的神经元中,AP刺激(0.2 Hz)诱发兴奋性突触后电流,其快速成分可被非N-甲基-D-天冬氨酸(NMDA)受体拮抗剂1,2,3,4-四氢-6-硝基-2,3-二氧苯并喹喔啉-7-磺酰胺(NBQX;3 μM,n = 7)阻断,慢速成分可被NMDA受体拮抗剂DL-2-氨基-5-磷酸戊酸(APV;50 μM,n = 8)阻断。尽管NBQX(3 μM,n = 14)消除了AP诱发的动作电位,但APV(50 μM,n = 9或500 μM,n = 6)或育亨宾(200 nM,n = 5或2 μM,n = 10)却没有。因此,尽管AP刺激激活了通过TS接收输入的NTS神经元上的非NMDA和NMDA受体,但突触传递仅需要非NMDA受体。