Relationship between central perceptivity of noradrenalin and oral dryness

皮层下器官（SFO）的激活会诱发饮酒行为，即口腔干燥。本研究采用全细胞膜片钳法记录NA及其类似物对大鼠SFO神经元的影响。在电流箝位模式下，在10-100 μM下施加NA可产生膜去极化（63%，17个响应神经元/27个被测神经元）和超极化（22%，6/27个神经元）。在电压箝位模式下，施加1 ~ 100 μM的NA产生向内电流（69%，42/61神经元）和向外电流（23%，14/61神经元）。这些电流在TTX存在或谷氨酸和GABA受体拮抗剂共同应用时保持不变。在NA存在下显示向内电流的大多数神经元（25/31个神经元）中，膜电导不受电压斜坡或超极化脉冲刺激的影响。应用α 1激动剂苯肾上腺素也获得了类似的反应。苯肾上腺素诱导的向内电流被α1拮抗剂吡唑嗪抑制。此外，α2激动剂可乐定降低自发性gaba能抑制性突触后电流的频率（4/10个神经元）。结果表明，大鼠SFO神经元突触后通过α1肾上腺素能受体激活，突触前α2肾上腺素能受体抑制gaba能抑制性突触输入可增强SFO神经元的激活。

Activation of the subfornical organ (SFO) induces drinking behavior, that is, oral dryness. In this study, the effects of NA and its analogues on SFO neurons in rat slice preparations were investigated by using whole cell patch clamp recording. In the current clamp mode, the application of NA at 10-100 μM produced membrane depolarization (63%, 17 responsive neurons /27 neurons tested) and hyperpolarization (22%, 6/27 neurons). In the voltage clamp mode, NA application at 1-100 μM produced inward currents (69%, 42/61 neurons) and outward currents (23%, 14/61 neurons). These currents were remained in the presence of TTX or in the coapplication of glutamate and GABA receptor antagonists. In most of the neurons (25/31 neurons) showing inward currents in the presence of NA, the membrane conductance was not changed by voltage ramps or hyperpolarizing pulse stimulation. Similar responses were obtained by the application of the αl agonist phenylephrine. The phenylephrine-induced inward currents were inhibited by the α1 antagonist prazosin. In addition, the α2 agonist clonidine decreased the frequency of spontaneous GABAergic inhibitory postsynaptic currents (4/10 neurons). The results suggest that SFO neurons in rats are activated postsynaptically through α1 adrenoceptors, and that the activation is enhanced by suppressing GABAergic inhibitory synaptic inputs through presynaptic α2 adrenoceptors.