ELECTROPHYSIOLOGICAL IDENTIFICATION OF FOREBRAIN CONNECTIONS OF THE SUBFORNICAL ORGAN

ELECTROPHYSIOLOGICAL IDENTIFICATION OF FOREBRAIN CONNECTIONS OF THE SUBFORNICAL ORGAN
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DOI:
10.1016/0006-8993(86)90118-6
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发表时间:
1986-09-10
期刊:
影响因子:
2.9
通讯作者:
MOGENSON, GJ
MOGENSON, GJ
中科院分区:
医学3区
文献类型:
--
作者:
GUTMAN, MB;CIRIELLO, J;MOGENSON, GJ

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17只大鼠经氨基脲麻醉后,观察下丘脑皮层下器官(SFO)内直接向下丘脑室旁核(PVH)、视上核(SON)和中隔核(NM)区域发送传出轴突的电生理神经元。对SFO区(n = 130)和三角核区(NT; n = 20)自发活动和沉默的神经元进行细胞外单单位记录。65个SFO单元在PVH、SON或NM刺激下被反向激活,其潜伏期对应于传导速度0.54 .+-。0.07 (n = 24), 0.44。0.05 (n = 17)和0.23。0.02 (n = 24) m/s。SFO单元轴突向NM的传导速度明显慢于PVH和SON。通过刺激这些前脑结构,另外11个单位在NT中被拮抗激活。发现67个单位对PVH、SON和NM的刺激有正交反应:SFO有58个,NT有9个。正交反应主要是兴奋或抑制。这些数据证明了SFO和前脑结构之间的双向通路,这可能参与了血源性血管紧张素II激活SFO时的发病和动脉压力反应。
Experiments were performed in 17 urethane-anesthetized rats to investigate electrophysiologically neurons in the subfornical organ (SFO), which send efferent axons directly to the region of the paraventricular nucleus of the hypothalamus (PVH), the supraoptic nucleus (SON) and the nucleus medianus (NM). Extracellular single unit recordings were made from spontaneously active and silent neurons in the region of SFO (n = 130) and the nucleus triangularis (NT; n = 20). Sixty-five units in SFO were antidromically activated by stimulation of either PVH, SON or NM with latencies corresponding to conduction velocities of 0.54 .+-. 0.07 (n = 24), 0.44 .+-. 0.05 (n = 17) and 0.23 .+-. 0.02 (n = 24) m/s, respectively. Axons of SFO units projecting to NM conducted at significantly slower velocities than those to PVH and SON. An additional 11 units were antidromically activated in NT by stimulation of these forebrain structures. Sixty-seven units were found to respond orthodromically to stimulation of PVH, SON and NM: 58 in SFO and 9 in NT. Orthodromic responses were primarily excitation or inhibition. These data have demonstrated bidirectional pathways between SFO and forebrain structures which are likely involved in the dipsogenic and arterial pressure responses to activation of SFO by blood-borne angiotensin II.