Urbanski R W, Sapru H N
Section of Neurosurgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark.
J Auton Nerv Syst. 1988 Dec;25(2-3):181-93. doi: 10.1016/0165-1838(88)90023-9.
Experiments were carried out in artificially ventilated pentobarbital-anesthetized male Wistar rats. Following microinjection of muscimol (GABA-mimetic) or kynurenic acid (KYN; glutamate antagonist) into the ventrolateral medullary depressor area (VLDA), microinjection of L-glutamate (GLU; 4.5 nmol) into the NTS elicited a pressor response. This pressor response was attenuated in a dose-dependent manner by microinjection of KYN (0.5-5 nmol) into the ventrolateral medullary pressor area (VLPA). A GLU-induced pressor response could also be elicited from the NTS when GABA receptors in the VLPA were blocked with the microinjection of bicuculline (GABA antagonist, 200 pmol) into this site. The same dose of bicuculline in the VLPA also blocked the depressor responses elicited from the VLDA. With the VLDA or VLPA functionally unimpaired, microinjection of GLU (4.5 nmol) into the NTS elicited a fall in blood pressure and heart rate. This depressor response was attenuated in a dose-dependent manner by the microinjections of KYN (2-20 nmol) into the VLDA. These results indicate that: (1) The NTS sends glutamatergic inputs to both the VLDA and the VLPA; the projection from the NTS to the VLPA mediates pressor responses while that from the NTS to the VLDA represents one component of the pathway mediating the depressor responses elicited from the NTS. (2) The pathway from the VLDA to the VLPA is GABA-ergic and represents another component of the pathway mediating depressor responses evoked from the NTS. (3) The bradycardia evoked from the NTS may involve a pathway from the NTS to the VLDA.
实验在人工通气的戊巴比妥麻醉雄性Wistar大鼠身上进行。向腹外侧延髓降压区（VLDA）微量注射蝇蕈醇（GABA模拟物）或犬尿喹啉酸（KYN；谷氨酸拮抗剂）后，向孤束核（NTS）微量注射L-谷氨酸（GLU；4.5 nmol）会引发升压反应。向腹外侧延髓升压区（VLPA）微量注射KYN（0.5 - 5 nmol）会以剂量依赖的方式减弱这种升压反应。当向VLPA微量注射荷包牡丹碱（GABA拮抗剂，200 pmol）阻断该部位的GABA受体时，也可从NTS引发GLU诱导的升压反应。VLPA中相同剂量的荷包牡丹碱也阻断了从VLDA引发的降压反应。在VLDA或VLPA功能未受损的情况下，向NTS微量注射GLU（4.5 nmol）会导致血压和心率下降。向VLDA微量注射KYN（2 - 20 nmol）会以剂量依赖的方式减弱这种降压反应。这些结果表明：（1）NTS向VLDA和VLPA均发送谷氨酸能输入；从NTS到VLPA的投射介导升压反应，而从NTS到VLDA的投射代表介导从NTS引发的降压反应的通路的一个组成部分。（2）从VLDA到VLPA的通路是GABA能的，代表介导从NTS引发的降压反应的通路的另一个组成部分。（3）从NTS引发的心动过缓可能涉及从NTS到VLDA的通路。
