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首页> 外文期刊>Brain research >Defense reaction mediated by NMDA mechanisms in the inferior colliculus is modulated by GABAergic nigro-collicular pathways.
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Defense reaction mediated by NMDA mechanisms in the inferior colliculus is modulated by GABAergic nigro-collicular pathways.

机译：下丘脑中NMDA机制介导的防御反应受GABA能性黑胶质细胞途径调节。

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Electrical stimulation of the inferior colliculus (IC) causes a behavioral activation together with autonomic responses similar to fear reactions to threatening situations. GABAergic mechanisms exert a tonic inhibitory control on the neural substrates of aversion in the IC insofar as local injections of GABA agonists or antagonists inhibit or mimic these defensive behaviors, respectively. Recently, we have shown that systemic injections of the GABA-A receptor agonist muscimol unexpectedly enhanced the freezing and escape responses provoked by gradual increases in the intensity of the electrical stimulation of the IC. Taking into account that the neural circuits mediated by excitatory amino acids (EAA) in the IC may be responsible for the integration of fear states, in the present study we examined whether the defensive behavior induced by local injections of NMDA into the IC is influenced by prior treatment with systemic muscimol and also whether this GABAergic control could be exerted by GABAergic fibers that project to the inferior colliculus from the substantia nigra pars reticulata (SNpr). Rats were implanted with two guide-cannulae aimed at the IC and SNpr through which drug microinfusions with glass micropipette could be made with reduced brain damage. One week after surgery, the animals received either NMDA (7 nmol/0.2 microl) or saline into the IC and were placed into the middle of an enclosure where behavioral responses such as freezing, crossings, jumping, rearing, and turnings could be measured as an indirect index of unconditioned fear. These animals were pretreated either with saline or muscimol (0.5 mg/kg, IP) or with brain injections of saline or muscimol (1 nmol/0.2 il into SNpr). NMDA applied into the IC produced a behavioral activation with significant increases in all behavioral measures. IP injections of muscimol or into the SNpr enhanced the defense reaction caused by microinjections of NMDA into the IC. These findings give support to the idea that unconditioned defensive responses generated in the IC may be mediated by NMDA mechanisms. Additionally, a reduction of the inhibitory control exerted by nigrocollicular GABAergic neurons seems to be responsible for the unexpected pro-aversive action of systemic injections of muscimol on the neural substrates of aversion mediated by NMDA in the IC.
机译：下丘脑（IC）的电刺激引起行为激活以及类似于对威胁情况的恐惧反应的自主反应。在局部注射GABA激动剂或拮抗剂分别抑制或模仿这些防御行为的范围内，GABA能机制对IC的厌恶神经基质施加强直抑制控制。最近，我们已经表明，全身注射GABA-A受体激动剂麝香酚出乎意料地增强了IC的电刺激强度逐渐增加引起的冻结和逃逸反应。考虑到IC中由兴奋性氨基酸（EAA）介导的神经回路可能与恐惧状态的整合有关，在本研究中，我们研究了将NMDA局部注入IC中引起的防御行为是否受到以下因素的影响：之前使用全身性麝香酚治疗，以及是否可以通过从黑质网状体（SNpr）投射到下丘的GABA能纤维来施加这种GABA能控制。大鼠植入了两个针对IC和SNpr的引导套管，通过它们可以用玻璃微量移液器进行药物微量输注，从而减少了脑损伤。手术后一周，动物将NMDA（7 nmol / 0.2 microl）或生理盐水注入IC内，并置于隔间的中间，可以测量行为反应，如冰冻，穿越，跳跃，饲养和转弯，如下所示：无条件恐惧的间接指标。这些动物用生理盐水或麝香酚（0.5 mg / kg，IP）或脑部注射生理盐水或麝香酚（1 mol / 0.2 il SNpr）进行预处理。应用于IC的NMDA产生了一种行为激活，所有行为指标均显着增加。 IP注射麝香酚或向SNpr注射可增强由NMDA微量注射至IC引起的防御反应。这些发现支持了IC中产生的无条件防御反应可能由NMDA机制介导的想法。此外，黑胶质胶体GABA能神经元施加的抑制控制作用的降低似乎是由ICDA介导的NMDA介导的muscimol全身性注射对厌恶的神经基质的出乎意料的促平均作用的原因。

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