Defense reaction mediated by XXXX mechanisms in the inferior colliculus is modulated by GABAergic nigro-collicular pathways.

@entity1522 @entity6341 @entity1246 @entity75 @entity143 @entity35
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 @entity1246 agonists or antagonists inhibit or mimic these defensive behaviors, respectively. Recently, we have shown that systemic injections of the @entity1246 -A receptor agonist @entity6341 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 @entity1522 (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 @entity143 into the IC is influenced by prior treatment with systemic @entity6341 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). @entity35 were implanted with two guide-cannulae aimed at the IC and SNpr through which drug microinfusions with glass micropipette could be made with reduced @entity75 . One week after surgery, the animals received either @entity143 (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 @entity6341 (0.5 mg/kg, IP) or with brain injections of saline or @entity6341 (1 nmol/0.2   l into SNpr). @entity143 applied into the IC produced a behavioral activation with significant increases in all behavioral measures. IP injections of @entity6341 or into the SNpr enhanced the defense reaction caused by microinjections of @entity143 into the IC. These findings give support to the idea that unconditioned defensive responses generated in the IC may be mediated by @entity143 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 @entity6341 on the neural substrates of aversion mediated by @entity143 in the IC.
