Abstract
Electrical stimulation of midbrain tectum structures, particularly the dorsal periaqueductal gray (dPAG) and inferior colliculus (IC), produces defensive responses, such as freezing and escape behavior. Freezing also ensues after termination of dPAG stimulation (post-stimulation freezing). These defensive reaction responses are critically mediated by Y-aminobutyric acid and 5-hydroxytryptamine mechanisms in the midbrain tectum. Neurokinins (NKs) also play a role in the mediation of dPAG stimulation-evoked fear, but how NK receptors are involved in the global processing and expression of fear at the level of the midbrain tectum is yet unclear. The present study investigated the role of NK-1 receptors in unconditioned defensive behavior induced by electrical stimulation of the dPAG and IC of male Wistar rats. Spantide (100 pmol/0.2 µL), a selective NK-1 antagonist, injected into these midbrain structures had anti-aversive effects on defensive responses and distress ultrasonic vocalizations induced by stimulation of the dPAG but not of the IC. Moreover, intra-dPAG injections of spantide did not influence post-stimulation freezing or alter exploratory behavior in rats subjected to the elevated plus maze. These results suggest that NK-1 receptors are mainly involved in the mediation of defensive behavior organized in the dPAG. Dorsal periaqueductal gray-evoked post-stimulation freezing was not affected by intra-dPAG injections of spantide, suggesting that NK-1-mediated mechanisms are only involved in the output mechanisms of defensive behavior and not involved in the processing of ascending aversive information from the dPAG.
Highlights
Electrical and chemical stimulation of the dorsal periaqueductal gray and inferior colliculus (IC) causes a characteristic pattern of active defense reactions, which include alertness, freezing, escape responses, and autonomic changes that resemble anxiety disorder [1,2]
As the intensity of the current applied to the dorsal periaqueductal gray (dPAG) and IC increased, the animals suddenly stopped their ongoing behavior, became immobile, and often urinated and defecated
The electrical stimulation applied to the dPAG would activate fibers of passage through this region, the volume of 0.2 μL does not spread in a tissue diameter higher than 0.4 mm in the midbrain tectum [27]
Summary
Electrical and chemical stimulation of the dorsal periaqueductal gray (dPAG) and inferior colliculus (IC) causes a characteristic pattern of active defense reactions, which include alertness, freezing, escape responses, and autonomic changes that resemble anxiety disorder [1,2]. Much evidence has implicated γ-aminobutyric acid (GABA), 5-hydroxytryptamine (5-HT), excitatory amino acids, nitric oxide, and opioids in the modulation of defense reactions in these midbrain tectum structures, but less is known about the involvement of neurokinin (NK)-mediated mechanisms in these responses (for a review, see Ref. 3). Substance P is widely distributed in the brain, including the amygdala, septum, hippocampus, and hypothalamus, and is involved in the regulation of affective behavior and the mediation of stress responses [4,5]. Substance P has been implicated in the mediation of fear in the dPAG [6,7]. Substance P has been shown to be involved in stress-, depression-, and anxiety-related behaviors [9,10]. The presence of substance P and NK receptors in the IC has been documented in the literature [11], to our knowledge, no study has investigated the possible role of NK-mediated mechanisms in the IC in Presented at the III Fórum em Neurobiologia do Estresse, Araraquara, SP, Brazil, September 8-10, 2011
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