Amygdaloid circuitry in the innate fear modulation

Abstract

Tonic immobility (IT) is a behavioral defensive innate fear triggered in situations of inescapable confrontation between predator-prey. This response is characterized by loss of righting reflex and the relative lack of responsiveness to environmental stimuli. Consistent studies have shown the involvement of different brain areas to modulate this response, including the periaqueductal gray, hypothalamus and amygdala. Considering the amygdala in particular our studies have shown the involvement of different neurotransmitter circuits (Brain Research Bulletin, 58: 13-19, 2002; Brain Research Bulletin, 60: 167-178, 2003; Brain Research Bulletin, 69: 356-364 , 2006; Brain Research Bulletin, 79: 358-364, 2009) among them systems cholinergic, opioidergic, serotonergic and GABAergic as well as interactions between these systems. Recently, we have demonstrated the involvement of receptors for corticotropin-releasing factor (CRF), the basolateral nucleus (BLA) or central (CEA) of the amygdala in the modulation of innate fear (Behavioural Brain Research, 225: 23-30, 2011, Advances in Bioscience and Biotechnology, 4: 20-27, 2013). In addition to the central and basolateral nucleus, medial nuclei / basomedial amygdala (Zoology Advances in Research, Vol. 1. Jenkins OP (ed.), Nova Science Publishers, New York, 2012, pp. 172-188) are closely related to behavioral modulation of innate and conditioned fear, possibly due to their reciprocal connections with hypothalamic nuclei responsible for the control of defensive behaviors. Thus, the goal of this project is to investigate the involvement of specific receptors for corticotropin-releasing factor, CRF1 and CRF2 basolateral and central nuclei of the amygdala in response modulation of IT in guinea pigs. In addition, a second step of this project will evaluate the participation of the GABAergic system (GABAA and GABAB) the medial nucleus / basomedial amygdala in modulating the response of IT in guinea pigs. In addition will assess the anatomical connections of the nucleus basomedial (BMA) of the amygdala in an attempt to substantiate the mechanisms of participation of this nucleus in the modulation of tonic immobility response. To exclude the possibility that the treatment promotes change in motor behavior, and change the response of IT nonspecifically, will be held the open field test, with all the drugs used in the study. (AU)