“…The findings of our study support a critical role of SP neurotransmission within the PAG in fear-potentiated startle and indicate more specifically that these effects may be mediated primarily by SP receptors in the rostral dlPAG. Perhaps not by coincidence, this is a region that receives a dense projection from the VMH (Bandler and Shipley, 1994;Canteras et al, 1994;Siegel et al, 1997), and approximately 30% of these projections contain SP (Dornan et al, 1990). However, the projections outlined in this paper went to a significantly more caudal region of the dlPAG than was targeted by any of the injections performed as part of the present study.…”
Section: Discussionmentioning
confidence: 57%
“…Lesions of the VMH have been shown to disrupt other affective behaviors (Colpaert and Wiepkema, 1976;de Oliveira et al, 1997;Dielenberg et al, 2001;Han et al, 1996;Sudakov, 1987). Moreover, SP-containing afferents from the VMH project to the periaqueductal gray (PAGFDornan et al, 1990), which in turn projects to the pontine startle reflex circuit (Cameron et al, 1995;Canteras et al, 1994;Fendt et al, 1994;Meloni and Davis, 1999;Siegel et al, 1997). Thus, it is conceivable that the SP-containing MeA-VMH-PAG-pontine circuit may participate in or be required for the full expression of fear-potentiated startle.…”
The neural pathways through which substance P (SP) influences fear and anxiety are poorly understood. However, the amygdala, a brain area repeatedly implicated in fear and anxiety processes, is known to contain large numbers of SP-containing neurons and SP receptors. Several studies have implicated SP neurotransmission within the amygdala in anxiety processes. In the present study, we evaluated the effects of site-specific infusions of an SP receptor antagonist, GR 82334, on conditioned fear responses using the fear-potentiated startle paradigm. GR 82334 infusion into the basolateral (BLA) or the medial (MeA) nuclei of the amygdala, but not into the central nucleus of the amygdala (CeA), dose dependently reduced fear-potentiated startle. Similar effects were obtained with GR 82334 infusion into the ventromedial nucleus of the hypothalamus (VMH), to which the MeA projects, and into the rostral dorsolateral periaqueductal gray (PAG), to which the VMH projects, but not into the deep layers of the superior colliculus/deep mesencephalic nucleus (dSC/DpMe), an output of the CeA previously shown to be important for fear-potentiated startle. Consistent with previous findings, infusion of the AMPA receptor antagonist, NBQX, into the dSC/DpMe, but not into the PAG, did disrupt fear-potentiated startle. These findings suggest that multiple outputs from the amygdala play a critical role in fear-potentiated startle and that SP plays a critical, probably modulatory role, in the MeA to VMH to PAG to the startle pathway based on these and data from others.
“…The findings of our study support a critical role of SP neurotransmission within the PAG in fear-potentiated startle and indicate more specifically that these effects may be mediated primarily by SP receptors in the rostral dlPAG. Perhaps not by coincidence, this is a region that receives a dense projection from the VMH (Bandler and Shipley, 1994;Canteras et al, 1994;Siegel et al, 1997), and approximately 30% of these projections contain SP (Dornan et al, 1990). However, the projections outlined in this paper went to a significantly more caudal region of the dlPAG than was targeted by any of the injections performed as part of the present study.…”
Section: Discussionmentioning
confidence: 57%
“…Lesions of the VMH have been shown to disrupt other affective behaviors (Colpaert and Wiepkema, 1976;de Oliveira et al, 1997;Dielenberg et al, 2001;Han et al, 1996;Sudakov, 1987). Moreover, SP-containing afferents from the VMH project to the periaqueductal gray (PAGFDornan et al, 1990), which in turn projects to the pontine startle reflex circuit (Cameron et al, 1995;Canteras et al, 1994;Fendt et al, 1994;Meloni and Davis, 1999;Siegel et al, 1997). Thus, it is conceivable that the SP-containing MeA-VMH-PAG-pontine circuit may participate in or be required for the full expression of fear-potentiated startle.…”
The neural pathways through which substance P (SP) influences fear and anxiety are poorly understood. However, the amygdala, a brain area repeatedly implicated in fear and anxiety processes, is known to contain large numbers of SP-containing neurons and SP receptors. Several studies have implicated SP neurotransmission within the amygdala in anxiety processes. In the present study, we evaluated the effects of site-specific infusions of an SP receptor antagonist, GR 82334, on conditioned fear responses using the fear-potentiated startle paradigm. GR 82334 infusion into the basolateral (BLA) or the medial (MeA) nuclei of the amygdala, but not into the central nucleus of the amygdala (CeA), dose dependently reduced fear-potentiated startle. Similar effects were obtained with GR 82334 infusion into the ventromedial nucleus of the hypothalamus (VMH), to which the MeA projects, and into the rostral dorsolateral periaqueductal gray (PAG), to which the VMH projects, but not into the deep layers of the superior colliculus/deep mesencephalic nucleus (dSC/DpMe), an output of the CeA previously shown to be important for fear-potentiated startle. Consistent with previous findings, infusion of the AMPA receptor antagonist, NBQX, into the dSC/DpMe, but not into the PAG, did disrupt fear-potentiated startle. These findings suggest that multiple outputs from the amygdala play a critical role in fear-potentiated startle and that SP plays a critical, probably modulatory role, in the MeA to VMH to PAG to the startle pathway based on these and data from others.
“…However, Cameron et al (7) have shown that none of the columns of the PAG send direct projections to the PVN. On the other hand, the l/dlPAG sends projections to the DMH (7,38,39), a region that has been implicated in diverse stress-induced effects, including activation of the hypothalamic-pituitary-adrenal axis. Stotz-Potter and colleagues have shown that microinjection of muscimol into the DMH nearly abolishes the increases in HR and MAP seen in this paradigm and also reduces the accompanying increases in plasma ACTH levels (46).…”
de Menezes RC, Zaretsky DV, Sarkar S, Fontes MA, DiMicco JA. Microinjection of muscimol into the periaqueductal gray suppresses cardiovascular and neuroendocrine response to air jet stress in conscious rats.
“…An increasing body of data further suggests that the serotonergic system also plays a principal role in the regulation of attack and defense [49][50][51][52][53]. It has been shown that 5-HT exerts an inhibitory influence on defensive forms of aggression through the activation of 5-HT 1A receptors [54,55]. However, activation of the 5-HT 2 receptor in the midbrain PAG potentiates defensive rage behavior [56].…”
Many studies have investigated different mechanisms of attack and defense in different species of higher brain animals including cats, rats, rodents, mice, and even in some bird species. However, detailed comparative analysis has not been carried out to understand the major similarities in the mechanisms of attack and defense across the different species of vertebrates. Although there are differences, there are also significant similarities as well, which warrant comparative assessment. By considering ethological ideas associated with the motivational defense system, we investigated the motor patterns of attack and defense in cats and rats, using the "resident-intruder" experimental paradigm. Our results reveal specific similarities and differences in the motor patterns of attack and defense in rats and cats. We discuss comparatively the mechanisms of attack and defense across different species of vertebrates, focusing on motor patterns, neuromodulating factors, brains neural substrates, and circuitry.
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