Evidence that substance P is utilized in medial amygdaloid facilitation of defensive rage behavior in the cat

Shaikh, Majid B.; Steinberg, Anda; Siegel, Allan

doi:10.1016/0006-8993(93)91070-9

Cited by 125 publications

(41 citation statements)

References 48 publications

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“…In fact, this pathway has previously been shown to be critical in mediating defensive rage and predatory attack in cats (Han et al, 1996;Shaikh et al, 1993). We found that GR 82334 infusions into the VMH also blocked fear-potentiated startle.…”

Section: Discussionsupporting

confidence: 51%

“…Early studies have shown that the VMH also is involved in fear and anxiety (Colpaert and Wiepkema, 1976;de Oliveira et al, 1997;Dielenberg et al, 2001;Han et al, 1996;Sudakov, 1987) and, interestingly, the VMH itself receives a heavy SPcontaining input from the MeA (Petrovich et al, 2001;Shaikh et al, 1993). In fact, this pathway has previously been shown to be critical in mediating defensive rage and predatory attack in cats (Han et al, 1996;Shaikh et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…It is unclear how the MeA influences fear-potentiated startle as it does not project directly to the startle reflex circuit, the dSC/DpMe, or the CeA (Canteras et al, 1995). However, the MeA does have heavy projections to the ventromedial nucleus of the hypothalamus (VMH), and this pathway was found to contain SP (Canteras et al, 1994(Canteras et al, , 1995Han et al, 1996;Shaikh et al, 1993). 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).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Substance P in the Amygdala, Ventromedial Hypothalamus, and Periaqueductal Gray on Fear-Potentiated Startle

Zhao

Yang

Walker

et al. 2008

Neuropsychopharmacol

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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.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Substance P in the Amygdala, Ventromedial Hypothalamus, and Periaqueductal Gray on Fear-Potentiated Startle

Zhao

Yang

Walker

et al. 2008

Neuropsychopharmacol

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“…In addition, an analysis of a behavioral quantitative trait locus in mouse showed that RGS2 modulated anxiety (Yalcin et al, 2004). In animals and humans, the amygdala is believed to control emotions such as fear and anxiety and behaviors such as impulsive violence (Phelps and LeDoux, 2005;Shaikh et al, 1993). Fear, anxiety and impulsive violence have all been proposed as risk factors for suicide (Sareen et al, 2005;Dumais et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Association of RGS2 Gene Polymorphisms with Suicide and Increased RGS2 Immunoreactivity in the Postmortem Brain of Suicide Victims

Cui

Nishiguchi

Ivleva

et al. 2007

Neuropsychopharmacol

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Regulators of G-protein signaling are a family of proteins that negatively regulate the intracellular signaling of G protein-coupled receptors, such as the serotonin receptor. Recent studies have suggested that one of these proteins, the regulator of G-protein signaling 2 (RGS2), plays an important part in anxiety and/or aggressive behavior. To explore the involvement of the RGS2 gene in the vulnerability to suicide, we screened Japanese suicide victims for sequence variations in the RGS2 gene and carried out an association study of RGS2 gene polymorphisms with suicide victims. In the eight identified polymorphisms that were identified by mutation screening, we genotyped four common single-nucleotide polymorphisms (SNPs) in the RGS2 gene, and found significant differences in the distribution of the SNP3 (C + 2971G, rs4606) genotypes and alleles of the SNP2 (C-395G, rs2746072) and the SNP3 between completed suicides and the controls. The distribution of the haplotype was also significantly different between the two groups (global po0.0001). Furthermore, RGS2 immunoreactivity significantly increased in the amygdala and the prefrontal cortex (Brodmann area 9 (BA9)) of the postmortem brain of the suicide subjects. These findings suggest that RGS2 is genetically involved in the biological susceptibility to suicide in the Japanese population.

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“…In cats, the medial amygdala and its major output region 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 BNST inhibit predatory attacks, whereas the central and basolateral nuclei facilitate this response [1,[42][43][44][45][46]. Our findings are in line with these reports by showing a muricide-specific activation of the central and basolateral nuclei.…”

Section: Comparisons With Earlier Findingsmentioning

confidence: 99%

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

Tulogdi

Biró

Barsvári

et al. 2015

Behavioural Brain Research

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Our recent studies showed that brain areas that are activated in a model of escalated aggression overlap with those that promote predatory aggression in cats. This finding raised the interesting possibility that the brain mechanisms that control certain types of abnormal aggression include those involved in predation. However, the mechanisms of predatory aggression are poorly known in rats, a species that is in many respects different from cats. To get more insights into such mechanisms, here we studied the brain activation patterns associated with spontaneous muricide in rats. Subjects not exposed to mice, and those which did not show muricide were used as controls. We found that muricide increased the activation of the central and basolateral amygdala, and lateral hypothalamus as compared to both controls; in addition, a ventral shift in periaqueductal gray activation was observed.Interestingly, these are the brain regions from where predatory aggression can be elicited, or enhanced by electrical stimulation in cats. The analysis of more than 10 other brain regions showed that brain areas that inhibited (or were neutral to) cat predatory aggression were not affected by muricide. Brain activation patterns partly overlapped with those seen earlier in the cockroach hunting model of rat predatory aggression, and were highly similar with those observed in the glucocorticoid dysfunction model of escalated aggression. These findings show that the brain mechanisms underlying predation are evolutionarily conservative, and indirectly support our earlier assumption regarding the involvement of predation-related brain mechanisms in certain forms of escalated social aggression in rats.

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Evidence that substance P is utilized in medial amygdaloid facilitation of defensive rage behavior in the cat

Cited by 125 publications

References 48 publications

Effects of Substance P in the Amygdala, Ventromedial Hypothalamus, and Periaqueductal Gray on Fear-Potentiated Startle

Effects of Substance P in the Amygdala, Ventromedial Hypothalamus, and Periaqueductal Gray on Fear-Potentiated Startle

Association of RGS2 Gene Polymorphisms with Suicide and Increased RGS2 Immunoreactivity in the Postmortem Brain of Suicide Victims

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

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