Neurochemical mechanisms of the defensive behavior in the dorsal midbrain

Brandão, Marcus Lira; Anseloni, V. Z.; Pandossio, José Eduardo; Araújo, João Luiz Vitorino; Castilho, V.M.

doi:10.1016/s0149-7634(99)00038-x

Cited by 256 publications

(172 citation statements)

References 114 publications

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“…Based on evidence from this and other laboratories, we have proposed that the IC contributes to some basic link between auditory inputs of aversive nature, and the generation and elaboration of defensive behavior in response to threat or danger (see Brandão et al (1999) for a review on this topic). Furthermore, we have shown that electrical stimulation of the IC of rats in intensity sufficient to induce escape behavior enhances subsequent fear-like behaviors when behaviorally tested in the elevated plusmaze test (Pandossio et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…One of these pathways is provided by projections from the central nucleus of the IC to the prefrontal cortex through the medial geniculate nucleus, amygdala and dorsomedial thalamus (Fuster, 1989;Brodal, 1992). It has been shown that this circuit is concerned with the processing of auditory information of an aversive nature which triggers fear-like behaviors (Maisonnette et al, Hoffman 1996;Brandão et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Troncoso¹,

Osaki²,

Mason³

et al. 2003

Neuropsychopharmacol

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Consistent evidence has shown that learning may be produced in paradigms using electrical stimulation of the inferior colliculus (IC) as unconditioned stimulus (UCS). Recent reports have also demonstrated that aversive stimulation of the IC, at the escape threshold, enhances dopamine (DA) release in the prefrontal cortex. The purpose of the present study was to determine whether dopaminergic mechanisms are involved in the Pavlovian conditioning and latent inhibition using IC stimulation as UCS and light as conditioned stimulus (CS). Rats were placed inside a shuttle box and subjected to a two-way avoidance paradigm. IC aversive electrical stimulation was used as UCS and shuttle box illumination as CS. The rats quickly learned to avoid or interrupt the IC stimulation. Apomorphine injections produced a dose-dependent increase in the number of avoidance responses. On the other hand, chlorpromazine administration promoted a dose-dependent reduction of the avoidance responses. Previous injections of chlorpromazine inhibited the effects of apomorphine. Also, previous exposure to unreinforced light weakened the strength of the conditioning. Apomorphine blocked this latent inhibition effect, which was antagonized by previous injections of chlorpromazine. These findings bring evidence for the involvement of DA in the setting up of adaptive responses to aversive states generated at the IC level, which may underlie stressful situations present in anxiety.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Troncoso¹,

Osaki²,

Mason³

et al. 2003

Neuropsychopharmacol

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show abstract

“…Other areas, which have been reported to be activated by subcutaneous nicotine injection in adolescents and/or adults (Park et al, 2006), including CeA, BNST, NAc, and SC, showed increased c-fos expression following intravenous drug administration with no significant effect of age. Acetalde- Interactions of nicotine and acetaldehyde J Cao et al hyde potentiated the effect of nicotine in two of these regions, SC and CeA, which are involved in defensive behaviors (Brandao et al, 1999). In contrast, this did not occur in NAc and BNST, which are more involved in the regulation of appetitive behaviors and neuroendocrine output (Swanson, 2000).…”

Section: Mechanismsmentioning

confidence: 99%

Acetaldehyde, a Major Constituent of Tobacco Smoke, Enhances Behavioral, Endocrine, and Neuronal Responses to Nicotine in Adolescent and Adult Rats

Cao

Belluzzi

Loughlin

et al. 2007

Neuropsychopharmacol

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We have previously shown that acetaldehyde, a constituent of tobacco smoke, increases nicotine self-administration in adolescent, but not adult, rats. The aim of this study was to determine whether acetaldehyde influences other behavioral, endocrine, or neuronal responses to nicotine at either age. Juvenile (postnatal day (P) 27) and adult (P90) male Sprague-Dawley rats were treated with saline, acetaldehyde (16 mg/kg/injection Â 2, i.v.), nicotine (30 mg/kg/injection Â 2, i.v.) or a combination of acetaldehyde and nicotine. Locomotion and center time were evaluated for 30 min in a novel open field, before measurement of plasma corticosterone levels and brain c-fos mRNA. Nicotine increased locomotor activity in juveniles but decreased it in adults; in contrast, center time was increased at both ages. Acetaldehyde potentiated nicotine's locomotor effects, but not center time. Nicotine induced c-fos expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults. Acetaldehyde potentiated nicotine-induced c-fos in CeA and SC, and activation of PVN c-fos expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed. Thus, acetaldehyde may modulate the interaction of nicotine and stress. Although pharmacokinetic studies showed that acetaldehyde did not change nicotine levels in either brain or serum, nicotine penetration into the brain was slower in juveniles as compared to adults.

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“…The periaqueductal gray (PAG) has been shown to be involved in the modulation of nociception (Fardin, et al, 1984;Liebeskind, et al, 1973;Morgan, et al, 1991;Morgan, et al, 1989), regulation of the autonomic system (Depaulis, et al, 1988;Hayward, et al, 2003), and in the expression of a variety of behaviors, including sexual (Sakuma and Pfaff, 1979), maternal (Lonstein and Stern, 1997), feeding (Van Erp, et al, 1993) and defensive behaviors (Blanchard, et al, 1981;Brandao, et al, 1999;Carrive, 1993;Depaulis, et al, 1992;Fanselow, 1991;Keay and Bandler, 2001) (for review see (Behbehani, 1995)). Canteras (2002) proposed that a medial hypothalamic defensive system (MHZ) mediates stimulus activation of the defense response elicited by a psychological threat stimulus, a predator.…”

Section: Introductionmentioning

confidence: 99%

“…These include glutamate agonists, γ-amino-butyric-acid (GABA), serotonin (5HT), cholecystokinin (CCK) and neuropeptides such as opioids and corticotropin releasing factor (CRF) (Brandao et al, 1999;Brandao, et al, 1982;Cardoso, et al, 1994;Carvalho-Netto, et al, 2007;Graeff, 1997;Jenck, et al, 1986;Melo, et al, 1992). Receptor binding studies have shown a substantial population of both CRF1 and CRF2 in the PAG (Merchenthaler, 1984;Swanson, et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

CRF type 1 receptors in the dorsal periaqueductal gray modulate anxiety-induced defensive behaviors

Litvin

Pentkowski

Blanchard

et al. 2007

Hormones and Behavior

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Neurochemical mechanisms of the defensive behavior in the dorsal midbrain

Cited by 256 publications

References 114 publications

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Acetaldehyde, a Major Constituent of Tobacco Smoke, Enhances Behavioral, Endocrine, and Neuronal Responses to Nicotine in Adolescent and Adult Rats

CRF type 1 receptors in the dorsal periaqueductal gray modulate anxiety-induced defensive behaviors

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