Escape behavior produced by the blockade of glutamic acid decarboxylase (GAD) in mesencephalic central gray or medial hypothalamus

Brandão, Marcus Lira; Scala, Georges Di; Bouchet, M.J.; Schmitt, Pierre

doi:10.1016/0091-3057(86)90547-2

Cited by 115 publications

(40 citation statements)

References 18 publications

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“…This finding is consistent with several reports showing that the neural substrate of aversion in the midbrain tectum is under tonic inhibitory control by GABA/benzodiazepine mechanisms (DiScala et al 1984;Brand¼o et al 1986Brand¼o et al , 1999Graeff 1990;Melo et al 1992;Pandossio and Brand¼o 1999). Moreover, it has been shown that benzodiazepine administration inhibits the expression of conditioned freezing to stimuli associated with foot-shocks (Kinscheck et al 1984;Fanselow and Helmstetter 1988;Fanselow 1991;Inoue et al 1996;Fendt and Fanselow 1999).…”

Section: Discussionsupporting

confidence: 91%

Role of benzodiazepine and serotonergic mechanisms in conditioned freezing and antinociception using electrical stimulation of the dorsal periaqueductal gray as unconditioned stimulus in rats

2002

Psychopharmacology

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(1) Conditioned freezing and antinociception are modulated by benzodiazepine mechanisms into dPAG. (2) 5-HT(2) receptors seem to regulate conditioned freezing behavior. However, conditioned antinociception was not affected by 13 nmol naltrexone. (3) Opioid mechanisms do not seem to be involved in the conditioned responses using electrical stimulation of the dPAG as unconditioned stimulus. Further studies with other opioid and 5-HT(2) receptor antagonists are still needed to confirm the conclusions drawn from the present work.

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Section: Discussionsupporting

confidence: 91%

Role of benzodiazepine and serotonergic mechanisms in conditioned freezing and antinociception using electrical stimulation of the dorsal periaqueductal gray as unconditioned stimulus in rats

2002

Psychopharmacology

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“…It has been shown that dPAG has a significant amount of GABAergic interneurons on which GAD blocking agents act, reducing the tonic inhibitory control exerted by GABA on the neural circuits of defensive behavior (Brandão et al 1986;DiScala and Sandner 1989;Aguiar and Brandão 1994). Indeed, defensive behaviors induced by the blockade of the GAD with semicarbazide were not affected by vPAG lesion.…”

Section: Vianna Et Almentioning

confidence: 90%

“…Also, it has been reported that glutamate microinjections in the same area produced freezing behavior (Krieger and Graeff 1985). Finally, microinjections into the dPAG of GABA receptor blockers or GABA inhibitors of glutamic acid decarboxylase (GAD), the enzyme responsible for GABA synthesis, produce fearlike behavior with a delay of action of ∼7 min (Brandão et al 1982(Brandão et al , 1986Schmitt et al 1985). Freezing, rapid running, and jumps characterize this response.…”

mentioning

confidence: 99%

Lesion of the Ventral Periaqueductal Gray Reduces Conditioned Fear but Does Not Change Freezing Induced by Stimulation of the Dorsal Periaqueductal Gray

Vianna¹,

Graeff²,

Landeira-Fernández³

et al. 2001

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Previously-reported evidence showed that freezing to a context previously associated with footshock is impaired by lesion of the ventral periaqueductal gray (vPAG). It has also been shown that stepwise increase in the intensity of the electrical stimulation of the dorsal periaqueductal gray (dPAG) produces alertness, then freezing, and finally escape. These aversive responses are mimicked by microinjections of GABA receptor antagonists, such as bicuculline, or blockers of the glutamic acid decarboxylase (GAD), such as semicarbazide, into the dPAG. In this work, we examined whether the expression of these defensive responses could be the result of activation of ventral portion of the periaqueductal gray. Sham- or vPAG electrolytic–lesioned rats were implanted with an electrode in the dPAG for the determination of the thresholds of freezing and escape responses. The vPAG electrolytic lesions were behaviorally verified through a context-conditioned fear paradigm. Results indicated that lesion of the vPAG disrupted conditioned freezing response to contextual cues associated with footshocks but did not change the dPAG electrical stimulation for freezing and escape responses. In a second experiment, lesion of the vPAG also did not change the amount of freezing and escape behavior produced by microinjections of semicarbazide into the dPAG. These findings indicate that freezing and escape defensive responses induced by dPAG stimulation do not depend on the integrity of the vPAG. A discussion on different neural circuitries that might underlie different inhibitory and active defensive behavioral patterns that animals display during threatening situations is presented.

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“…DPAG has been shown to contain a significant number of GABAergic interneurons that play an important inhibitory role on the regulation of defensive behavior (Brandão et al 1986;DiScala & Sandner 1989). For example, DPAG microinjections of GABA receptor antagonists or inhibitors of glutamic acid decarboxylase, the enzyme responsible for GABA synthesis, produced unambiguous active defensive responses such as running and jumping (Brandão et al 1982(Brandão et al , 1986Schmitt et al 1985). Therefore, intraperitoneal injection of high doses of PTZ in the Shenberg et al (2001) study might have led to a decrease in GABA A receptor function within the DPAG, thus facilitating escape reactions induced by stimulation of this area.…”

Section: Discussionmentioning

confidence: 99%

Effects of contextual fear conditioning and pentylenetetrazol on panic-like reactions induced by dorsal periaqueductal gray stimulation with N-methyl-D-aspartate.

Galvão

Larrubia

Hommes

et al. 2010

Psychology & Neuroscience

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Electrical or chemical stimulation of the dorsal periaqueductal gray (DPAG) has been accepted as an animal model of panic attacks. This study investigates the influence of anticipatory anxiety in the occurrence of panic-like behavior induced by N-methyl-Daspartate (NMDA) microinjection into the DPAG of rats. Behavioral (i.e., contextual fear conditioning) and pharmacological (i.e., pentylenetetrazol) manipulations were employed as animal models of anticipatory anxiety. In the first experiment, animals exposed to contextual cues that had been previously associated with electric footshocks through contextual fear conditioning were less likely than non-conditioned control animals to display defensive reactions such as running and jumping in response to microinjection of NMDA (0.3 µl of 15.0 µg/µl) into the DPAG. In the second experiment, rats were injected intraperitoneally with the anxiogenic drug pentylenetetrazol (PTZ, 15 mg/kg) 5 minutes before receiving intra-DPAG microinfusion with the same dose of NMDA as in Experiment 1. Panic-related behaviors were registered in an experimental arena immediately after NMDA microinfusion. As compared with saline pre-treated animals, PTZ significantly attenuated NMDA-induced panic-like reactions. These results further demonstrate the usefulness of DPAG chemical stimulation as an animal model of panic attacks and suggest that behavioral and pharmacological activation of the brain mechanisms underlying anticipatory anxiety might exert an antipanic-like effect.

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Escape behavior produced by the blockade of glutamic acid decarboxylase (GAD) in mesencephalic central gray or medial hypothalamus

Cited by 115 publications

References 18 publications

Role of benzodiazepine and serotonergic mechanisms in conditioned freezing and antinociception using electrical stimulation of the dorsal periaqueductal gray as unconditioned stimulus in rats

Role of benzodiazepine and serotonergic mechanisms in conditioned freezing and antinociception using electrical stimulation of the dorsal periaqueductal gray as unconditioned stimulus in rats

Lesion of the Ventral Periaqueductal Gray Reduces Conditioned Fear but Does Not Change Freezing Induced by Stimulation of the Dorsal Periaqueductal Gray

Effects of contextual fear conditioning and pentylenetetrazol on panic-like reactions induced by dorsal periaqueductal gray stimulation with N-methyl-D-aspartate.

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