Avril Nuche-Bricaire

Publications (3)11.79 Total impact

• Article: GABAA ρ receptor mechanisms in the rat amygdala and its role in the modulation of fear and anxiety

  Candy Flores-Gracia, Avril Nuche-Bricaire, Minerva Crespo-Ramírez, Ricardo Miledi, Kjell Fuxe, Miguel Pérez de la Mora
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  ABSTRACT: RationaleAccumulating evidence for the presence of GABAA ρ receptors within the amygdala which differ from other members of the GABAA receptor family in both subunit composition and functional properties has been recently obtained. ObjectivesThis work was conducted to study whether GABAA ρ receptors may have a putative role in the amygdaloid modulation of fear and anxiety. ResultsIt was found that the bilateral intra-amygdaloid administration (6–240pmol/side) of (1,2,5,6-tetrahydropyridine-4-yl)methylphosphinic acid, a selective GABAA ρ receptor antagonist, reduced dose-dependently the exploration of the open arms of the elevated plus-maze without affecting locomotion and increased the plasma levels of corticosterone. In contrast, bicuculline in the dose range used (1.8–60pmol/side) induced seizures, but had no effects on the exploration of the maze. ConclusionsIt is suggested that GABAA ρ receptors may have a role in the amygdaloid modulation of fear and anxiety. KeywordsAnxiety-Amygdala-GABA C receptors-GABA ρ receptors-Elevated plus-maze-Corticosterone-Intercalated paracapsular islands
  Psychopharmacologia 04/2012; 212(4):475-484. · 4.08 Impact Factor
• Article: GABA(A) ρ receptor mechanisms in the rat amygdala and its role in the modulation of fear and anxiety.

  Candy Flores-Gracia, Avril Nuche-Bricaire, Minerva Crespo-Ramírez, Ricardo Miledi, Kjell Fuxe, Miguel Pérez de la Mora
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  ABSTRACT: Accumulating evidence for the presence of GABA(A) ρ receptors within the amygdala which differ from other members of the GABA(A) receptor family in both subunit composition and functional properties has been recently obtained. This work was conducted to study whether GABA(A) ρ receptors may have a putative role in the amygdaloid modulation of fear and anxiety. It was found that the bilateral intra-amygdaloid administration (6-240 pmol/side) of (1,2,5,6-tetrahydropyridine-4-yl)methylphosphinic acid, a selective GABA(A) ρ receptor antagonist, reduced dose-dependently the exploration of the open arms of the elevated plus-maze without affecting locomotion and increased the plasma levels of corticosterone. In contrast, bicuculline in the dose range used (1.8-60 pmol/side) induced seizures, but had no effects on the exploration of the maze. It is suggested that GABA(A) ρ receptors may have a role in the amygdaloid modulation of fear and anxiety.
  Psychopharmacologia 12/2010; 212(4):475-84. · 4.08 Impact Factor
• Article: Role of the amygdaloid cholecystokinin (CCK)/gastrin-2 receptors and terminal networks in the modulation of anxiety in the rat. Effects of CCK-4 and CCK-8S on anxiety-like behaviour and [3H]GABA release.

  Miguel Pérez de la Mora, Ana María Hernández-Gómez, Yexel Arizmendi-García, Kirsten X Jacobsen, Daniel Lara-García, Candy Flores-Gracia, Minerva Crespo-Ramírez, Andrea Gallegos-Cari, Avril Nuche-Bricaire, Kjell Fuxe
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  ABSTRACT: The amygdala plays a key role in fear and anxiety. The intercalated islands are clusters of glutamate-responsive GABAergic neurons rich in cholecystokinin (CCK)-2 receptors which control the trafficking of nerve impulses from the cerebral cortex to the central nucleus of amygdala. In this study, the nature of the CCK-glutamate-GABA interactions within the rat rostral amygdala, and their relevance for anxiety, were studied. CCK/gastrin-like immunoreactive nerve terminals were found to be mainly restricted to the paracapsular intercalated islands and the rostrolateral part of the main intercalated island. Behaviourally, the bilateral microinjection of CCK-4 (0.043-4.3 pmol/side) or CCK-8S (4.3 pmol/side) into the rostrolateral amygdala reduced the open-arm exploration in the elevated plus-maze without affecting locomotion. In contrast, neither CCK-4 nor CCK-8S (0.043-4.3 pmol/side) had any effects in the shock-probe burying test as compared with their saline-treated controls. Biochemically, CCK-4 (0.3 and 1.5 microm), unlike CCK-8S, enhanced significantly the K(+)-stimulated release of [(3)H]GABA from amygdala slices. These effects were fully prevented by prior superfusion of the slices with either the selective CCK-2 receptor antagonist CR2945 (3 microm), or 6,7-dinitroquinoxaline-2,3(1H,4H)-dione (DNQX), 10 microm, a glutamatergic (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist. It is suggested that CCK modulates glutamate-GABA mechanisms by acting on CCK-2 receptors via volume transmission occurring at the level of the basolateral amygdaloid nucleus and/or by synaptic or perisynaptic volume transmission in the region of the rostrolateral main and paracapsular intercalated islands, resulting in subsequent disinhibition of the central amygdaloid nucleus and anxiety or panic-like behaviour.
  European Journal of Neuroscience 01/2008; 26(12):3614-30. · 3.63 Impact Factor