Hippocampal 5-HT receptors and consolidation of stressful memories

Guimarães, Francisco Silveira; Bel, Elaine Aparecida Del; Padovan, Cláudia Maria; Netto, Sueli Mendonça; Almeida, R.Titze de

doi:10.1016/0166-4328(93)90098-b

Cited by 106 publications

(56 citation statements)

References 40 publications

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“…A key mechanism of action of antidepressant agents is to enhance the efficacy of 5-HT neurotransmission, which occurs following chronic treatment. In the hippocampus, this would restore the capacity to tolerate chronic stress (for reviews of this topic and original references, see references [20][21] ).…”

Section: Anxietymentioning

confidence: 99%

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Graeff

2007

Rev. Bras. Psiquiatr.

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A b s t r a c t Objective: This article focuses on the differential activation of the hypothalamic-pituitary-adrenal axis in generalized anxiety disorder and panic disorder. Method: The results of recently reported reviews of the literature are summarized and discussed. Results: The results of experimental studies that assayed adrenocorticotropic hormone, cortisol and prolactin show that real-life panic attacks, as well as those induced by selective panicogenic agents such as lactate and carbon dioxide, do not activate the hypothalamic-pituitary-adrenal axis. Agonists of the cholecystokinin receptor B such as the cholecystokinin-4 peptide and pentagastrin increase stress hormones regardless of the occurrence of a panic attack and, thus, seem to activate the hypothalamicpituitary-adrenal axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increase anxiety in both normal people and panic patients (caffeine, yohimbine, serotonergic agonists) raise stress hormone levels. Conclusions: In addition to the differences in symptomatology and pharmacological response, generalized anxiety disorder and panic disorder affect stress hormones in distinct ways. While anticipatory anxiety and generalized anxiety disorder activate both the hypothalamic-pituitary-adrenal and the sympathoadrenal axes, panic attack causes major sympathetic activation, but has little effect on the hypothalamic-pituitaryadrenal axis.Descriptors: Stress; Hormones; Anxiety disorders; Hypothalamus; Pituitary-adrenal system Resumo Objetivo: Este artigo discute a ativação diferencial do eixo hipotálamo-pituitária-adrenal no transtorno de ansiedade generalizada e no transtorno de pânico. Método: Resultados de recentes revisões da literatura são resumidos e discutidos. Resultados: Os resultados de estudos experimentais que dosaram o hormônio adrenocorticotrópico, o cortisol e a prolactina mostram que ataques de pânico espontâneos, bem como os provocados por agentes panicogênicos seletivos -como lactato de sódio e dióxido de carbono -, não ativam o eixo hipotálamo-pituitária-adrenal. Agonistas do receptor de colecistocinina do tipo B, como o peptídeo colecistocinina-4 e pentagastrina, elevam os hormônios de estresse, independentemente da ocorrência de um ataque de pânico, parecendo ativar diretamente o eixo hipotálamo-pituitária-adrenal. O antagonista benzodiazepínico flumazenil não eleva o nível dos hormônios de estresse; porém, este agente farmacológico não induz ataques de pânico de modo consistente. Agentes farmacológicos que aumentam a ansiedade em pacientes de pânico (cafeína, ioimbina, agonistas serotonérgicos), assim como em pessoas saudáveis, elevam o nível dos hormônios de estresse. Conclusões: Além das diferenças na sintomatologia e na resposta farmacológica, o transtorno de ansiedade generalizada e o transtorno de pânico afetam os hormônios de estresse de modo distinto. Enquanto a ansiedade antecipatória e o transtorno de ansied...

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Section: Anxietymentioning

confidence: 99%

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Graeff

2007

Rev. Bras. Psiquiatr.

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“…For example, rats submitted to 2 h of restraint show an exploratory deficit of new environments such as an open arena 24 h after the stress (2)(3)(4)(5), suggesting that previous stressful experiences may modify the animal response to new aversive stimuli (2). Neurochemical changes such as an increase in benzodiazepine receptor affinity in the frontal cortex (6) or an increase in the 5HIAA serotonin metabolite in the same region and in the hippocampus and raphe nuclei (7) have also been reported.…”

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confidence: 99%

“…We have recently shown that the restraintinduced decreased activity is also evident when the animal is exposed to the elevated plus-maze, an animal model of anxiety (2)(3)(4)(5).…”

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Restraint-induced hypoactivity in an elevated plus-maze

Padovan

Guimarães

2000

Braz J Med Biol Res

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109

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Rodents submitted to restraint stress show decreased activity in an elevated plus-maze (EPM) 24 h later. The objective of the present study was to determine if a certain amount of time is needed after stress for the development of these changes. We also wanted to verify if behavioral tolerance of repeated daily restraint would be detectable in this model. Male Wistar rats were restrained for 2 h and tested in the EPM 1, 2, 24 or 48 h later. Another group of animals was immobilized daily for 2 h for 7 days, being tested in the EPM 24 h after the last restraint period. Restraint induced a significant decrease in the percent of entries and time spent in the open arms, as well as a decrease in the number of enclosed arm entries. The significant effect in the number of entries and the percentage of time spent in the open arms disappeared when the data were submitted to analysis of covariance using the number of enclosed arm entries as a covariate. This suggests that the restraint-induced hypoactivity influences the measures of open arm exploration. The modifications of restraint-induced hypoactivity are evident 24 or 48 h, but not 1 or 2 h, after stress. In addition, rats stressed daily for seven days became tolerant to this effect.

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“…Aversive stimuli such as an electric footshock can induce rotational behavior in rats (14) and it has been suggested that turnings may be part of the defensive repertoire of these animals (15). Rearings are often used to evaluate exploratory activity (16) and a decrease in exploratory drive has been observed in rats submitted to stressful events (17). Many studies suggest that grooming behavior is increased by a mild aversive stimulus; however, the response varies with the degree of fear and the habituation to the stressful situation (18).…”

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Defense reaction induced by a metabotropic glutamate receptor agonist microinjected into the dorsal periaqueductal gray of rats

Molchanov

Guimarães

1999

Braz J Med Biol Res

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The behavioral effects of trans-(±)-1-amino-1,3-cyclopentanedicarboxylic acid (t-ACPD), a metabotropic glutamate receptor (mGluR) agonist, or 0.9% (w/v) saline, injected into the dorsal periaqueductal gray (DPAG), was investigated. Male Wistar rats showed defense reactions characterized by jumps toward the top edges of the cages (saline = 0 vs t-ACPD = 6.0, medians P<0.05) and gallops (saline = 0 vs t-ACPD = 10.0, medians P<0.05) during the 60-s period after the beginning of the injection. In another experiment animals were placed inside an open arena for 5 min immediately after injection. Their behavior was recorded by a video camera and a computer program analyzed the videotapes. Eleven of fifteen rats injected with t-ACPD showed a short-lasting (about 1 min) flight reaction. No saline-treated animal showed this reaction (P<0.0005, chi-square test). The drug induced an increase in turning behavior (P = 0.002, MANOVA) and a decrease in the number of rearings (P<0.001, MANOVA) and grooming episodes (P<0.001, MANOVA). These results suggest that mGluRs play a role in the control of defense reactions in the DPAG.

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Hippocampal 5-HT receptors and consolidation of stressful memories

Cited by 106 publications

References 40 publications

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Restraint-induced hypoactivity in an elevated plus-maze

Defense reaction induced by a metabotropic glutamate receptor agonist microinjected into the dorsal periaqueductal gray of rats

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