Regulation of 5‐HT Receptors and the Hypothalamic‐Pituitary‐Adrenal Axis

López, Juan F.; Vázquez, Delia M.; Chalmers, Derek T.; Watson, Stanley J.

doi:10.1111/j.1749-6632.1997.tb52357.x

Cited by 88 publications

(51 citation statements)

References 106 publications

(110 reference statements)

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“…In support of this hypothesis is the fact that dysregulation of the HPA axis, which controls glucocorticoid levels is particularly common in severe forms of depression and in those patients with suicidal ideation or attempts (Lopez et al 1997).…”

Section: Discussionmentioning

confidence: 98%

Increased Temporal Cortex ER Stress Proteins in Depressed Subjects Who Died by Suicide

Bown

Wang

MacQueen

et al. 2000

Neuropsychopharmacology

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Regulation of ER stress proteins, such as the 78-kilodalton glucose regulated protein (GRP78) by chronic treatment with mood stabilizing drugs suggests that this family of proteins may be involved in the pathophysiology of mood disorders. Indeed, increased levels of GRP78, GRP94, and calreticulin, a third member of the ERCurrent theories of the pathophysiology of mood disorders suggest that prolonged increases in glucocorticoid levels, likely the result of prolonged environmental stress, lead to biochemical changes in cortical and limbic neurons that leave individuals vulnerable to depression (Duman et al. 1997). A number of studies have found evidence of neuronal atrophy and loss of hippocampal neurons in response to stress (Magarinos et al. 1996;Uno et al. 1989;Sapolsky et al. 1985), and a report of reduced hippocampal volumes in elderly patients with histories of depression suggests that analogous processes may occur in individuals with depression (Sheline et al. 1996). Some models of mood disorders (Hyman and Nestler 1996; Post 1992) have attempted to incorporate the notion of compensatory processes into an understanding of the pathophysiologic changes that occur in patients with mood disorders, but few studies have tested these notions empirically (Post 1992). Part of the difficulty has been identifying neuroprotective mechanisms that may be of relevance for mood disorders.Recently, we found that treatment with the mood stabilizing drugs, valproate and carbamazepine, increased expression of the 78-kilodalton glucose-regulated protein (GRP78) . GRP78 is a member of the ER stress protein family that includes GRP94 and calreticulin, all of which function as Ca 2 ϩ binding proteins and molecular chaperones to assist in the regulation of protein folding (Gething 1997). These proteins have neuroprotective properties, are induced by seizures and ischemic damage, and may be involved in Alzheimer's disease pathology (Yu et al. 1999;Lowenstein et al. 1994;Hamos et al. 1991).Increased expression of ER stress proteins by mood stabilizing drugs suggest that these proteins may be in- METHODS Postmortem brain tissue was obtained from the StanleyFoundation Neuropathology Consortium (4 groups of n ϭ 15 age-and sex-matched subjects, i.e., subjects with bipolar disorder (BD), subjects with Major Depressive Disorder (MDD), subjects with schizophrenia (SCZ), and non-psychiatric, non-neurologic comparison subjects) (Johnston et al. 1997). Details on dissection and clinical characteristics have been previously published (Dowlatshahi et al. 1998(Dowlatshahi et al. , 1999. Briefly, all medical records for psychiatric cases were reviewed by two psychiatrists. Diagnosis was determined according to DSM-IV criteria. If there was disagreement about the diagnosis, a third psychiatrist read the records. If a diagnosis could not be established, a family member was then interviewed. All interviewed relatives were first degree except for two (one aunt and one father-in-law). Similarly, a clinical interview was performed with a family member...

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Section: Discussionmentioning

confidence: 98%

Increased Temporal Cortex ER Stress Proteins in Depressed Subjects Who Died by Suicide

Bown

Wang

MacQueen

et al. 2000

Neuropsychopharmacology

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“…Tricyclic antidepressants, whose modes of action include modulation of noradrenaline and serotonergic systems, have been shown to alter CRH in the PVN and hippocampal corticosteroid receptor expression in adult animal studies (Brady et al, 1991;López et al, 1998López et al, , 1997. Desipramine (DES), in particular, has selective noradrenaline reuptake inhibitor properties, and its administration to chronically stressed adult rats prevents the downregulation of hippocampal mineralocorticoid and serotonin 1a receptors, and the elevation of CORT levels that results from chronic stress (López et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Impact of Maternal Deprivation on Brain Corticotropin-Releasing Hormone Circuits: Prevention of CRH Receptor-2 mRNA Changes by Desipramine Treatment

Vázquez

Eskandari

Phelka

et al. 2002

Neuropsychopharmacol

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Corticotropin-releasing hormone (CRH) acts within the brain and pituitary to coordinate the overall endocrinological and behavioral stress response. From postnatal day (PND) 4 to 14, the infant rat displays minimal adrenal response to mild stress. However, maternal deprivation alters the pituitary-adrenal system such that the infants become responsive to specific stimuli. We hypothesized that maternal deprivation would also affect CRH brain circuits. Since tricyclic antidepressants have been shown to decrease the adrenal response to stress in adult rats, we hypothesized that CRH-related changes induced by maternal deprivation would be prevented by this treatment. Thus, we investigated CRH-related molecules on animals that were maternally deprived on PND 13 compared with nondeprived animals. We found that maternal deprivation caused alterations in the gene expression of both CRH receptors (CRHr) 1 and 2 in specific brain regions, and that some of these effects were augmented by chronic isotonic saline injections. There was a significant increase in CRH, CRHr1, and r2 mRNA in the cortex. In amygdala, CRHr1 and r2 mRNAs were decreased. CRHr2 mRNA was also decreased in the ventromedial nucleus of the hypothalamus, whereas an increase was detected in the hippocampal pyramidal cells. One week of desipramine (DES) administration preceding the maternal deprivation event prevented all the deprivation-induced changes in CRHr2 mRNA, regardless of the direction of the original change. We also found that chronic injection treatments enhanced the adrenocortical response and improved the efficiency of negative feedback in maternal deprivation animals. These results demonstrate that maternal deprivation elicits modifications of CRH brain circuits in a site-specific manner, and that the regulation of CRHr2 gene expression is mediated by mechanisms different from those involved with the modulation of CRHr1 in the infant rat.

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“…To our knowledge, no stress research has focused on cortical 5-HT1Br density. But it has been suggested that chronic stress decreases hippocampal 5-HT1Br binding (Mendelson & McEwen, 1992) and hippocampal 5-HT 1B mRNA expression (Lopez et al, 1997). Our findings added that chronic stress down-regulates 5-HT1Br binding not only in the hippocampus, but also in some subregions of the PFC, such as the prelimbic and orbitolateral cortices.…”

Section: -Ht 1b Receptor Density and Stress-induced Aggressionmentioning

confidence: 43%

“…More interestingly, the microinjection of 5-HT1Br agonists into the PFC decreases aggressive behavior (Centenaro et al, 2008;da Veiga et al, 2011;De Almeida et al, 2006;Veiga, Miczek, Lucion, & Almeida, 2007). Therefore, our findings suggest the possibility that chronic stress down-regulates 5-HT1Br densities in the prelimbic and orbitolateral cortices of the right hemisphere, which, in turn, escalates aggressive behavior (Lopez et al, 1997), although further research is needed to test this hypothesis. Dopamine D 2 receptor density and stress-suppressed aggression In contrast to our results of 5-HT1Br binding analysis, only 1-day immobilization stress altered D2r density in the striatum, and no change in striatal D2r density was found under 5-and 10-day immobilization stress.…”

Section: -Ht 1b Receptor Density and Stress-induced Aggressionmentioning

confidence: 67%

“…In addition to T, neurochemical systems, especially serotonergic and dopaminergic systems, are commonly associated with aggressive behavior (de Almeida, Ferrari, Parmigiani, & Miczek, 2005). For example, 5-HT 1B receptor (5-HT1Br) function contributes to the control of aggressive behavior in rodents (de Boer & Koolhaas, 2005;Lopez, Vazquez, Chalmers, & Watson, 1997;Olivier & van Oorschot, 2005;Saudou et al, 1994). Furthermore, decreased levels of 5-HT neurotransmission, specifically located in the prefrontal cortex (PFC), and increased levels of dopamine in the nucleus accumbens are promoted after aggression (van Erp & Miczek, 2000).…”

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confidence: 99%

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Aggression is suppressed by acute stress but induced by chronic stress: Immobilization effects on aggression, hormones, and cortical 5-HT1B/ striatal dopamine D2 receptor density

Yohe

Suzuki²,

Lucas

2012

Cogn Affect Behav Neurosci

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Although it has been established by a number of investigators that a variety of stressors are associated with the induction of aggressive behavior, two specific issues remain unanswered. First, it is unclear whether the contexts surrounding stressors (e.g., stressor length and chance of winning over opponents) change outcomes regarding aggressive behavior. Second, if a relationship exists between stress and aggressive behavior, altered levels of stressrelated hormone (e.g., corticosterone [CORT]), as well as aggression-related biomarkers (e.g., testosterone [T], density of prefronto-cortical 5-HT 1B receptor and striatal dopamine D 2 receptor [D2r]) may contribute to changes in aggressive behavior. Thus, we examined how immobilization (with a 1-, 5-, or 10-day exposure) would impact (1) a longitudinal course of aggression toward different-sized opponents, (2) levels of CORT and T, and (3) densities of 5-HT 1B receptor (5-HT1Br) in the prefrontal cortex (PFC) and D2r in the striatum. It was found that, regardless of small or large opponents, a single 2-h exposure to immobilization reduced aggressive behavior (stress-suppressed aggression) over time, whereas repeated (10-day) exposure to immobilization escalated aggressive behavior (stress-induced aggression). These stress effects persisted up to 1 week of recovery from immobilization stress. Moreover, immobilized rats demonstrated elevated levels of T, but not CORT, as compared with controls. Finally, acute immobilization altered D2r densities in the shell of the nucleus accumbens, and chronic immobilization changed 5-HT1Br in the PFC, including the downregulation of 5-HT1Br densities in the right prelimbic and orbitolateral cortices. The potential relationships among stress, aggression, and 5-HT1Br/D2r roles are discussed.

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Regulation of 5‐HT Receptors and the Hypothalamic‐Pituitary‐Adrenal Axis

Cited by 88 publications

References 106 publications

Increased Temporal Cortex ER Stress Proteins in Depressed Subjects Who Died by Suicide

Increased Temporal Cortex ER Stress Proteins in Depressed Subjects Who Died by Suicide

Impact of Maternal Deprivation on Brain Corticotropin-Releasing Hormone Circuits: Prevention of CRH Receptor-2 mRNA Changes by Desipramine Treatment

Aggression is suppressed by acute stress but induced by chronic stress: Immobilization effects on aggression, hormones, and cortical 5-HT1B/ striatal dopamine D2 receptor density

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