Elevated plasma corticosterone level and depressive behavior in experimental temporal lobe epilepsy

Mazarati, Andréy; Shin, Don; Kwon, Young Se; Bragin, Anatol; Pineda, Eduardo; Tio, Delia L.; Taylor, Anna N.; Sankar, Raman

doi:10.1016/j.nbd.2009.02.018

Cited by 134 publications

(135 citation statements)

References 32 publications

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“…and phenytoin (50 mg/kg, i.p.) [2,3,7]. In control animals (further defined as naïve), pilocarpine was substituted with saline.…”

Section: Status Epilepticus and Spontaneous Seizuresmentioning

confidence: 99%

“…To confirm the development of chronic epilepsy, animals were subjected to continuous 2 or more weeks of video monitoring for the detection of stage 4 to 5 seizures (i.e., rearing and/or rearing and falling). To avoid immediate effects of spontaneous seizures on outcome measurements, all assays were performed on verification that no seizures had developed for at least 6 hours prior to or during the test [2,3,7].…”

Section: Status Epilepticus and Spontaneous Seizuresmentioning

confidence: 99%

“…Active swimming (attempts to escape) and immobility (movements purposed only to maintain the head above the water) were recorded. The increased immobility time has been regarded as an equivalent of hopelessness and despair [2,3,7].…”

Section: Forced Swim Testmentioning

confidence: 99%

“…Corticosterone (CORT) was measured using radioimmunoassay (Immunochem Double Antibody Corticosterone 125 I radioimmunoassay kit, MP Biomedicals, Orangeburg, NY) in 10 μl plasma samples. The dysregulation of the HPA axis consists of the failure of DEX to suppress plasma CORT and of the exacerbated increase of plasma CORT in response to CRH [3,7,12].…”

Section: Taste Preference Testmentioning

confidence: 99%

“…In turn, the compromised serotonergic transmission is due to the functional upregulation of presynaptic serotonin type 1A (5-HT1A) receptors [3], which normally control 5-HT release from raphe nuclei on a negative feedback basis [4][5][6]. Finally, the upregulation of 5-HT1A autoreceptors is driven by the dysregulation of the hypothalamo-pituitaryadrenocortical (HPA) axis [1,7], which (dysregulation) by itself represents a neuroendocrine hallmark of chronic stress [8]. At the same time, behavioral impairment indicative of anhedonia has not been associated with the deficit of serotonergic transmission [2].…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-1beta Causes Fluoxetine Resistance in an Animal Model of Epilepsy-Associated Depression

et al. 2012

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Depression represents a common comorbidity of epilepsy and is frequently resistant to selective serotonin reuptake inhibitors (SSRI). We tested the hypothesis that the SSRI resistance in epilepsy associated depression may be a result of a pathologically enhanced interleukin-1β (IL1-β) signaling, and consequently that the blockade of IL1-β may restore the effectiveness of SSRI. Epilepsy and concurrent depression-like impairments were induced in Wistar rats by pilocarpine status epilepticus (SE). The effects of the 2-week long treatment with fluoxetine, interleukin-1 receptor antagonist (IL-1ra), and their combination were examined using behavioral, biochemical, neuroendocrine, and autoradiographic assays. In post-SE rats, depression-like impairments included behavioral deficits indicative of hopelessness and anhedonia; the hyperactivity of the hypothalamo-pituitaryadrenocortical axis; the diminished serotonin output from raphe nucleus; and the upregulation of presynaptic serotonin 1-A (5-HT1A) receptors. Fluoxetine monotherapy exerted no antidepressant effects, whereas the treatment with IL-1ra led to the complete reversal of anhedonia and to a partial improvement of all other depressive impairments. Combined administration of fluoxetine and IL-1ra completely abolished all hallmarks of epilepsy-associated depressive abnormalities, with the exception of the hyperactivity of the hypothalamopituitary-adrenocortical axis, the latter remaining only partially improved. We propose that in certain forms of depression, including but not limited to depression associated with epilepsy, the resistance to SSRI may be driven by the pathologically enhanced interleukin-1β signaling and by the subsequent upregulation of presynaptic 5-HT1A receptors. In such forms of depression, the use of interleukin-1β blockers in conjunction with SSRI may represent an effective therapeutic approach.

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“…and phenytoin (50 mg/kg, i.p.) [2,3,7]. In control animals (further defined as naïve), pilocarpine was substituted with saline.…”

Section: Status Epilepticus and Spontaneous Seizuresmentioning

confidence: 99%

Section: Status Epilepticus and Spontaneous Seizuresmentioning

confidence: 99%