Animal models of depression: Parallels and correlates to severe depression in humans

Jesberger, James A.; Richardson, Jeremy

doi:10.1016/0006-3223(85)90156-8

Cited by 149 publications

(40 citation statements)

References 91 publications

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“…Both 5HT and DA play important roles in the setpoint for HPA reactivity (Korte et al, 1991;Stokes et al, 1987) and glucococorticoids in turn regulate the expression and function of the receptors for these two transmitters (Aghajanian et al, 1993;Young, 1994). It would therefore be worthwhile to investigate the extent to which early glucocorticoid exposure elicits persistent changes in HPA responses through its effects on 5HT and DA systems, or whether these animals display behavioral anomalies akin to those found in animal models of depression that involve deficient monoamine function (Jesberger and Richardson, 1985;Kelly et al, 1997;Song, 2000). One potential strategy is to use selective receptor antagonists to isolate the participation of specific 5HT and DA inputs in the functional outcomes .…”

Section: Discussionmentioning

confidence: 99%

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Slotkin

Kreider

Tate

et al. 2005

Neuropsychopharmacol

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Glucocorticoid administration to preterm infants is associated with neurodevelopmental disorders. We treated developing rats with dexamethasone (Dex) at 0.05, 0.2, or 0.8 mg/kg, doses below or spanning the range in clinical use, testing the effects of administration during three different stages: gestational days 17-19, postnatal days 1-3 or postnatal days 7-9. In adulthood, we assessed the impact on synaptic biomarkers for serotonin (5-hydroxytryptamine (5HT)) systems. Across all three regimens, Dex administration evoked upregulation of cerebrocortical 5HT 1A and 5HT 2 receptors and the presynaptic 5HT transporter, greatest for 5HT 1A receptors. The effects were fully evident even at the lowest dose. In contrast, 5HT levels in the cerebral cortex and hippocampus showed disparate patterns of temporal sensitivity, with no change after gestational treatment, an increase with the early postnatal regimen, and a decrease with the later postnatal exposure. None of the changes in 5HT concentrations were offset by adaptive changes in the fractional 5HT turnover rate. Furthermore, the critical period of sensitivity seen for 5HT levels differed from that of dopamine even within the same brain region. These findings suggest that developmental exposure to Dex during the critical neurodevelopmental period corresponding to its use in preterm infants, elicits selective changes in 5HT and dopaminergic synaptic function over and above its effects on general aspects of neural cell development, below the threshold for somatic growth impairment, and even at doses below those used clinically. Accordingly, adverse neurobehavioral consequences may be inescapable in glucocorticoid therapy of preterm infants. Neuropsychopharmacology (2006) 31, 904-911.

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Section: Discussionmentioning

confidence: 99%

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Slotkin

Kreider

Tate

et al. 2005

Neuropsychopharmacol

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“…It represents the theoretical basis of the origin and development of depression, as the model is a combination of cognitive and neurovegetative abnormalities and genetic susceptibility (Jesberger and Richardson, 1985;Henn et al, 1993;Nestler et al, 2002). In this animal model, however, the behavioral deficits can be seen for only a few days (2-3 days).…”

Section: Introductionmentioning

confidence: 99%

Single and Repeated Stress-Induced Modulation of Phospholipase C Catalytic Activity and Expression: Role in LH Behavior

Dwivedi

Mondal

Rizavi

et al. 2004

Neuropsychopharmacol

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PI-PLC, a critical enzyme of the phosphoinositide (PI) signaling pathway, mediates many physiological functions in the brain, including cellular plasticity. Stress-induced learned helplessness (LH) in animals serves as a model of behavioral depression. Recently, we observed that repeated stress prolongs the duration of LH behavior in rats, enabling us to compare neurobiologic abnormalities in acute and chronic depression. Here we examine whether LH behavior is associated with alterations in phospholipase C (PLC), and whether repetition of inescapable shock has similar or dissimilar effects on PLC to those of the single-stress paradigm. Rats were exposed to inescapable shock either once on day 1, or twice, on days 1 and 7. Rats were tested for escape latency on days 2 and 4 after day 1 inescapable shock or on days 2, 8, and 14 after day 1 and 7 inescapable shock. PI-PLC activity and mRNA and protein expression of three different PLC isozymes were determined in the frontal cortex and hippocampus. Higher escape latencies were observed in LH rats tested on day 2 after single inescapable shock and on day 14 after repeated inescapable shock. Single inescapable shock reduced PI-PLC activity in the frontal cortex and hippocampus of LH rats. On the other hand, repeated inescapable shock not only reduced PI-PLC activity in these brain areas of LH rats but also selectively decreased the expression of PLC b 1 and PLC g 1 isozymes. Our results suggest different responsiveness at the level of PI-PLC after single vs repeated stress, and that reductions in PLC may be critical in the pathophysiology of depression and other stress-related disorders.

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“…Chronic deprivation of olfaction, the primary sensory mode in rats, constitutes a stress of high intensity, and the behavioral deficits induced by OB are primarily the result of alterations in neuronal functions, which is supported by the phenomenon that the behavioral deficits can be reversed by antidepressant treatments although the olfactory bulbs are nonexistent (van Riezen et al, 1977;Jesberger and Richardson, 1988;Mar et al, 2000;O'Neil and Moore, 2003). The depression symptom-resembling deficits in OB rats can be normalized by chronic, not acute, antidepressant treatments (Jesberger and Richardson, 1985;Kelly et al, 1997). In previous preliminary study, treating OB rats with SA-4503 for 1 week did not significantly ameliorate the behavioral deficits, which were ameliorated after treating for 2 weeks in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…The olfactory bulbs have extensive neural connections with the structures of the limbic system and other parts of the brain, and they influence many emotional aspects of behavioral and other brain output functions (Jesberger and Richardson, 1985). Bilateral olfactory bulbectomy in rodents produces neuroanatomical deficits analogous to the cortical/ allocortical degeneration in depressive patients that is, in general, not dependent on particular structures (Holmes, 2003).…”

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confidence: 99%

Role ofN-Methyl-D-aspartate Receptors in Antidepressant-Like Effects of σ₁Receptor Agonist 1-(3,4-Dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine Dihydrochloride (SA-4503) in Olfactory Bulbectomized Rats

Wang¹,

Noda²,

Tsunekawa³

et al. 2007

J Pharmacol Exp Ther

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In the present study, we aimed to investigate the role of N-methyl-D-aspartate (NMDA) receptors in the antidepressant-like effects of a 1 receptor agonist, 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA-4503), in the olfactory bulbectomized (OB) rat model of depression. A symptomatologybased behavioral investigation was made by reconstructing in OB rats the symptoms of depression, such as psychomotor agitation, loss of interest, and cognitive dysfunction, using a typical antidepressant, desipramine, as a positive control. Repeated treatment with SA-4503 ameliorated the behavioral deficits in OB rats resembling depression symptoms in the open-field test, sexual behavior test, and cued and contextual fear-conditioning test. SA-4503 displayed advantages over desipramine in the sexual behavior test. SA-4503 also reversed the decrease in the protein expression of NMDA receptor subunit (NR)1, but not NR2A or NR2B, in the prefrontal cortex, hippocampus, and amygdala of OB rats. The behavioral and neurochemical effects of SA-4503 were blocked by combined treatment with a specific 1 receptor antagonist, N,N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)ethylamine monohydrochloride (NE-100). Furthermore, the effects of SA-4503 on the performance of OB rats in the behavioral tests were abrogated by acute treatment with an NMDA receptor antagonist, (Ϫ)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801). The present study indicated for the first time that the 1 receptor agonist SA-4503 may have effects on depressive symptoms such as agitation, loss of interest, and impaired cognition, which are mediated by NMDA receptors.

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Animal models of depression: Parallels and correlates to severe depression in humans

Cited by 149 publications

References 91 publications

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Single and Repeated Stress-Induced Modulation of Phospholipase C Catalytic Activity and Expression: Role in LH Behavior

Role ofN-Methyl-D-aspartate Receptors in Antidepressant-Like Effects of σ₁Receptor Agonist 1-(3,4-Dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine Dihydrochloride (SA-4503) in Olfactory Bulbectomized Rats

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Animal models of depression: Parallels and correlates to severe depression in humans

Cited by 149 publications

References 91 publications

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Single and Repeated Stress-Induced Modulation of Phospholipase C Catalytic Activity and Expression: Role in LH Behavior

Role ofN-Methyl-D-aspartate Receptors in Antidepressant-Like Effects of σ1Receptor Agonist 1-(3,4-Dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine Dihydrochloride (SA-4503) in Olfactory Bulbectomized Rats

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Role ofN-Methyl-D-aspartate Receptors in Antidepressant-Like Effects of σ₁Receptor Agonist 1-(3,4-Dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine Dihydrochloride (SA-4503) in Olfactory Bulbectomized Rats