Acute Stress-induced Changes in Hippocampal/Prefrontal Circuits in Rats: Effects of Antidepressants

Rocher, Cyril; Spedding, Michael; Muñoz, Carmen; Jay, Thérèse M.

doi:10.1093/cercor/bhg122

Cited by 284 publications

(208 citation statements)

References 46 publications

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“…This cortical region is another area in which dopamine has been tied to depression (specifically mesolimbic pathways) (Jentsch et al 2000) and D2 dopamine receptor expression in the prefrontal cortex may be a target for RA (Vincent et al 1995). The hippocampus modulates dopaminergic function in the medial prefrontal cortex (Peleg-Raibstein et al 2005) and deficits in hippocampal function lead to a downstream effect on orbitofrontal function Rocher et al 2004). Based on these findings alterations in hippocampal-medial prefrontal function have been hypothesized to play a role in neuropsychiatric symptoms (Peleg-Raibstein et al 2005).…”

Section: Ra and The Frontal Cortexmentioning

confidence: 99%

The neurobiology of retinoic acid in affective disorders

Bremner

McCaffery

2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

147

154

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Current models of affective disorders implicate alterations in norepinephrine, serotonin, dopamine, and CRF/cortisol; however treatments targeted at these neurotransmitters or hormones have led to imperfect resolution of symptoms, suggesting that the neurobiology of affective disorders is incompletely understood. Until now retinoids have not been considered as possible contributors to affective disorders. Retinoids represent a family of compounds derived from Vitamin A that perform a large number of functions, many via the vitamin A product, retinoic acid. This signaling molecule binds to specific retinoic acid receptors in the brain which, like the glucocorticoid and thyroid hormone receptors, are part of the nuclear receptor superfamily and regulate gene transcription. Research in the field of retinoic acid in the CNS has focused on the developing brain, in part stimulated by the observation that isotretinoin (13-cis retinoic acid), an isomer of retinoic acid used in the treatment of acne, is highly teratogenic for the CNS. More recent work has suggested that retinoic acid may influence the adult brain; animal studies indicated that the administration of isotretinoin is associated with alterations in behavior as well as inhibition of neurogenesis in the hippocampus. Clinical evidence for an association between retinoids and depression includes case reports in the literature, studies of health care databases, and other sources. A preliminary PET study in human subjects showed that isotretinoin was associated with a decrease in orbitofrontal metabolism. Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain ; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.

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Section: Ra and The Frontal Cortexmentioning

confidence: 99%

The neurobiology of retinoic acid in affective disorders

Bremner

McCaffery

2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

147

154

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“…AJ Devall and TA Lovick da Costa Gomez and Behbehani, 1995;Figueiredo et al, 2002;Girotti et al, 2006;Salchner and Singewald, 2002;Gerrits et al, 2003;Rizvi et al, 1991;Rocher et al, 2004;Brown et al, 2005;Floyd et al, 2000;Keay and Bandler, 2001). In particular, activation of the orbitofrontal cortex has been shown to induce biphasic changes in nociceptive threshold: hypoalgesia followed by a delayed hyperalgesia, and both effects could be blocked by inhibiting transmission through the ventrolateral PAG (Zhang et al, 1997).…”

Section: Stress-induced Hyperalgesia In Female Ratsmentioning

confidence: 99%

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Devall¹,

Lovick²

2010

Neuropsychopharmacol

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The effect of acute exposure to mild anxiogenic stress on cutaneous nociceptive threshold was investigated in female Wistar rats at different stages of the estrous cycle. Baseline tail flick latencies did not change significantly during the cycle. However after brief exposure to vibration stress (4 Hz for 5 min), rats in late diestrus, but not at other cycle stages, developed a hyperalgesia (decrease in tail flick latency). Animals in late diestrus revealed a more than fivefold increase in the density of Fos-like immunoreactive nuclei in the dorsolateral, lateral, and ventrolateral columns in the caudal half of the periaqueductal gray matter (PAG). There was no change in the density of Fos-like immunoreactive nuclei in the PAG in rats in estrus and early diestrus, although rats in proestrus showed a smaller (50%) but significant increase. Rats undergoing withdrawal from a progesterone dosing regimen (5 mg/kg i.p. twice daily for 6 days) designed to mimic the fall in progesterone that occurs naturally during late diestrus, exhibited a stress-induced hyperalgesia that was similar to animals in late diestrus and a significant increase in Fos-positive cells in the PAG. We suggest that falling levels of progesterone during late diestrus may be a predisposing factor for the development of stress-induced hyperalgesia, which is linked to differential activation of descending pain control circuits in the PAG. Similar changes in women, when progesterone levels fall during the late luteal phase of the menstrual cycle, may contribute to the development of premenstrual symptoms that include increased anxiety and hyperalgesia.

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“…LTP is an important physiological derivate of learning and memory formation (Rioult-Pedotti et al, 2000). Deficient LTP and left prefrontal hypo-activity are present in depression and are restituted after antidepressant treatment; thus, respective restitution of brain physiology and reduction of symptoms seem to be associated (Henriques and Davidson., 1991;Rocher et al, 2004;Norman et al, 2007). Taken together, these findings suggest that the enhancement of cortical excitability and LTP-like plasticity may contribute to adaptive changes induced by antidepressant treatment and therefore improve learning and cognition.…”

Section: Functional Relevancementioning

confidence: 79%