Repeated restraint-induced modulation of long-term potentiation in the dentate gyrus of the mouse

Spyrka, Jadwiga; Hess, Grzegorz

doi:10.1016/j.brainres.2010.01.031

Cited by 21 publications

(18 citation statements)

References 23 publications

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“…The reverse, however, was seen in the ventral-most part of the hippocampus (Maggio and Segal, 2011). The effects in the DG were variable (Gerges et al, 2001;Pavlides et al, 2002;Alfarez et al, 2003;Aleisa et al, 2006a,b,c;Dumas et al, 2010;Spyrka and Hess, 2010), and reduced LTD was observed in the bed nucleus stria terminalis (McElligott et al, 2010) and nucleus accumbens (Wang et al, 2010).…”

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confidence: 97%

“…Some 922 of the above-mentioned studies demonstrated that particular molecules are critical for the electrophysiological changes to occur, such as calcineurin and Ca 2ϩ /calmodulin-dependent protein kinase II (Aleisa et al, 2006a,b,c), NR2B subunits, inhibitor of nuclear factor-B (Christoffel et al, 2011), and brain-derived neurotrophic factor (Zhou et al, 2000;Radecki et al, 2005;Aleisa et al, 2006c). Compounds that prevented or normalized the development of changes in neural activity include nicotine (Aleisa et al, 2006a,b,c), antidepressants (Von Frijtag et al, 2001;Kole et al, 2002Kole et al, , 2004Kessal et al, 2006;Holderbach et al, 2007;Wang et al, 2010;Holm et al, 2011), ketamine (Li et al, 2011), memantine (Quan et al, 2011), antiglucocorticoids Karst and Joëls, 2007;Spyrka and Hess, 2010), and phenytoin (Zheng et al, 2004), whereas ␤-amyloid exacerbated the effects of chronic stress (Srivareerat et al, 2009;Tran et al, 2011). However, it is unclear whether these compounds 1) directly interfere with chronic-stress-dependent signaling pathways, 2) tap indirectly into the same pathways, or 3) compensate for/ counteract the effects of chronic stress through independent mechanisms.…”

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confidence: 99%

“…A nice exception is a study by Spyrka and Hess (2010), who examined LTP in the dentate gyrus at 1, 3, 7, 14, and 21 days of restraint (neck) stress. They observed that the induction of LTP was reduced after 3 and 7 days of restraint, but enhanced after 14 or 21 days, through a GR-and MR-dependent mechanism, respectively.…”

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confidence: 99%

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Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

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2012

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“…Among stresses, restraint (immobilization) stress is a convenient method to induce psychological (escape reaction) and/or physical stress (muscle work), which result in restricted mobility and aggression [20,21]. Restraint stress induces changes in the brain, including suppression of long-term potentiation, neurogenesis and physiological changes [5,22,23]. One of the prominent changes is release of glucocorticoid hormones from the adrenal cortex [24]: Glucocorticoids under stress promote the catabolism of glycogen, muscle, and fat to obtain the energy required for immediate adaptive response to stress.…”

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confidence: 99%

Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

et al. 2011

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Restraint stress produces physiological changes including suppression of long-term potentiation in the brain. We observed the effects of repeated stress on ischemic damage associated with corticosteroid hormone receptors in gerbils. Animals were placed into restrainers for 5 h (between 09:30 h and 14:30 h) for 21 consecutive days prior to induction of transient cerebral ischemia. The animals were divided into 4 groups; (1) sham-operated-control-group (sham-group), (2) ischemia-operated-control-group (ischemia-group), (3) sham-operated-stress-group (stressed-sham-group), and (4) ischemia-operated-stress-group (stressed-ischemia-group). We found that serum corticosterone level in the ischemia-group was highest (374% of the sham-group) 12 h after ischemia/reperfusion and its level in the stressed-ischemia-group was significantly lower than the ischemia-group. Locomotor activity in the ischemia-group was significantly increased (295% of the sham-group) at 1 day post-ischemia; however, the locomotor activity in the stressed-ischemia-group was less increased compared to the ischemia-group. Cresyl violet positive (CV(+)) cells were significantly decreased in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) of the 4 days post-ischemia-group, while 79.4% of CV(+) cells were detected in the CA1 of the stressed-ischemia-group. Also, a few NeuN (neuron-specific soluble nuclear antigen)(+) cells were detected in the SP of the 4 days post-ischemia-group; however, in the 4 days stressed-post-ischemia-group, 77.2% of NeuN(+) neurons were found in the SP. Glial fibrillary acidic protein(+) astrocytes in the CA1 in the stressed-ischemia-groups were similar to those in the ischemia-groups; however, ionized calcium-binding adapter molecule 1(+) microglia in the stressed-ischemia-groups were less activated compared to the ischemia-groups. Mineralocorticoid receptor (MCR) and glucocorticoid receptor (GR) immunoreactivity in the SP of the stressed-ischemia-group were higher than the ischemia-group; at 4 days post-ischemia, MCR and GR immunoreactivity were expressed in non-pyramidal cells. In brief, our results indicate that repeated restraint stress significantly increase levels of corticosteroid hormone receptors and attenuates neuronal damage in the ischemic hippocampal CA1 region.

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“…This synaptic metaplasticity occurred not only by electrophysiological manipulations but also by exposure to stress. For example, unconditioned fear stress such as elevated platform stress or exposure to novel circumstances suppressed high frequency stimulation (tetanus)-induced long-term potentiation (LTP) in the hippocampal CA1 field (3,4); however, they enhanced the magnitude of LTP in another hippocampal subregion, the dentate gyrus (DG) (5,6). These differential metaplastic changes mimic those induced by basolateral amygdala (BLA) activation; electrical stimulation of BLA suppressed LTP in the CA1 field (7) but enhanced LTP in DG (7 -9).…”

Section: Introductionmentioning

confidence: 99%

Synaptic Modulation via Basolateral Amygdala on the Rat Hippocampus–Medial Prefrontal Cortex Pathway in Fear Extinction

et al. 2013

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Abstract. The present study elucidated the functional role of modulatory effects of basolateral amygdala (BLA) on synaptic transmission in the rat hippocampus-medial prefrontal cortex (mPFC) pathway, compared with the hippocampal dentate gyrus (DG). Exposure to conditioned fear stress (CFS) or prior BLA activation enhanced tetanus-induced long-term potentiation (LTP) in DG. A similar synaptic response was found by low frequency stimulation (LFS) prior to tetanus. In mPFC, they did not affect LTP, but prior BLA activation, as well as pretreatment with the Nmethyl-d-aspartate (NMDA)-receptor antagonist MK-801 (0.1 mg/kg, i.p.), suppressed LFSprimed LTP. This BLA-mediated synaptic pattern was mimicked by synaptic changes observed in the fear extinction process; prior BLA activation suppressed the synaptic potentiation responsible for extinction retrieval and attenuated decreases in fear-related freezing behavior. These data suggest that LFS-primed LTP in mPFC is related to the neural basis of extinction. Extinctionrelated synaptic potentiation did not occur in a juvenile stress model that exhibited extinction deficit. In addition, LFS-primed LTP was suppressed in this model, which was reversed by the NMDA-receptor agonist d-cycloserine (15 mg/kg, i.p.). These findings suggest that modulatory effects of BLA on synaptic function in the hippocampus-mPFC pathway play a significant role in fear extinction in rats.

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Repeated restraint-induced modulation of long-term potentiation in the dentate gyrus of the mouse

Cited by 21 publications

References 23 publications

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

Synaptic Modulation via Basolateral Amygdala on the Rat Hippocampus–Medial Prefrontal Cortex Pathway in Fear Extinction

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