Infralimbic kappa opioid and muscarinic M1 receptor interactions in the concurrent modulation of anxiety and memory

Wall, Philip M.; Messier, Claude

doi:10.1007/s00213-001-0979-9

Cited by 95 publications

(69 citation statements)

References 64 publications

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“…It is conceivable that the deficits in novel object recognition may be attributable to endogenous opioid-mediated deficits in attention. Reports have shown that administration of exogenous KOR agonists suppress attention in a model of fear conditioning (Iordanova et al, 2006) and increase omissions and correct response latencies in a fivechoice serial reaction time task (Paine et al, 2007), although KOR antagonist (nor-BNI) administration was also shown to disrupt aspects of attention related to working memory in mice (Wall and Messier, 2002). The novel object recognition test may be configured differently to examine attention (Silvers et al, 2007), but the present study did not examine this effect.…”

Section: Discussioncontrasting

confidence: 55%

Endogenous κ Opioid Activation Mediates Stress-Induced Deficits in Learning and Memory

Carey

Lyons²,

Shay³

et al. 2009

J. Neurosci.

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We hypothesized that mice subjected to prolonged stress would demonstrate decreased performance in a learning and memory task attributable to the endogenous activation of the opioid receptor (KOR). C57BL/6J mice were tested using the novel object recognition (NOR) assay at various time points after exposure to repeated forced swim stress (FSS). Unstressed mice demonstrated recognition of the novel object at the end of a procedure using three 10-min object interaction phases, with a recognition index (RI) for the novel object of 71.7 Ϯ 3.4%. However, 1 h after exposure to FSS, vehicle-pretreated mice displayed a significant deficit in performance (RI ϭ 58.

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Section: Discussioncontrasting

confidence: 55%

Endogenous κ Opioid Activation Mediates Stress-Induced Deficits in Learning and Memory

Carey

Lyons²,

Shay³

et al. 2009

J. Neurosci.

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“…In addition, antalarmin treatment normalized stress-increased same arm return ratio (treatment: F 1, 24 ¼ 8.757, p ¼ 0.007; interaction: F 1, 24 ¼ 4.663, p ¼ 0.041; Figure 5b), which reflects certain aspects of attention (Wall and Messier, 2002;Wietrzych et al, 2005). In each sample phase of the temporal order memory test, all groups of mice explored the two copies of an identical object similarly (Supplementary Figure S7d).…”

Section: Blockade Of Crf 1 Prevents Early-life Stress-induced Cognitimentioning

confidence: 88%

“…The total distance traveled, number of arm entries, spontaneous alternation ratio (Wang et al, 2013), and same arm return ratio (Wall and Messier, 2002;Wietrzych et al, 2005) were measured.…”

Section: Behavioral Testingmentioning

confidence: 99%

Stress during a Critical Postnatal Period Induces Region-Specific Structural Abnormalities and Dysfunction of the Prefrontal Cortex via CRF1

Yang

Liao

Uribe-Mariño

et al. 2014

Neuropsychopharmacol

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During the early postnatal period, environmental influences play a pivotal role in shaping the development of the neocortex, including the prefrontal cortex (PFC) that is crucial for working memory and goal-directed actions. Exposure to stressful experiences during this critical period may disrupt the development of PFC pyramidal neurons and impair the wiring and function of related neural circuits. However, the molecular mechanisms of the impact of early-life stress on PFC development and function are not well understood. In this study, we found that repeated stress exposure during the first postnatal week hampered dendritic development in layers II/III and V pyramidal neurons in the dorsal agranular cingulate cortex (ACd) and prelimbic cortex (PL) of neonatal mice. The deleterious effects of early postnatal stress on structural plasticity persisted to adulthood only in ACd layer V pyramidal neurons. Most importantly, concurrent blockade of corticotropin-releasing factor receptor 1 (CRF 1 ) by systemic antalarmin administration (20 mg/g of body weight) during early-life stress exposure prevented stress-induced apical dendritic retraction and spine loss in ACd layer V neurons and impairments in PFC-dependent cognitive tasks. Moreover, the magnitude of dendritic regression, especially the shrinkage of apical branches, of ACd layer V neurons predicted the degree of cognitive deficits in stressed mice. Our data highlight the region-specific effects of early postnatal stress on the structural plasticity of prefrontal pyramidal neurons, and suggest a critical role of CRF 1 in modulating early-life stress-induced prefrontal abnormalities.

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“…However, performance of all mutant mice remained above the chance level, which for Y-maze performance, is calculated at 22.2%. Furthermore, the error analysis showed that reduced performance in the Y-maze correlated for doubleand RXR␥ single-mutants with a higher number of alternate arm returns and not with the same arm returns, thus being a further indication of reduced attention/working memory in these mutant animals (Holcomb et al 1999;Wall and Messier 2002). Thus, the reduction of spontaneous alternation indicates that in agreement with results from DNMTP test, an inactivation of RXR␥ alone or in parallel with RAR␤ leads to reduction, but not complete absence of spatial working memory.…”

Section: Discussionmentioning

confidence: 99%

“…For efficient alternation, mice need to use working memory, and thus, they should maintain an ongoing record of most recently visited arms, and continuously update such a record. A mouse with an impaired working memory cannot remember which arm it has just visited, and thus shows decreased spontaneous alternation (Holcomb et al 1999;Wall and Messier 2002).…”

Section: Y-maze Spontaneous Alternationmentioning

confidence: 99%

Working memory deficits in retinoid X receptor γ-deficient mice

Wietrzych¹,

Méziane²,

Sutter³

et al. 2005

Learn. Mem.

114

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Retinoid signaling has been recently shown to be required for mnemonic functions in rodents. To dissect the behavioral and molecular mechanisms involved in this requirement, we have analyzed the spatial and recognition working memory in mice carrying null mutations of retinoid receptors RAR␤ and RXR␥. Double mutants appeared deficient in spatial working memory as tested in spontaneous alternation in the Y-maze and delayed nonmatch to place (DNMTP) test in the T-maze. These mutant mice did acquire, however, spatial place reference or right/left discrimination tasks in the T-maze set-up, indicating that basic sensorimotor functions, spatial orientation, and motivational factors are unlikely to account for deficits in working memory-sensitive tasks. Double-mutant mice were also deficient in novel object recognition at intermediate, but not short delays. RXR␥ appeared to be the functionally predominant receptor in modulation of the working memory, as RXR␥, but not RAR␤ single null mutant mice exhibited deficits similar to those observed in the double mutants. The mechanism of this modulation is potentially related to functions of RXR␥ in frontal and perirhinal cortex, structures in which we detected RXR␥ expression and which are functionally implicated in working memory processes.Retinoic acid (RA, the major active form of vitamin A) is involved in the control of functions of several adult organs, including brain. Diet-induced or age-related reduction of retinoic acid levels was recently reported to lead to mnemonic deficits in spatial learning and memory in rats (Cocco et al. 2002) or relational memory in mice (Etchamendy et al. 2001(Etchamendy et al. , 2003. In view of the pleiotropic effects of RA, several dysfunctions may be involved in the generation of these deficits. Thus, one of the first steps in elucidating the molecular mechanisms underlying the modulation of mnemonic functions by retinoids is to determine which RA-signaling pathway(s) is implicated in this control.In vertebrates, the retinoid signal is mediated by two families of nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), each family comprising three isotypes, ␣ ␤, and ␥ with several isoforms for each isotype (Chambon 1996). These receptors are ligand-dependent transcriptional regulators acting as RAR/RXR heterodimers (Chambon 1996;Kastner et al. 1997). As RARs and RXRs are expressed in the adult mouse brain (Krezel et al. 1999;Zetterstrom et al. 1999) they can be directly implicated in control of brain functions. The concomitant null mutation of RAR␤ and RXR␥ or the null mutation of RAR␤ alone have been linked with spatial long-term memory deficits observed in the place-reference version of the Morris water-maze task (Chiang et al. 1998). Whether the inability of RAR␤/RXR␥ double mutants to learn this task could be related to deficits in the working memory, which actually would be the primary origin of deficient performance of these mutants in the water-maze task, was not investigated in this latter study....

show abstract

Infralimbic kappa opioid and muscarinic M1 receptor interactions in the concurrent modulation of anxiety and memory

Cited by 95 publications

References 64 publications

Endogenous κ Opioid Activation Mediates Stress-Induced Deficits in Learning and Memory

Endogenous κ Opioid Activation Mediates Stress-Induced Deficits in Learning and Memory

Stress during a Critical Postnatal Period Induces Region-Specific Structural Abnormalities and Dysfunction of the Prefrontal Cortex via CRF1

Working memory deficits in retinoid X receptor γ-deficient mice

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