Chronic neonatal N-methyl-d-aspartate receptor blockade induces learning deficits and transient hypoactivity in young rats

Latysheva, N. V.; Rayevsky, K.S.

doi:10.1016/s0278-5846(03)00110-6

Cited by 49 publications

(28 citation statements)

References 48 publications

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“…One possibility for the male-specific attenuation of morphine tolerance by MK-801 in the hot plate assay could involve motor impairment due to a number of factors, including neurobehavioral toxicity or adaptations that could oppose repeated MK-801-induced behavioral effects such as baseline hypoactivity after repeated hyperactivity (42) or changes in motor coordination after repeated ataxia (12), which could confound the hot plate response. However, in the first experiment, using lower doses of MK-801 and morphine (Fig.…”

Section: Discussionmentioning

confidence: 99%

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Bryant

Eitan²,

Sinchak

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Multiple studies demonstrate that coadministration of N-methyl-D-aspartate (NMDA) receptor antagonists with the opioid agonist morphine attenuates the development of analgesic tolerance. Sex differences in the effects of noncompetitive, but not competitive NMDA receptor antagonists on acute morphine analgesia, have been reported in mice, yet the role of sex in modulation of morphine tolerance by NMDA receptor antagonists has yet to be addressed. Therefore, we tested whether there is a sex difference in the effect of NMDA receptor antagonists on the development of morphine analgesic tolerance in C57BL/6J mice. Acutely, at a dose required to affect morphine tolerance in male mice, the noncompetitive NMDA receptor antagonist dizocilpine (MK-801) prolonged morphine analgesia similarly in both sexes in the hot plate and tail withdrawal assays. In the hot plate assay, coadministration of MK-801 or the competitive antagonist 3-(2-carboxpiperazin-4-yl)propyl-1-phosphanoic acid (CPP) with morphine attenuated the development of tolerance in male mice, while having no effect in females. Like normal and sham females, ovariectomized mice were similarly insensitive to the attenuation of morphine tolerance by MK-801 in the hot plate assay. Surprisingly, in the tail withdrawal assay, MK-801 facilitated the development of morphine-induced hyperalgesia and tolerance in males but not females. The results demonstrate that male mice are more sensitive to modulation of nociception and morphine analgesia after repeated coadministration of NMDA receptor antagonists. Furthermore, the underlying mechanisms are likely to be different from those mediating the sex difference in the modulation of acute morphine analgesia that has previously been reported.

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Section: Discussionmentioning

confidence: 99%

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Bryant

Eitan²,

Sinchak

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…MDMs release soluble neurotoxins, and, after paracrine and autocrine amplification, such factors diffuse to affect regions distant from their primary locale. Because the activation of NMDA receptors can affect memory and learning (Latysheva and Rayevsky, 2003), we examined whether treatment with an NMDA antagonist such as memantine could improve synaptic transmission and plasticity and ameliorate subsequent neuropathology in the hippocampus, a brain region representative of learning and memory and apart from the initial source of the MP neurotoxins.…”

Section: Discussionmentioning

confidence: 99%

Memantine Protects Hippocampal Neuronal Function in Murine Human Immunodeficiency Virus Type 1 Encephalitis

Anderson¹,

Gendelman²,

Xiong³

2004

J. Neurosci.

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Memantine, a low-to-moderate-affinity NMDA receptor antagonist, can be used to treat cognitive impairment associated with Alzheimer's disease. However, its potential neuroprotective effects for human immunodeficiency virus type 1-associated (HIV-1-associated) dementia are less well appreciated. To this end we studied hippocampal synaptic function in a severe combined immunodeficient (SCID) mouse model of HIV-1 encephalitis (HIVE). Human monocyte-derived macrophages (MDMs) infected with HIV-1 ADA were injected stereotactically into the caudate and putamen of SCID mice, generating HIVE. These brain subregions are among those most affected in humans. Impaired synaptic transmission and long-term potentiation (LTP) were detected in the CA1 region of hippocampal brain slices of HIVE mice. Memantine-treated HIVE mice showed significant improvements in synaptic function during frequency facilitation tests and LTP induced by high-frequency stimulation when compared with untreated animals. Immunocytochemical measures of neuronal antigens mirrored the neuronal physiological tests. These results demonstrate that memantine attenuates hippocampal synaptic impairment in murine HIVE and provide a rationale for its use in infected humans who experience cognitive decline.

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“…NMDA receptor antagonist treatment during early brain development also produces long-term changes in behavior including reduced performance in spatial learning [10][11][12] and working memory tasks [7,13], hyperlocomotion [7,14] and impaired prepulse inhibition (PPI), a measure of sensorimotor gating [4,7,15]. Interestingly, Wang et al [7] showed that pre-treatment with the antipsychotic drug olanzapine, prevented the deficits in PPI and other neurochemical changes reported.…”

Section: Introductionmentioning

confidence: 99%

Altered Dopamine Receptor and Dopamine Transporter Binding and Tyrosine Hydroxylase mRNA Expression Following Perinatal NMDA Receptor Blockade

Bois

Hsu

et al. 2008

Neurochem Res

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This study examined how perinatal phencyclidine (PCP) treatment would affect dopamine D2 receptor and dopamine transporter (DAT) binding at different stages after treatment cessation. Female rat pups received injections of PCP (10 mg/kg, s.c.) or saline on postnatal day (PN)7, 9 and 11. D2 receptor and transporter binding was examined at four time-points (PN12, 18, 32 and 96) following injections. PCP treatment altered D2 receptor binding throughout development, with a final end-point of 22-33% decreased binding at adulthood in the nucleus accumbens and caudate putamen (P < 0.01), accompanied by a small but significant increase in DAT binding in the caudate putamen. Tyrosine hydroxylase mRNA expression was also significantly increased by 25% (P < 0.05) in the ventral tegmental area of adult rats, suggesting that this model may produce a long-term increase in dopamine output. This study demonstrates that early insult to the brain from NMDA receptor hypofunction alters the dopaminergic system at different stages of development.

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Chronic neonatal N-methyl-d-aspartate receptor blockade induces learning deficits and transient hypoactivity in young rats

Cited by 49 publications

References 48 publications

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Memantine Protects Hippocampal Neuronal Function in Murine Human Immunodeficiency Virus Type 1 Encephalitis

Altered Dopamine Receptor and Dopamine Transporter Binding and Tyrosine Hydroxylase mRNA Expression Following Perinatal NMDA Receptor Blockade

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