2008
DOI: 10.1111/j.1530-0277.2008.00760.x
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Electrophysiological Effects of Dizocilpine (MK‐801) in Adult Rats Exposed to Ethanol During Adolescence

Abstract: The effects of MK-801 on hippocampal EEG variability and P3 ERP amplitude and latency are significantly attenuated after a prolonged withdrawal period following adolescent EtOH exposure. However, the inhibitory effects of MK-801 on cortical and hippocampal EEG power were enhanced in rats exposed to EtOH during adolescence. Taken together, these data suggest protracted changes in NMDA systems following adolescent EtOH exposure.

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Cited by 15 publications
(23 citation statements)
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References 84 publications
(116 reference statements)
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“…These data suggest an important role of the glutamatergic NMDA system in the generation of the P3 ERP (Ehlers et al, 1992). More recently, we provided evidence of protracted changes in NMDA systems in cortical and hippocampal neurophysiological activity following adolescent ethanol exposure in rats (Criado et al, 2008a). In that study, we showed that MK-801 significantly reduced P3 ERP amplitude and increased P3 ERP latency in control, but not in adolescent rats exposed to ethanol.…”
Section: Discussionmentioning
confidence: 98%
See 1 more Smart Citation
“…These data suggest an important role of the glutamatergic NMDA system in the generation of the P3 ERP (Ehlers et al, 1992). More recently, we provided evidence of protracted changes in NMDA systems in cortical and hippocampal neurophysiological activity following adolescent ethanol exposure in rats (Criado et al, 2008a). In that study, we showed that MK-801 significantly reduced P3 ERP amplitude and increased P3 ERP latency in control, but not in adolescent rats exposed to ethanol.…”
Section: Discussionmentioning
confidence: 98%
“…However, the consequences of adolescent ethanol exposure on the expression of NMDAR subunits in the cortex and hippocampus in vivo are just beginning to be understood (Sircar and Sircar, 2006; Pascual et al, 2009). Characterizing the effects of adolescent versus adult ethanol exposure on the expression of NMDAR subunits could provide important information on the unique mechanisms that may mediate the neurophysiological consequences of adolescent ethanol exposure previously shown in our laboratory (Slawecki et al, 2004; Criado et al, 2008a, 2008b). The objective of the present study was to determine whether expression of the NR1, NR2A and NR2B subunits in the hippocampus and frontal cortex is influenced by chronic ethanol exposure and/or withdrawal in adolescent versus adult rats.…”
mentioning
confidence: 98%
“…We recently determined the role of NMDA receptors in the development of long-term compensatory neurophysiological changes following adolescent EtOH exposure and found that MK-801 significantly reduced P3 ERP amplitude and increased P3 ERP latency in control, but not in EtOH-exposed rats [14]. These data suggest neuroadaptive changes in NMDA-mediated regulation of the P3 ERP component following adolescent EtOH exposure.…”
Section: Discussionmentioning
confidence: 99%
“…The mechanism for these effects of alcohol exposure was not identified, but subsequent studies suggested a potential role for changes in NMDA receptor expression and/or function. Rats exposed to ethanol vapor for 12 h/day as juveniles through late adolescence/young adulthood (P24-P60) exhibited significant changes in both cortical and hippocampal EEG following a challenge with the NMDA receptor antagonist MK-801 (Criado et al, 2008). Additionally, expression of NR1 and NR2A subunits in the hippocampus were increased and decreased following 24-hr and 2-week withdrawal, respectively, from alcohol vapor exposure that occurred for 14 h/day starting in the juvenile period (P23-P37) (Pian et al, 2010).…”
Section: Alcohol and Adolescencementioning
confidence: 99%