Source Paper
Activation of Glutamatergic Neurotransmission by Ketamine: A Novel Step in the Pathway from NMDA Receptor Blockade to Dopaminergic and Cognitive Disruptions Associated with the Prefrontal Cortex
Bita Moghaddam, Barbara Adams, Anita Verma, Darron Daly
Journal of Neuroscience • 1997
Systemic LY293558 Pretreatment
Objective: To assess the effects of systemic AMPA/kainate receptor antagonist LY293558 pretreatment on ketamine-induced dopamine activation and impairment of spatial delayed alternation performance in the prefrontal cortex
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Equipment2
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Protocol Steps
Systemic LY293558 Pretreatment
Administer AMPA/kainate receptor antagonist LY293558 systemically prior to ketamine treatment
Note: Pretreatment timing relative to ketamine administration not specified
View evidence from paper
“systemic pretreatment with AMPA/kainate receptor antagonist LY293558”
Ketamine Administration
Administer ketamine at specified dose following LY293558 pretreatment
Note: Dose-response study tested 10, 20, 30, 50, and 200 mg/kg doses
View evidence from paper
“low doses of ketamine (10, 20, and 30 mg/kg) increase glutamate outflow in the PFC”
Microdialysis Measurement
Measure glutamate and dopamine outflow in the prefrontal cortex using microdialysis in conscious rats
Note: Measurements taken in conscious animals
View evidence from paper
“A thorough dose-response study using microdialysis in conscious rats indicated that low doses of ketamine”
Spatial Delayed Alternation Task
Assess cognitive performance on spatial delayed alternation, a PFC-sensitive task
Note: Task used to measure ketamine-induced cognitive impairment
View evidence from paper
“ketamine-induced activation of dopamine release and impairment of spatial delayed alternation in the rodent, a PFC-sensitive cognitive task”