Abstract
Long-term memory of cocaine-associated context was established by conditioned place preference learning. After 1 week, exposure to context in the absence of cocaine (memory retrieval) was paired with one of the following treatments: saline, scopolamine (muscarinic acetylcholine receptor antagonist), dizocilpine (MK-801; noncompetitive N-methyl-D-aspartate antagonist) or D-cycloserine (partial N-methyl-D-aspartate agonist). In subsequent conditioned place preference tests, place preference was suppressed in the drug-treated groups but not saline-treated groups. Results suggest that the amnesic agents, scopolamine and MK-801, disrupted reconsolidation of cocaine-associated contextual memory. In contrast, the mnemonic agent D-cycloserine might have facilitated extinction learning during context exposure in the absence of cocaine. Challenge administration of cocaine reinstated place preference in all groups except the MK-801 group, suggesting that suppression of conditioned response may or may not suppress memory evoked by drug-context reexposure.
| Original language | English |
|---|---|
| Pages (from-to) | 777-780 |
| Number of pages | 4 |
| Journal | NeuroReport |
| Volume | 18 |
| Issue number | 8 |
| DOIs | |
| State | Published - May 1 2007 |
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Keywords
- Cocaine
- Conditioned place preference
- Extinction
- Reconsolidation
- Reinstatement
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Long-term memory of cocaine-associated context : Disruption and reinstatement. / Kelley, Jonathan B.; Anderson, Karen L.; Itzhak, Yossef.
In: NeuroReport, Vol. 18, No. 8, 01.05.2007, p. 777-780.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Long-term memory of cocaine-associated context
T2 - Disruption and reinstatement
AU - Kelley, Jonathan B.
AU - Anderson, Karen L.
AU - Itzhak, Yossef
PY - 2007/5/1
Y1 - 2007/5/1
N2 - Long-term memory of cocaine-associated context was established by conditioned place preference learning. After 1 week, exposure to context in the absence of cocaine (memory retrieval) was paired with one of the following treatments: saline, scopolamine (muscarinic acetylcholine receptor antagonist), dizocilpine (MK-801; noncompetitive N-methyl-D-aspartate antagonist) or D-cycloserine (partial N-methyl-D-aspartate agonist). In subsequent conditioned place preference tests, place preference was suppressed in the drug-treated groups but not saline-treated groups. Results suggest that the amnesic agents, scopolamine and MK-801, disrupted reconsolidation of cocaine-associated contextual memory. In contrast, the mnemonic agent D-cycloserine might have facilitated extinction learning during context exposure in the absence of cocaine. Challenge administration of cocaine reinstated place preference in all groups except the MK-801 group, suggesting that suppression of conditioned response may or may not suppress memory evoked by drug-context reexposure.
AB - Long-term memory of cocaine-associated context was established by conditioned place preference learning. After 1 week, exposure to context in the absence of cocaine (memory retrieval) was paired with one of the following treatments: saline, scopolamine (muscarinic acetylcholine receptor antagonist), dizocilpine (MK-801; noncompetitive N-methyl-D-aspartate antagonist) or D-cycloserine (partial N-methyl-D-aspartate agonist). In subsequent conditioned place preference tests, place preference was suppressed in the drug-treated groups but not saline-treated groups. Results suggest that the amnesic agents, scopolamine and MK-801, disrupted reconsolidation of cocaine-associated contextual memory. In contrast, the mnemonic agent D-cycloserine might have facilitated extinction learning during context exposure in the absence of cocaine. Challenge administration of cocaine reinstated place preference in all groups except the MK-801 group, suggesting that suppression of conditioned response may or may not suppress memory evoked by drug-context reexposure.
KW - Cocaine
KW - Conditioned place preference
KW - Extinction
KW - Reconsolidation
KW - Reinstatement
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U2 - 10.1097/WNR.0b013e3280c1e2e7
DO - 10.1097/WNR.0b013e3280c1e2e7
M3 - Article
VL - 18
SP - 777
EP - 780
JO - NeuroReport
JF - NeuroReport
SN - 0959-4965
IS - 8
ER -