Glycine Site Antagonist (HA-966) Treatment — David L. Walker | ReplicateScience
Experiments/Glycine Site Antagonist (HA-966) Treatment
Source Paper
Facilitation of Conditioned Fear Extinction by Systemic Administration or Intra-Amygdala Infusions of d-Cycloserine as Assessed with Fear-Potentiated Startle in Rats
David L. Walker, Kerry J. Ressler, Kwok-Tung Lu, Michael Davis
Objective: To evaluate whether HA-966, a glycine-recognition site antagonist, blocks the facilitating effects of D-cycloserine on conditioned fear extinction as measured by fear-potentiated startle in rats
Materials & Equipment Checklist
6 items2 from ConductScience
Gather these items before starting the experiment. Check off items as you prepare.
Equipment2
not specified • not specified • not specified • not specified
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Protocol Steps
View Abstract
NMDA receptor antagonists block conditioned fear extinction when injected systemically and also when infused directly into the amygdala. Here we evaluate the ability of d -cycloserine (DCS), a partial agonist at the strychnine-insensitive glycine-recognition site on the NMDA receptor complex, to facilitate conditioned fear extinction after systemic administration or intra-amygdala infusions. Rats received 10 pairings of a 3.7 sec light and a 0.4 mA footshock (fear conditioning). Fear-potentiated startle (increased startle in the presence vs the absence of the light) was subsequently measured before and after 30, 60, or 90 presentations of the light without shock (extinction training). Thirty non-reinforced light presentations produced modest extinction, and 60 or 90 presentations produced nearly complete extinction (experiment 1). DCS injections (3.25, 15, or 30 mg/kg) before 30 non-reinforced light exposures dose-dependently enhanced extinction (experiment 2) but did not influence fear-potentiated startle in rats that did not receive extinction training (experiment 3). These effects were blocked by HA-966, an antagonist at the glycine-recognition site (experiment 4). Neither DCS nor HA-966 altered fear-potentiated startle when injected before testing (experiment 5). The effect of systemic administration was mimicked by intra-amygdala DCS (10 μg/side) infusions (experiment 6). These results indicate that treatments that promote NMDA receptor activity after either systemic or intra-amygdala administration promote the extinction of conditioned fear.
1
Fear Conditioning
Rats received fear conditioning with paired presentations of light and footshock
Note: Measured as increased startle in presence vs absence of light
View evidence from paper
“Fear-potentiated startle (increased startle in the presence vs the absence of the light) was subsequently measured before and after”
3
HA-966 Administration
HA-966, a glycine-recognition site antagonist, was administered to block D-cycloserine effects
not specifiednot specified
Note: Specific dose and route not detailed in provided text
View evidence from paper
“These effects were blocked by HA-966, an antagonist at the glycine-recognition site (experiment 4)”
4
Extinction Training
Rats received non-reinforced light presentations without shock to test extinction learning
30, 60, or 90 presentations of light without shocknot specified
Note: 30 presentations produced modest extinction; 60 or 90 presentations produced nearly complete extinction
View evidence from paper
“30, 60, or 90 presentations of the light without shock (extinction training). Thirty non-reinforced light presentations produced modest extinction, and 60 or 90 presentations produced nearly complete extinction”
