Pretraining infusion of DSP-4 into the amygdala impaired retention in the inhibitory avoidance task: involvement of norepinephrine but not serotonin in memory facilitation.
The present study investigated the involvement of amygdala noradrenergic (NE) and serotonergic (5-HT) systems in memory storage processing. Rats bearing chronic cannulae in the amygdala were trained on a one-trial inhibitory avoidance task and tested for retention 24 hrs later. Five days prior to training, rats received intra-amygdala infusion of vehicle or various doses of N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP-4)-a NE-specific neurotoxin when given peripherally. Results showed that pretraining intra-amygdala infusion of 10.0 micrograms or 30.0 micrograms of DSP-4 impaired retention. Further, 30.0 micrograms of DSP-4 also abolished the memory enhancing effect of epinephrine (E) injected peripherally. However, local infusion of DSP-4 depleted not only NE but also 5-HT and DA substantially. Subsequent experiments found that the retention deficit induced by 30.0 micrograms of DSP-4 could be ameliorated by 0.2 microgram NE but not by 5-HT at a wide range of doses infused into the amygdala shortly after training, which ascribed the deficit to depletion of NE. After protecting the 5-HT terminals by a pretreatment of fluoxetine (15.0 mg/kg), pretraining intra-amygdala infusion of 30.0 micrograms DSP-4 shifted the memory-enhancing dose of E from 0.1 mg/kg to 1.0 mg/kg. In contrast, pretraining intra-amygdala infusion of 15.0 micrograms 5,7-dihydroxytryptamine (5,7-DHT) or DSP-4 with a pretreatment of desipramine (DMI, 25.0 mg/kgx2) to protect NE terminals failed to impair retention or attenuate the memory enhancing effect of 0.1 mg/kg E injected peripherally. These findings, taken together, suggest that the memory modulatory effect of peripheral E involved, at least partially, the amygdala NE system.
Liang
K C
KC
Department of Psychology, National Taiwan University, Taiwan, ROC. kcliang@ms.cc.ntu.edu.tw
D015116:5,7-Dihydroxytryptamine / Q000494:pharmacology; D000322:Adrenergic Agonists / Q000494:pharmacology; D000647:Amnesia / Q000139:chemically induced / Q000188:drug therapy; D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects*; D001522:Behavior, Animal / Q000187:drug effects; D001596:Benzylamines / Q000494:pharmacology*; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D005473:Fluoxetine / Q000494:pharmacology; D008297:Male; D008568:Memory / Q000187:drug effects / Q000502:physiology*; D008845:Microinjections; D014179:Neurotransmitter Uptake Inhibitors / Q000494:pharmacology*; D009638:Norepinephrine / Q000172:deficiency / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000502:physiology; D018490:Serotonin Agents / Q000494:pharmacology; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology
D015116:5,7-Dihydroxytryptamine; D000322:Adrenergic Agonists; D001596:Benzylamines; D004837:Epinephrine; D005473:Fluoxetine; D014179:Neurotransmitter Uptake Inhibitors; D009638:Norepinephrine; D012701:Serotonin; D018490:Serotonin Agents; D017367:Selective Serotonin Reuptake Inhibitors; C012102:DSP 4