TY - JOUR
T1 - Effects of antidepressant treatment on inhibitory avoidance behavior and amygdaloid β-Adrenoceptors in rats
AU - Daws, Lynette C.
AU - Lopez, Ray
AU - Frazer, Alan
N1 - Funding Information:
This work was supported by USPHS (MH 29094) and research funds from the VA. The authors gratefully acknowledge the excellent technical assistance of Sabrina Fister, Anna Domyan-cic, and Douglas Davis. The authors extend their appreciation to Dr. Irwin Lucki for his useful comments on this manuscript, and to Drs. Glenn Toney and Paul Scott for their valuable input.
PY - 1998/10
Y1 - 1998/10
N2 - Chronic treatment of rats with a variety of antidepressants results in the down-regulation of β1-adrenoceptors in the amygdaloid nuclei. The present study sought to determine if this specific neurochemical effect caused an alteration in inhibitory avoidance conditioning, a behavior considered to be mediated by β-adrenoceptors in the amygdala. Rats treated chronically with either desipramine (DMI) or phenelzine (PHEN), which down-regulate β1-adrenoceptors in the amygdala, or fluoxetine (FLUOX), which does not do this, did not exhibit a deficit in the retention of the inhibitory avoidance task. However, when scopolamine was given prior to acquisition of the task in a dose that, by itself, did not affect retention, DMI- and PHEN-treated rats showed a marked deficit in retention. This effect was also observed after acute administration of these drugs, although they did not down-regulate amygdaloid β1-adrenoceptors at this time. It seems that the ability of these antidepressants to potentiate the amnesic effect of scopolamine is unrelated to their effect on β1-adrenoceptor number in the amygdala and that the extent of antidepressant-induced amygdaloid β1-adrenoceptor down-regulation is not sufficient, by itself, to cause a deficit in an inhibitory avoidance task. Copyright (C) 1998 American College of Neuropsychopharmacology.
AB - Chronic treatment of rats with a variety of antidepressants results in the down-regulation of β1-adrenoceptors in the amygdaloid nuclei. The present study sought to determine if this specific neurochemical effect caused an alteration in inhibitory avoidance conditioning, a behavior considered to be mediated by β-adrenoceptors in the amygdala. Rats treated chronically with either desipramine (DMI) or phenelzine (PHEN), which down-regulate β1-adrenoceptors in the amygdala, or fluoxetine (FLUOX), which does not do this, did not exhibit a deficit in the retention of the inhibitory avoidance task. However, when scopolamine was given prior to acquisition of the task in a dose that, by itself, did not affect retention, DMI- and PHEN-treated rats showed a marked deficit in retention. This effect was also observed after acute administration of these drugs, although they did not down-regulate amygdaloid β1-adrenoceptors at this time. It seems that the ability of these antidepressants to potentiate the amnesic effect of scopolamine is unrelated to their effect on β1-adrenoceptor number in the amygdala and that the extent of antidepressant-induced amygdaloid β1-adrenoceptor down-regulation is not sufficient, by itself, to cause a deficit in an inhibitory avoidance task. Copyright (C) 1998 American College of Neuropsychopharmacology.
KW - Amygdala
KW - Desipramine
KW - Fluoxetine
KW - Inhibitory avoidance
KW - Phenelzine
KW - β-Adrenoceptors
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U2 - 10.1016/S0893-133X(98)00016-5
DO - 10.1016/S0893-133X(98)00016-5
M3 - Article
C2 - 9718593
AN - SCOPUS:0031783572
SN - 0893-133X
VL - 19
SP - 300
EP - 313
JO - Neuropsychopharmacology
JF - Neuropsychopharmacology
IS - 4
ER -