Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant‐negative cAMP response element‐binding protein (CREB) in forebrain

Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant‐negative... Electrophysiological and behavioural experiments were performed in transgenic mice expressing a dominant‐negative form of cAMP response element‐binding protein (CREBA133) in the limbic system. In control littermate in vitro slice preparation, tetanizing the lateral amygdala–basolateral amygdala (BLA) pathway with a single train (100 Hz for 1 s) produced short‐term potentiation (STP) in the BLA. Five trains (10‐s interstimulus interval) induced long‐term potentiation (LTP), which was completely blocked by the N‐methyl‐ d‐aspartate (NMDA) receptor antagonist d(–)‐2‐amino‐5‐phosphonopentanoic acid (AP5; 50 μm). When GABAergic (γ‐aminobutyric acid) inhibition was blocked by picrotoxin (10 μm), LTP became more pronounced. Low‐frequency stimulation (1 Hz for 15 min) induced either long‐term depression (LTD) or depotentiation. LTD remained unaffected by AP5 (50 μm) or by the L‐ and T‐type Ca2+‐channel blockers nifedipine (20 μm) and Ni2+ (50 μm), but was prevented by picrotoxin (10 μm), indicating a GABAergic link in the expression of LTD in the BLA. When conditioned fear was tested, a mild impairment was seen in one of three transgenic lines only. Although high levels of mRNA encoding CREBA133 lead to downregulation of endogenous CREB, expression of LTP and depotentiation were unaltered in BLA of these transgenic animals. These results could suggest that residual CREB activity was still present or that CREB per se is dispensable. Alternatively, other CREB‐like proteins were able to compensate for impaired CREB function. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant‐negative cAMP response element‐binding protein (CREB) in forebrain

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Publisher
Wiley
Copyright
Copyright © 2000 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1046/j.1460-9568.2000.00108.x
Publisher site
See Article on Publisher Site

Abstract

Electrophysiological and behavioural experiments were performed in transgenic mice expressing a dominant‐negative form of cAMP response element‐binding protein (CREBA133) in the limbic system. In control littermate in vitro slice preparation, tetanizing the lateral amygdala–basolateral amygdala (BLA) pathway with a single train (100 Hz for 1 s) produced short‐term potentiation (STP) in the BLA. Five trains (10‐s interstimulus interval) induced long‐term potentiation (LTP), which was completely blocked by the N‐methyl‐ d‐aspartate (NMDA) receptor antagonist d(–)‐2‐amino‐5‐phosphonopentanoic acid (AP5; 50 μm). When GABAergic (γ‐aminobutyric acid) inhibition was blocked by picrotoxin (10 μm), LTP became more pronounced. Low‐frequency stimulation (1 Hz for 15 min) induced either long‐term depression (LTD) or depotentiation. LTD remained unaffected by AP5 (50 μm) or by the L‐ and T‐type Ca2+‐channel blockers nifedipine (20 μm) and Ni2+ (50 μm), but was prevented by picrotoxin (10 μm), indicating a GABAergic link in the expression of LTD in the BLA. When conditioned fear was tested, a mild impairment was seen in one of three transgenic lines only. Although high levels of mRNA encoding CREBA133 lead to downregulation of endogenous CREB, expression of LTP and depotentiation were unaltered in BLA of these transgenic animals. These results could suggest that residual CREB activity was still present or that CREB per se is dispensable. Alternatively, other CREB‐like proteins were able to compensate for impaired CREB function.

Journal

European Journal of NeuroscienceWiley

Published: Jul 1, 2000

References

  • Induction of long‐term potentiation in the basolateral amygdala does not depend on NMDA receptor activation
    Chapman, Chapman; Bellavance, Bellavance
  • Spaced training induces normal long‐term memory in CREB mutant mice
    Kogan, Kogan; Frankland, Frankland; Blendy, Blendy; Coblentz, Coblentz; Marowitz, Marowitz; Schütz, Schütz; Silva, Silva
  • Emotion: clues from the brain
    LeDoux, LeDoux
  • Excitatory transmission in the basolateral amygdala
    Rainnie, Rainnie; Asprodini, Asprodini; Shinnick‐Gallagher, Shinnick‐Gallagher
  • Induction of LTD in the dentate gyrus in vitro is NMDA receptor independent, but dependent on Ca2+ influx via low‐voltage‐activated Ca2+ channels and release of Ca2+ from intracellular stores
    Wang, Wang; Rowan, Rowan; Anwyl, Anwyl

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