Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

Rammes, G; Steckler, T; Kresse, A; Schütz, G; Zieglgänsberger, W; Lutz, B.
Synaptic plasticity in the basolateral amygdala in transgenic mice expressing dominant-negative cAMP response element-binding protein (CREB) in forebrain.
Eur J Neurosci. 2000; 12(7): 2534-2546.
Web of Science PubMed FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Kresse Adelheid
Altmetrics:

Dimensions Citations:

Plum Analytics:
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 microM). When GABAergic (gamma-aminobutyric acid) inhibition was blocked by picrotoxin (10 microM), 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 microM) or by the L- and T-type Ca2+-channel blockers nifedipine (20 microM) and Ni2+ (50 microM), but was prevented by picrotoxin (10 microM), 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.
Find related publications in this database (using NLM MeSH Indexing)
2-Amino-5-phosphonovalerate - pharmacology
Acoustic Stimulation - pharmacology
Amygdala - physiology
Animals - physiology
Calcium Channel Blockers - pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - pharmacology
Calcium-Calmodulin-Dependent Protein Kinases - genetics
Conditioning (Psychology) - physiology
Cyclic AMP Response Element-Binding Protein - genetics
Electrophysiology - genetics
Electroshock - genetics
Excitatory Amino Acid Antagonists - pharmacology
Exploratory Behavior - physiology
Fear - physiology
GABA Antagonists - pharmacology
Gene Expression Regulation, Enzymologic - pharmacology
Genes, Dominant - pharmacology
Habituation, Psychophysiologic - physiology
Hippocampus - chemistry
Long-Term Potentiation - physiology
Male - physiology
Membrane Potentials - drug effects
Mice - drug effects
Mice, Inbred C57BL - drug effects
Mice, Transgenic - drug effects
Neuronal Plasticity - physiology
Nickel - pharmacology
Nifedipine - pharmacology
Picrotoxin - pharmacology
Promoter Regions (Genetics) - physiology
Prosencephalon - chemistry
Receptors, N-Methyl-D-Aspartate - physiology

Find related publications in this database (Keywords)
amygdala
long-term depression
long-term potentiation
transgenic mice
© Med Uni Graz Impressum