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*D. E. BUSH, A. GEKKER, J. E. LEDOUX; Fear conditioning is a form of Pavlovian learning that endows an initially
neutral conditioned stimulus (e.g. a tone) with fear-eliciting properties
by association with an aversive unconditioned stimulus (e.g. a footshock).
The amygdala is essential for the acquisition and maintenance of fear
conditioning, and is known to receive substantial inputs from midbrain
ascending noradrenergic neurons. Amygdala beta-adrenergic receptors have
been implicated in fear memory reconsolidation, but thus far little is
known about the role of these receptors in fear memory acquisition and
consolidation. We therefore assessed the effects of pre-training intra-amygdala
propranolol, a beta-adrenergic antagonist, on short-term memory (STM)
and long-term memory (LTM) for auditory fear conditioning. Male Sprague-Dawley
rats were pretreated with propranolol (0, 0.1 or 1 µg; in 0.25 µl
aCSF) microinjections into the lateral amygdala, approximately 45 min
prior to the commencement of auditory fear conditioning. Fear conditioning
consisted of three 30-sec tone (5kHz, 80dB SPL) presentations that each
co-terminated with a mild footshock (1sec, 0.6mA). Testing for tone-elicited
freezing in the absence of footshock took place in a distinct context,
either 3 hrs (STM) or 48 hrs (LTM) after fear conditioning. Results showed
that pre-training intra-amygdala propranolol significantly disrupted freezing
in both STM and LTM tests. Propranolol microinjections into surrounding
regions outside the lateral amygdala had no effect. These results indicate
that amygdala beta-adrenergic receptors are important during the early
stages of fear memory formation. Further experiments are underway to determine
whether amygdala beta-adrenergic receptors contribute to fear memory acquisition,
or to an early phase of memory consolidation |
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