Regular Article
Amygdala β-Noradrenergic Influences on Memory Storage Involve Cholinergic Activation

https://doi.org/10.1006/nlme.1996.0006Get rights and content

Abstract

These experiments examined the involvement of the amygdaloid complex as a site of interaction of adrenergic and muscarinic cholinergic influences on memory storage. Male Sprague–Dawley rats (60 days old; 250–300 g) were given a single training trial in an inhibitory avoidance task and a retention test trial 48 h later. Immediately after training buffer control or drug solutions (0.5 μl) were infused into the amygdala and, in the first experiment only, other drugs were administered intraperitoneally (ip). The first experiment examined the effects of post-training systemic injections of the muscarinic agonist oxotremorine (100.0 μg/kg) administered alone or together with intraamygdala injections of either the muscarinic antagonist atropine (1.0 μg) or the β-noradrenergic antagonist propranolol (0.3 μg). Oxotremorine enhanced retention and atropine, but not propranolol, attenuated the effects of oxotremorine. In the second experiment intraamygdala infusions of the β-noradrenergic agonist clenbuterol (10.0 ng) were administered either alone or together with atropine (1.0 μg). Clenbuterol enhanced retention and atropine blocked the effects of clenbuterol. In the third experiment intraamygdala infusions of oxotremorine (3, 10, 30, or 100 ng) were administered either alone or together with propranolol (0.3 μg). Oxotremorine (3.0 and 10.0 ng) enhanced retention and propranolol did not block the effects of oxotremorine. These findings are consistent with the view that memory storage is regulated by an interaction of β-noradrenergic and cholinergic influences and suggest that the noradrenergic influences are mediated by the release of acetylcholine and activation of muscarinic cholinergic receptors within the amygdala.

References (0)

Cited by (95)

  • Memory Modulation

    2017, Learning and Memory: A Comprehensive Reference
  • Memory-enhancing intra-basolateral amygdala clenbuterol infusion reduces post-burst afterhyperpolarizations in hippocampal CA1 pyramidal neurons following inhibitory avoidance learning

    2015, Neurobiology of Learning and Memory
    Citation Excerpt :

    While one prior study found a 3 ng dose of clenbuterol was memory-enhancing, a 10 ng dose was ineffective (Introini-Collison et al., 1991). Another study found a 10 ng dose was memory-enhancing, while a 30 ng dose was ineffective (Introini-Collison et al., 1996). Yet another study found a 10 ng dose of clenbuterol was memory-enhancing, but doses orders of magnitudes higher were ineffective (Ferry & McGaugh, 1999).

  • Corticosterone and propranolol's role on taste recognition memory

    2014, Pharmacology Biochemistry and Behavior
  • How the amygdala affects emotional memory by altering brain network properties

    2014, Neurobiology of Learning and Memory
    Citation Excerpt :

    A ß-adrenoceptor antagonist administered into the amygdala post-training was shown to impair memory, while concurrent infusion of norepinephrine blocked this memory impairment (Gallagher et al., 1981). Many subsequent studies found that post-training infusions of norepinephrine or ß-adrenoceptor agonists into the amygdala (or selectively into the BLA) enhance memory consolidation for a wide variety of training experiences (Bianchin, Mello e Souza, Medina, & Izquierdo, 1999; Ferry & McGaugh, 1999; Hatfield & McGaugh, 1999; Huff, Wright-Hardesty, Higgins, Matus-Amat, & Rudy, 2005; Introini-Collison, Dalmaz, & McGaugh, 1996; Introini-Collison, Miyazaki, & McGaugh, 1991; Introini-Collison, Saghafi, Novack, & McGaugh, 1992; Lalumiere, Buen, & McGaugh, 2003; Lalumiere, Nawar, & McGaugh, 2005; Liang et al., 1986; Liang, Chen, & Huang, 1995; Liang, McGaugh, & Yao, 1990; Roozendaal, Castello, Vedana, Barsegyan, & McGaugh, 2008). Experiments investigating the role of amygdala norepinephrine in modulating memory consolidation have generally used emotionally arousing training conditions that induce the release of high levels of norepinephrine in the amygdala.

View all citing articles on Scopus
View full text