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Second-order fear conditioning prevented by blocking NMDA receptors in amygdala.
Nature. 1997 Jul 31; 388(6641):471-4.Nat

Abstract

Antagonists of NMDA (N-methyl-D-aspartate)-type glutamate receptors disrupt several forms of learning. Although this might indicate that NMDA-receptor-mediated processes are critical for synaptic plasticity, there may be other mechanisms by which NMDA-receptor antagonism could interfere with learning. For instance, fear conditioning would be blocked by microinfusion of the NMDA-receptor antagonist AP5 (D,L-2-amino-5-phosphonovalerate) into the basolateral amygdala if AP5 inhibited routine synaptic transmission, thereby reducing the ability of stimuli to activate amygdala neurons. In second-order fear conditioning, the reinforcer is a fear-eliciting conditioned stimulus rather than an unconditioned stimulus. Expression of conditioned fear is amygdala-dependent and so provides a behavioural assessment of the ability of the reinforcer to activate amygdala neurons in the presence of AP5. We report here that intra-amygdala AP5 actually enhances expression of conditioned fear to the conditioned stimulus that provides the reinforcement signal for second-order conditioning. Nevertheless, acquisition of second-order fear conditioning is completely blocked. Our findings strongly support the view that NMDA receptors are critically involved in synaptic plasticity.

Authors+Show Affiliations

Department of Psychology, Yale University, Ribicoff Research Facilities of the Connecticut Mental Health Center, New Haven 06508, USA. jonathan.gewirtz@yale.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9242405

Citation

Gewirtz, J C., and M Davis. "Second-order Fear Conditioning Prevented By Blocking NMDA Receptors in Amygdala." Nature, vol. 388, no. 6641, 1997, pp. 471-4.
Gewirtz JC, Davis M. Second-order fear conditioning prevented by blocking NMDA receptors in amygdala. Nature. 1997;388(6641):471-4.
Gewirtz, J. C., & Davis, M. (1997). Second-order fear conditioning prevented by blocking NMDA receptors in amygdala. Nature, 388(6641), 471-4.
Gewirtz JC, Davis M. Second-order Fear Conditioning Prevented By Blocking NMDA Receptors in Amygdala. Nature. 1997 Jul 31;388(6641):471-4. PubMed PMID: 9242405.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Second-order fear conditioning prevented by blocking NMDA receptors in amygdala. AU - Gewirtz,J C, AU - Davis,M, PY - 1997/7/31/pubmed PY - 2001/3/23/medline PY - 1997/7/31/entrez SP - 471 EP - 4 JF - Nature JO - Nature VL - 388 IS - 6641 N2 - Antagonists of NMDA (N-methyl-D-aspartate)-type glutamate receptors disrupt several forms of learning. Although this might indicate that NMDA-receptor-mediated processes are critical for synaptic plasticity, there may be other mechanisms by which NMDA-receptor antagonism could interfere with learning. For instance, fear conditioning would be blocked by microinfusion of the NMDA-receptor antagonist AP5 (D,L-2-amino-5-phosphonovalerate) into the basolateral amygdala if AP5 inhibited routine synaptic transmission, thereby reducing the ability of stimuli to activate amygdala neurons. In second-order fear conditioning, the reinforcer is a fear-eliciting conditioned stimulus rather than an unconditioned stimulus. Expression of conditioned fear is amygdala-dependent and so provides a behavioural assessment of the ability of the reinforcer to activate amygdala neurons in the presence of AP5. We report here that intra-amygdala AP5 actually enhances expression of conditioned fear to the conditioned stimulus that provides the reinforcement signal for second-order conditioning. Nevertheless, acquisition of second-order fear conditioning is completely blocked. Our findings strongly support the view that NMDA receptors are critically involved in synaptic plasticity. SN - 0028-0836 UR - https://www.unboundmedicine.com/medline/citation/9242405/Second_order_fear_conditioning_prevented_by_blocking_NMDA_receptors_in_amygdala_ L2 - https://doi.org/10.1038/41325 DB - PRIME DP - Unbound Medicine ER -