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Posttraining inactivation of excitatory afferent input to the locus coeruleus impairs retention in an inhibitory avoidance learning task.
Neurobiol Learn Mem. 2000 Mar; 73(2):127-40.NL

Abstract

These experiments examined whether the nucleus paragigantocellularis (PGi) contributes to memory storage processing via its ascending excitatory influence on locus coeruleus (LC) neuronal activity. Activation of the LC leads to memory enhancement and also results in a widespread release of norepinephrine in target structures, such as the amygdala and hippocampus. Infusion of norepinephrine into either structure also improves memory for several types of learned responses. Thus, the capacity for norepinephrine to modulate memory within limbic structures may be contingent upon the functional connections between PGi and the LC. To examine this hypothesis, male Sprague-Dawley rats were implanted with cannula aimed above PGi (Experiments 1 and 2) or 1.5 mm dorsal or medial to PGi (Experiment 3). Immediately following inhibitory avoidance training (0.45 mA, 0. 5 s), phosphate-buffered saline, lidocaine (Experiment 1), or 12.5 or 25 nmol/0.5 microl of the GABA agonist muscimol (Experiment 2) was infused into PGi. On a retention test given 48 h later, the latency to reenter the footshock compartment was significantly shorter for subjects given either lidocaine or 12.5 or 25.0 nmol of muscimol compared to controls. In Experiment 3, infusion of lidocaine or muscimol into areas 1.5 mm dorsal or medial to PGi did not significantly alter retention, indicating that the memory impairment observed in Experiments 1 and 2 was site specific and not due to the spread of drug to cell groups surrounding PGi. These findings suggest that PGi may serve a vital function in relaying biologically relevant information to forebrain structures involved in memory via its excitatory influence on the LC.

Authors+Show Affiliations

Department of Psychology, University of Virginia, Charlottesville, Virginia 22903, USA.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

10704323

Citation

Clayton, E C., and C L. Williams. "Posttraining Inactivation of Excitatory Afferent Input to the Locus Coeruleus Impairs Retention in an Inhibitory Avoidance Learning Task." Neurobiology of Learning and Memory, vol. 73, no. 2, 2000, pp. 127-40.
Clayton EC, Williams CL. Posttraining inactivation of excitatory afferent input to the locus coeruleus impairs retention in an inhibitory avoidance learning task. Neurobiol Learn Mem. 2000;73(2):127-40.
Clayton, E. C., & Williams, C. L. (2000). Posttraining inactivation of excitatory afferent input to the locus coeruleus impairs retention in an inhibitory avoidance learning task. Neurobiology of Learning and Memory, 73(2), 127-40.
Clayton EC, Williams CL. Posttraining Inactivation of Excitatory Afferent Input to the Locus Coeruleus Impairs Retention in an Inhibitory Avoidance Learning Task. Neurobiol Learn Mem. 2000;73(2):127-40. PubMed PMID: 10704323.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Posttraining inactivation of excitatory afferent input to the locus coeruleus impairs retention in an inhibitory avoidance learning task. AU - Clayton,E C, AU - Williams,C L, PY - 2000/3/8/pubmed PY - 2000/5/16/medline PY - 2000/3/8/entrez SP - 127 EP - 40 JF - Neurobiology of learning and memory JO - Neurobiol Learn Mem VL - 73 IS - 2 N2 - These experiments examined whether the nucleus paragigantocellularis (PGi) contributes to memory storage processing via its ascending excitatory influence on locus coeruleus (LC) neuronal activity. Activation of the LC leads to memory enhancement and also results in a widespread release of norepinephrine in target structures, such as the amygdala and hippocampus. Infusion of norepinephrine into either structure also improves memory for several types of learned responses. Thus, the capacity for norepinephrine to modulate memory within limbic structures may be contingent upon the functional connections between PGi and the LC. To examine this hypothesis, male Sprague-Dawley rats were implanted with cannula aimed above PGi (Experiments 1 and 2) or 1.5 mm dorsal or medial to PGi (Experiment 3). Immediately following inhibitory avoidance training (0.45 mA, 0. 5 s), phosphate-buffered saline, lidocaine (Experiment 1), or 12.5 or 25 nmol/0.5 microl of the GABA agonist muscimol (Experiment 2) was infused into PGi. On a retention test given 48 h later, the latency to reenter the footshock compartment was significantly shorter for subjects given either lidocaine or 12.5 or 25.0 nmol of muscimol compared to controls. In Experiment 3, infusion of lidocaine or muscimol into areas 1.5 mm dorsal or medial to PGi did not significantly alter retention, indicating that the memory impairment observed in Experiments 1 and 2 was site specific and not due to the spread of drug to cell groups surrounding PGi. These findings suggest that PGi may serve a vital function in relaying biologically relevant information to forebrain structures involved in memory via its excitatory influence on the LC. SN - 1074-7427 UR - https://www.unboundmedicine.com/medline/citation/10704323/Posttraining_inactivation_of_excitatory_afferent_input_to_the_locus_coeruleus_impairs_retention_in_an_inhibitory_avoidance_learning_task_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1074-7427(99)93924-2 DB - PRIME DP - Unbound Medicine ER -