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Memory-enhancing intra-basolateral amygdala clenbuterol infusion reduces post-burst afterhyperpolarizations in hippocampal CA1 pyramidal neurons following inhibitory avoidance learning.
Neurobiol Learn Mem. 2015 Mar; 119:34-41.NL

Abstract

Activation of the basolateral amygdala can modulate the strength of fear memories, including those in single-trial inhibitory avoidance (IA) tasks. Memory retention, measured by the latency to re-enter a dark-compartment paired 24h earlier with a footshock, varies with intensity of this aversive stimulus. When higher intensity footshocks were used, hippocampal CA1 pyramidal neurons exhibited reduced afterhyperpolarizations (AHPs) 24h post-trial, an effect blocked by immediate post-trial inactivation of the basolateral complex of the amygdala (BLA). Similar AHP reductions in CA1 have been observed in a number of learning tasks, with time courses appropriate to support memory consolidation. When less intense footshocks were used for IA training of Sprague-Dawley rats, immediate post-trial infusion of the β-adrenergic agonist clenbuterol into BLA was required to enhance hippocampal Arc protein expression 45 min later and to enhance memory retention tested 48 h later. Here, using Long-Evans rats and low-intensity footshocks, we confirmed that bilateral immediate post-trial infusion of 15 ng/0.5 μl of the β-adrenergic agonist clenbuterol into BLA significantly enhances memory for an IA task. Next, clenbuterol was infused into one BLA immediately post-training, with vehicle infused into the contralateral BLA, then hippocampal CA1 neuron AHPs were assessed 24 h later. Only CA1 neurons from hemispheres ipsilateral to post-trial clenbuterol infusion showed learning-dependent AHP reductions. Excitability of CA1 neurons from the same trained rats, but from the vehicle-infused hemispheres, was identical to that from untrained rats receiving unilateral clenbuterol or vehicle infusions. Peak AHPs, medium and slow AHPs, and accommodation were reduced only with the combination of IA training and unilateral BLA β-receptor activation. Similar to previous observations of BLA adrenergic memory-related enhancement of Arc protein expression in hippocampus, increased CA1 neuronal excitability in the fear-modulated IA task was activated by immediate post-trial β-receptor activation of the ipsilateral BLA.

Authors+Show Affiliations

University of Texas at Dallas, Cognition & Neuroscience Program, Behavioral & Brain Sciences, Richardson, TX 75080-3021, United States.University of Texas at Dallas, Cognition & Neuroscience Program, Behavioral & Brain Sciences, Richardson, TX 75080-3021, United States. Electronic address: tres@utdallas.edu.

Pub Type(s)

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

Language

eng

PubMed ID

25613546

Citation

Lovitz, E S., and L T. Thompson. "Memory-enhancing Intra-basolateral Amygdala Clenbuterol Infusion Reduces Post-burst Afterhyperpolarizations in Hippocampal CA1 Pyramidal Neurons Following Inhibitory Avoidance Learning." Neurobiology of Learning and Memory, vol. 119, 2015, pp. 34-41.
Lovitz ES, Thompson LT. Memory-enhancing intra-basolateral amygdala clenbuterol infusion reduces post-burst afterhyperpolarizations in hippocampal CA1 pyramidal neurons following inhibitory avoidance learning. Neurobiol Learn Mem. 2015;119:34-41.
Lovitz, E. S., & Thompson, L. T. (2015). Memory-enhancing intra-basolateral amygdala clenbuterol infusion reduces post-burst afterhyperpolarizations in hippocampal CA1 pyramidal neurons following inhibitory avoidance learning. Neurobiology of Learning and Memory, 119, 34-41. https://doi.org/10.1016/j.nlm.2014.12.004
Lovitz ES, Thompson LT. Memory-enhancing Intra-basolateral Amygdala Clenbuterol Infusion Reduces Post-burst Afterhyperpolarizations in Hippocampal CA1 Pyramidal Neurons Following Inhibitory Avoidance Learning. Neurobiol Learn Mem. 2015;119:34-41. PubMed PMID: 25613546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Memory-enhancing intra-basolateral amygdala clenbuterol infusion reduces post-burst afterhyperpolarizations in hippocampal CA1 pyramidal neurons following inhibitory avoidance learning. AU - Lovitz,E S, AU - Thompson,L T, Y1 - 2015/01/19/ PY - 2014/08/14/received PY - 2014/11/12/revised PY - 2014/12/19/accepted PY - 2015/1/24/entrez PY - 2015/1/24/pubmed PY - 2015/12/15/medline KW - Afterhyperpolarizations KW - Amygdalo-hippocampal circuitry KW - Beta agonist KW - Emotional memory KW - Medium AHPs KW - Slow AHPs SP - 34 EP - 41 JF - Neurobiology of learning and memory JO - Neurobiol Learn Mem VL - 119 N2 - Activation of the basolateral amygdala can modulate the strength of fear memories, including those in single-trial inhibitory avoidance (IA) tasks. Memory retention, measured by the latency to re-enter a dark-compartment paired 24h earlier with a footshock, varies with intensity of this aversive stimulus. When higher intensity footshocks were used, hippocampal CA1 pyramidal neurons exhibited reduced afterhyperpolarizations (AHPs) 24h post-trial, an effect blocked by immediate post-trial inactivation of the basolateral complex of the amygdala (BLA). Similar AHP reductions in CA1 have been observed in a number of learning tasks, with time courses appropriate to support memory consolidation. When less intense footshocks were used for IA training of Sprague-Dawley rats, immediate post-trial infusion of the β-adrenergic agonist clenbuterol into BLA was required to enhance hippocampal Arc protein expression 45 min later and to enhance memory retention tested 48 h later. Here, using Long-Evans rats and low-intensity footshocks, we confirmed that bilateral immediate post-trial infusion of 15 ng/0.5 μl of the β-adrenergic agonist clenbuterol into BLA significantly enhances memory for an IA task. Next, clenbuterol was infused into one BLA immediately post-training, with vehicle infused into the contralateral BLA, then hippocampal CA1 neuron AHPs were assessed 24 h later. Only CA1 neurons from hemispheres ipsilateral to post-trial clenbuterol infusion showed learning-dependent AHP reductions. Excitability of CA1 neurons from the same trained rats, but from the vehicle-infused hemispheres, was identical to that from untrained rats receiving unilateral clenbuterol or vehicle infusions. Peak AHPs, medium and slow AHPs, and accommodation were reduced only with the combination of IA training and unilateral BLA β-receptor activation. Similar to previous observations of BLA adrenergic memory-related enhancement of Arc protein expression in hippocampus, increased CA1 neuronal excitability in the fear-modulated IA task was activated by immediate post-trial β-receptor activation of the ipsilateral BLA. SN - 1095-9564 UR - https://www.unboundmedicine.com/medline/citation/25613546/Memory_enhancing_intra_basolateral_amygdala_clenbuterol_infusion_reduces_post_burst_afterhyperpolarizations_in_hippocampal_CA1_pyramidal_neurons_following_inhibitory_avoidance_learning_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1074-7427(14)00218-4 DB - PRIME DP - Unbound Medicine ER -