title: Low-frequency stimulation induces a pathway-specific late phase of LTP in the amygdala that is mediated by PKA and dependent on protein synthesis.
abstract: Activity-dependent changes in synaptic efficacy are thought to be the key cellular mechanism for the formation and storage of both explicit and implicit memory. Different patterns of stimulation can elicit different changes in the efficiency on excitatory synaptic transmission. Here, we examined the synaptic changes in the amygdala of adult mice produced by low-frequency stimulation (1 Hz, 15 min, LFS). We first compared the synaptic changes induced by LFS in three different synaptic pathways of amygdala: cortical-lateral amygdala, thalamic-lateral amygdala, and lateral-basolateral amygdala pathways. We find that the plastic changes induced by LFS are different between synaptic pathways. Low-frequency stimulation selectively elicits a slow onset and protein synthesis-dependent late-phase LTP in the cortical-lateral amygdala pathway, but not in the thalamic-lateral or lateral-basolateral pathways. We next analyzed LTP induced by LFS in the cortical-lateral amygdala pathway and found that three PKA-coupling neurotransmitter receptors are involved: 5-HT4, Dopamine D1, and beta-adrenergic receptors. Antagonists of these receptors block the LFS L-LTP, but the effects of agonists of these receptors are clearly different. These results indicate that the threshold for the induction of LFS L-LTP is different among these pathways and that the maintenance of LFS L-LTP requires a cross-talk among multiple neurotransmitters.
authors.affiliation: Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York, New York 10032, USA. yyh3@columbia.edu
authors.forename: Yan-You
authors.initials: YY
authors.lastname: Huang
authors.forename: Eric R
authors.initials: ER
authors.lastname: Kandel
mesh_terms: D000679:Amygdala / Q000166:cytology* / Q000201:enzymology*; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D004558:Electric Stimulation; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009434:Neural Pathways; D009924:Organ Culture Techniques; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D020239:Receptor Cross-Talk / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D044422:Receptors, Serotonin, 5-HT4 / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D013788:Thalamus / Q000166:cytology
chemical_list: D011500:Protein Synthesis Inhibitors; D011943:Receptors, Adrenergic, beta; D044422:Receptors, Serotonin, 5-HT4; D000841:Anisomycin; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases