ArticleNeurobiology of learning and memory2012
Mitogen-activated protein kinase in the amygdala plays a critical role in lithium chloride-induced taste aversion learning.
Article in Neurobiology of learning and memory, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- A neural mechanism for learning from delayed postingestive feedback.bioRxiv : the preprint server for biology · 2024Article
- Amphetamine-induced activation of neurons within the rat nucleus of the solitary tract.Physiology & behavior · 2019Article
- Current Development Status of MEK Inhibitors.Molecules (Basel, Switzerland) · 2017Review
- Parabrachial calcitonin gene-related peptide neurons mediate conditioned taste aversion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Acquisition and expression of conditioned taste aversion differentially affects extracellular signal regulated kinase and glutamate receptor phosphorylation in rat prefrontal cortex and nucleus accumbens.Frontiers in behavioral neuroscience · 2014Article
- Memory of conditioned taste aversion is erased by inhibition of PI3K in the insular cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Article
- The role of protein phosphorylation in the gustatory cortex and amygdala during taste learning.Experimental neurobiology · 2012Article
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2 authors at 1 institution in 1 country.
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Abstract
The intracellular mitogen-activated protein kinase (MAPK) pathway in the brain is necessary for the formation of a variety of memories including conditioned taste aversion (CTA) learning. However, the functional role of MAPK activation in the amygdala during lithium chloride (LiCl)-induced CTA learning has not been established. In the present study, we investigated if local microinjection of SL327, a MAPK kinase inhibitor, into the rat amygdala could alleviate LiCl-induced CTA learning. Our results revealed that acute administration of a high dose of LiCl (0.15M, 12 ml/kg, i.p.) rapidly increased the level of phosphorylated MAPK (pMAPK)-positive cells in the central nucleus of the amygdala (CeA) and nucleus of the solitary tract (NTS) of rats as measured by immunohistochemistry. Local microinjection of SL327 (1 μg/0.5 μl/hemisphere) into the CeA 10 min before LiCl administration decreased both the strength of LiCl-induced CTA paired with 0.125% saccharin and the level of LiCl-induced pMAPK-positive cells in the CeA, but not in the NTS. Our data suggest that the intracellular signaling cascade of the MAPK pathway in the CeA plays a critical role in the processing of visceral information induced by LiCl for CTA learning.
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