Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.

Learning to fear dangerous situations requires the participation of basolateral amygdala (BLA). In the present study, we provide evidence that BLA is necessary for the synaptic strengthening occurring during memory formation in the cerebellum in rats. In the cerebellar vermis the parallel fibers (PF...

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Main Authors: Lan Zhu, Tiziana Sacco, Piergiorgio Strata, Benedetto Sacchetti
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3031621?pdf=render
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spelling doaj-bafc7625f5f4462f9b97ef74e90072a52020-11-25T00:07:13ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0161e1667310.1371/journal.pone.0016673Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.Lan ZhuTiziana SaccoPiergiorgio StrataBenedetto SacchettiLearning to fear dangerous situations requires the participation of basolateral amygdala (BLA). In the present study, we provide evidence that BLA is necessary for the synaptic strengthening occurring during memory formation in the cerebellum in rats. In the cerebellar vermis the parallel fibers (PF) to Purkinje cell (PC) synapse is potentiated one day following fear learning. Pretraining BLA inactivation impaired such a learning-induced long-term potentiation (LTP). Similarly, cerebellar LTP is affected when BLA is blocked shortly, but not 6 h, after training. The latter result shows that the effects of BLA inactivation on cerebellar plasticity, when present, are specifically related to memory processes and not due to an interference with sensory or motor functions. These data indicate that fear memory induces cerebellar LTP provided that a heterosynaptic input coming from BLA sets the proper local conditions. Therefore, in the cerebellum, learning-induced plasticity is a heterosynaptic phenomenon that requires inputs from other regions. Studies employing the electrically-induced LTP in order to clarify the cellular mechanisms of memory should therefore take into account the inputs arriving from other brain sites, considering them as integrative units. Based on previous and the present findings, we proposed that BLA enables learning-related plasticity to be formed in the cerebellum in order to respond appropriately to new stimuli or situations.http://europepmc.org/articles/PMC3031621?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Lan Zhu
Tiziana Sacco
Piergiorgio Strata
Benedetto Sacchetti
spellingShingle Lan Zhu
Tiziana Sacco
Piergiorgio Strata
Benedetto Sacchetti
Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
PLoS ONE
author_facet Lan Zhu
Tiziana Sacco
Piergiorgio Strata
Benedetto Sacchetti
author_sort Lan Zhu
title Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
title_short Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
title_full Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
title_fullStr Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
title_full_unstemmed Basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
title_sort basolateral amygdala inactivation impairs learning-induced long-term potentiation in the cerebellar cortex.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2011-01-01
description Learning to fear dangerous situations requires the participation of basolateral amygdala (BLA). In the present study, we provide evidence that BLA is necessary for the synaptic strengthening occurring during memory formation in the cerebellum in rats. In the cerebellar vermis the parallel fibers (PF) to Purkinje cell (PC) synapse is potentiated one day following fear learning. Pretraining BLA inactivation impaired such a learning-induced long-term potentiation (LTP). Similarly, cerebellar LTP is affected when BLA is blocked shortly, but not 6 h, after training. The latter result shows that the effects of BLA inactivation on cerebellar plasticity, when present, are specifically related to memory processes and not due to an interference with sensory or motor functions. These data indicate that fear memory induces cerebellar LTP provided that a heterosynaptic input coming from BLA sets the proper local conditions. Therefore, in the cerebellum, learning-induced plasticity is a heterosynaptic phenomenon that requires inputs from other regions. Studies employing the electrically-induced LTP in order to clarify the cellular mechanisms of memory should therefore take into account the inputs arriving from other brain sites, considering them as integrative units. Based on previous and the present findings, we proposed that BLA enables learning-related plasticity to be formed in the cerebellum in order to respond appropriately to new stimuli or situations.
url http://europepmc.org/articles/PMC3031621?pdf=render
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