(Q51075451)

28 March 2018

title

A role for amygdaloid PKA and PKC in the acquisition of long-term conditional fear memories in rats. (English)

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28 March 2018

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1

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28 March 2018

Stephen Maren

series ordinal

3

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28 March 2018

author name string

Holt W

series ordinal

2

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28 March 2018

language of work or name

English

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publication date

1 September 2000

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28 March 2018

Behavioural Brain Research

published in

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28 March 2018

volume

114

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28 March 2018

page(s)

145-152

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28 March 2018

issue

1-2

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28 March 2018

The MAPK cascade is required for mammalian associative learning.

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Why we think plasticity underlying Pavlovian fear conditioning occurs in the basolateral amygdala

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Postsynaptic induction and PKA-dependent expression of LTP in the lateral amygdala.

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cAMP contributes to mossy fiber LTP by initiating both a covalently mediated early phase and macromolecular synthesis-dependent late phase.

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Cross talk between ERK and PKA is required for Ca2+ stimulation of CREB-dependent transcription and ERK nuclear translocation.

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Stimulation of cAMP response element (CRE)-mediated transcription during contextual learning.

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Amygdalar NMDA receptors are critical for new fear learning in previously fear-conditioned rats.

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NMDA and non-NMDA receptors contribute to synaptic transmission between the medial geniculate body and the lateral nucleus of the amygdala.

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An essential role for postsynaptic calmodulin and protein kinase activity in long-term potentiation.

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Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP

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Synaptic transmission and plasticity in the amygdala. An emerging physiology of fear conditioning circuits

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Overtraining does not mitigate contextual fear conditioning deficits produced by neurotoxic lesions of the basolateral amygdala.

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Neurotoxic basolateral amygdala lesions impair learning and memory but not the performance of conditional fear in rats.

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Long-term potentiation in the amygdala: a mechanism for emotional learning and memory.

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Synaptic plasticity in the basolateral amygdala induced by hippocampal formation stimulation in vivo.

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Control of memory formation through regulated expression of a CaMKII transgene

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Fear conditioning induces a lasting potentiation of synaptic currents in vitro.

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Fear conditioning enhances different temporal components of tone-evoked spike trains in auditory cortex and lateral amygdala.

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LTP is accompanied by commensurate enhancement of auditory-evoked responses in a fear conditioning circuit.

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Fear conditioning induces associative long-term potentiation in the amygdala

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Stress persistently increases NMDA receptor-mediated binding of [3H]PDBu (a marker for protein kinase C) in the amygdala, and re-exposure to the stressful context reactivates the increase.

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Toward a molecular explanation for long-term potentiation.

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Lack of a temporal gradient of retrograde amnesia following NMDA-induced lesions of the basolateral amygdala assessed with the fear-potentiated startle paradigm.

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Retrograde abolition of conditional fear after excitotoxic lesions in the basolateral amygdala of rats: absence of a temporal gradient

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N-methyl-D-aspartate receptors in the basolateral amygdala are required for both acquisition and expression of conditional fear in rats.

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Identifiers

DOI

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28 March 2018

PubMed ID

10996055

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28 March 2018