PMID- 24631390
OWN - NLM
STAT- MEDLINE
DCOM- 20141212
LR  - 20161125
IS  - 1872-7549 (Electronic)
IS  - 0166-4328 (Linking)
VI  - 266
DP  - 2014 Jun 1
TI  - NMDA receptor activation and PKC but not PKA lead to the modification of the 
      long-term potentiation in the insular cortex induced by conditioned taste 
      aversion: differential role of kinases in metaplasticity.
PG  - 58-62
LID - S0166-4328(14)00146-6 [pii]
LID - 10.1016/j.bbr.2014.02.049 [doi]
AB  - It has been reported that training in behavioral tasks modifies the ability to 
      induce long-term potentiation (LTP) in an N-methyl-D-aspartate receptor 
      (NMDAR)-dependent manner. This receptor leads to calcium entry into neuronal 
      cells, promoting the activation of protein kinases as protein kinase A (PKA) and 
      protein kinase C (PKC), which contribute significantly to the formation of 
      different types of memories and play a pivotal role in the expression of LTP. Our 
      previous studies involving the insular cortex (IC) have demonstrated that 
      induction of LTP in the basolateral amygdaloid nucleus (BLA)-IC projection prior 
      to conditioned taste aversion (CTA) training enhances the retention of this task. 
      Recently, we showed that CTA training triggers a persistent impairment in the 
      ability to induce subsequent synaptic plasticity on the BLA-IC pathway in a 
      protein synthesis-dependent manner, but the underlying molecular mechanisms 
      remain unclear. In the present study we investigated whether the blockade of 
      NMDAR, as well as the inhibition of PKC and PKA affects the CTA-dependent 
      impairment of the IC-LTP. Thus, CTA-trained rats received high frequency 
      stimulation in the Bla-IC projection in order to induce LTP 48 h after the 
      aversion test. The NMDAR antagonist CPP and the specific inhibitors for PKC 
      (chelerythrine) and PKA (KT-5720) were intracortically administered during the 
      acquisition session. Our results show that the blockade of NMDAR and the 
      inhibition of PKC activity prevent the CTA memory-formation as well as the IC-LTP 
      impairment. Nevertheless, PKA inhibition prevents the memory formation of taste 
      aversion but produces no interference with the CTA-dependent impairment of the 
      IC-LTP. These findings reveal the differential roles of protein kinases on 
      CTA-dependent modification of IC-LTP enhancing our understanding of the effects 
      of memory-related changes on synaptic function.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Rodriguez-Duran, Luis F
AU  - Rodriguez-Duran LF
AD  - Division de Investigacion y Estudios de Posgrado, Facultad de Psicologia, 
      Universidad Nacional Autonoma de Mexico, Mexico D.F., Mexico.
FAU - Escobar, Martha L
AU  - Escobar ML
AD  - Division de Investigacion y Estudios de Posgrado, Facultad de Psicologia, 
      Universidad Nacional Autonoma de Mexico, Mexico D.F., Mexico. Electronic address: 
      mescobar@unam.mx.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140311
PL  - Netherlands
TA  - Behav Brain Res
JT  - Behavioural brain research
JID - 8004872
RN  - 0 (Benzophenanthridines)
RN  - 0 (Carbazoles)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Piperazines)
RN  - 0 (Pyrroles)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 58HV29I28S (KT 5720)
RN  - 98Y1I8ZD4M (3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid)
RN  - E3B045W6X0 (chelerythrine)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
SB  - IM
MH  - Animals
MH  - Avoidance Learning/drug effects/*physiology
MH  - Benzophenanthridines/pharmacology
MH  - Carbazoles/pharmacology
MH  - Cerebral Cortex/drug effects/*physiology
MH  - Cyclic AMP-Dependent Protein Kinases/*metabolism
MH  - Electric Stimulation
MH  - Enzyme Inhibitors/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Long-Term Potentiation/drug effects/*physiology
MH  - Male
MH  - Piperazines/pharmacology
MH  - Protein Kinase C/metabolism
MH  - Pyrroles/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Taste/drug effects/*physiology
OTO - NOTNLM
OT  - CTA
OT  - LTP
OT  - Metaplasticity
OT  - NMDAR
OT  - PKA
OT  - PKC
EDAT- 2014/03/19 06:00
MHDA- 2014/12/17 06:00
CRDT- 2014/03/18 06:00
PHST- 2013/09/26 00:00 [received]
PHST- 2014/02/20 00:00 [revised]
PHST- 2014/02/27 00:00 [accepted]
PHST- 2014/03/18 06:00 [entrez]
PHST- 2014/03/19 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
AID - S0166-4328(14)00146-6 [pii]
AID - 10.1016/j.bbr.2014.02.049 [doi]
PST - ppublish
SO  - Behav Brain Res. 2014 Jun 1;266:58-62. doi: 10.1016/j.bbr.2014.02.049. Epub 2014 
      Mar 11.