Literature DB >> 16406707

Input-specific long-term potentiation in the rat lateral amygdala of horizontal slices.

Christian Drephal1, Manja Schubert, Doris Albrecht.   

Abstract

Long-term potentiation (LTP) at input synapses to the lateral nucleus of the amygdala (LA) is a candidate mechanism for memory storage during fear learning. Cellular mechanisms of LTP have been nearly exclusively investigated in coronal brain slices. In our experiments, we used a horizontal brain slice preparation of rats that preserved most of the connections to cortical areas and the hippocampus. The stimulation electrodes were located either within the external capsule (EC) or the LA. The aim of the present study was to investigate the mechanisms of LTP induced either by weak theta burst stimulation (TBS) or strong high frequency stimulation (HFS) using the two different stimulation sites. Whereas both TBS and HFS of afferences running through the LA induced stable LTP, TBS failed to induce LTP of EC-inputs to the LA. The present findings also show that LTP in the LA exhibits vulnerability at different time windows after induction. The time window was dependent on the kind of stimulated afferences. Later LTP becomes resistant to disruption by low frequency stimulation. We could show that both used inputs depended on NMDA receptors for LTP-induction. LTP induced by stimulation of fibers within the LA was not altered by nifedipine (10 microM). In contrast, EC-induced LTP was dependent on L-type voltage-gated calcium channels (VGCC). Finally, we found a higher magnitude of LTP in females using TBS, whereas HFS did not cause gender-specific differences. Our study supports the conclusion that the form of LA-LTP depend on which afferences are activated and what pattern of stimulation is used to induce LTP.

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Year:  2006        PMID: 16406707     DOI: 10.1016/j.nlm.2005.11.004

Source DB:  PubMed          Journal:  Neurobiol Learn Mem        ISSN: 1074-7427            Impact factor:   2.877


  9 in total

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4.  Angiotensin-(1-7)-induced plasticity changes in the lateral amygdala are mediated by COX-2 and NO.

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9.  Glutamate receptor GluA1 subunit is implicated in capsaicin induced modulation of amygdala LTP but not LTD.

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  9 in total

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