12,174 research outputs found
Blockade of amygdala metabotropic glutamate receptor subtype 1 impairs fear extinction
No full textThe metabotropic glutamate receptor subtype 1 (mGluR1) is thought to be crucial for several forms of memory, but its role in memory extinction has not been determined. Here, we examined a role of mGluR1 in the extinction of conditioned fear using microinjection of an mGluR1 antagonist, CPCCOEt, into the lateral amygdala (LA), a critical structure for fear conditioning and extinction. Intra-LA injection of 3 mu g CPCCOEt impaired extinction that was initiated 48 h after the conditioning, but not that initiated 2 h after the conditioning, indicating that the effectiveness of CPCCOEt depends upon the length of time since fear conditioning. The CPCCOEt injection failed to alter an mGluR1-like receptor (mGluR5)-dependent acquisition of fear memory, further supporting the specificity of the injected CPCCOEt on mGluR1. Together, our results suggest that amygdala mGluR1 plays a critical role in the extinction of learned fear, but not in the acquisition of fear memory. (c) 2007 Elsevier Inc. All rights reserved.
GSK-3β activation is required for ZIP-induced disruption of learned fear
No full textThe myristoylated zeta inhibitory peptide (ZIP), which was originally developed as a protein kinase C/M zeta (PKC zeta/PKM zeta) inhibitor, is known to produce the loss of different forms of memories. However, ZIP induces memory loss even in the absence of PKM zeta, and its mechanism of action, therefore, remains elusive. Here, through a kinome-wide screen, we found that glycogen synthase kinase 3 beta (GSK-3 beta) was robustly activated by ZIP in vitro. ZIP induced depotentiation (a cellular substrate of memory erasure) of conditioning-induced potentiation at LA synapses, and the ZIP-induced depotentiation was prevented by a GSK-3 beta inhibitor, 6-bromoindirubin-3-acetoxime (BIO-acetoxime). Consistently, GSK-3 beta inhibition by BIO-acetoxime infusion or GSK-3 beta knockdown by GSK-3 beta shRNA in the LA attenuated ZIP-induced disruption of learned fear. Furthermore, conditioned fear was decreased by expression of a non-inhibitable form of GSK-3 beta in the LA. Our findings suggest that GSK-3 beta activation is a critical step for ZIP-induced disruption of memory.
Extinction of cued fear memory involves a distinct form of depotentiation at cortical input synapses onto the lateral amygdala
No full textThe amygdala is known to be a critical storage site of conditioned fear memory. Among the two major pathways to the lateral amygdala (LA), the cortical pathway is known to display a presynaptic long-term potentiation which is occluded with fear conditioning. Here we show that fear extinction results in a net depression of conditioning-induced potentiation at cortical input synapses onto the LA (C-LA synapses). Fear conditioning induced a significant potentiation of excitatory postsynaptic currents at C-LA synapses compared with naive and unpaired controls, whereas extinction apparently reversed this potentiation. Paired-pulse low-frequency stimulation (pp-LFS) induced synaptic depression in the C-LA pathway of fear-conditioned rats, but not in naive or unpaired controls, indicating that the pp-LFS-induced depression is specific to associative learning-induced changes (pp-LFS-induced depotentiation(ex vivo)). Importantly, extinction occluded pp-LFS-induced depotentiation(ex vivo), suggesting that extinction shares some mechanisms with the depotentiation. pp-LFS-induced depotentiation(ex vivo) required NMDA receptor (NMDAR) activity, consistent with a previous finding that blockade of amygdala NMDARs impaired fear extinction. In addition, pp-LFS-induced depotentiation(ex vivo) required activity of group II metabotropic glutamate receptors (mGluRs), known to be present at presynaptic terminals, but not AMPAR internalization, consistent with a presynaptic mechanism for pp-LFS-induced depotentiation(ex vivo). This result is in contrast with another form of ex vivo depotentiation in the thalamic pathway that requires both group I mGluR activity and AMPAR internalization. We thus suggest that extinction of conditioned fear involves a distinct form of depotentiation at C-LA synapses, which depends upon both NMDARs and group II mGluRs.
Author Identification from Song Lyrics
No full textMachine Learning (ML) tools have been used extensively in a wide variety of domains
recently. Due the enormous amount of data being produced, machine learning techniques
are being heavily used to make sense of data & derive meaningful results. Using machine
learning tools, we can turn the data into knowledge.
Music is one of the truest forms of art. Bangladesh has a great history of music with a
great tradition of song writing over centuries. Authorship attribution is the way of
identifying the author from a linguistic corpus.
This paper demonstrates a guideline to identify the author of a Bengali song from the
lyrics of that song using machine learning. This research work presents the first work on
machine learning approach for author attribution from the lyrics of a song. Here six
methods of machine learning are used for the author identification and high accuracies
have been achieved from these methods. It is observed that Naïve Bayes method provides
higher accuracy in comparison with the other methods
Song
No full textAuthor attribution from Rudolph, 240. Printed on yellow paper with black ink. Set to the tune of "Happy land of Canaan". First line "You Rebels come along and listen to my song"
Fear conditioning occludes late-phase long-term potentiation at thalamic input synapses onto the lateral amygdala in rat brain slices
No full textLate-phase long-term potentiation (L-LTP) of excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala (T-LA synapses) has been proposed as a cellular substrate for long-term fear memory. This notion is evidenced primarily by previous reports in which the same pharmacological treatments block both T-LA L-LTP and the consolidation of fear memory. In this study, we report that fear conditioning occludes L-LTP at T-LA synapses in brain slices prepared after fear memory consolidation. L-LTP was restored either when synaptic depotentiation was induced prior to L-LTP induction in brain slices prepared from conditioned rats or when brain slices were prepared from conditioned rats that had been exposed to subsequent fear extinction, which is a behavior paradigm known to induce in vivo synaptic depotentiation at T-LA synapses. These results suggest that fear conditioning recruits L-LTP-like mechanisms that are reversible and saturable at T-LA synapses. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
Modulation of fear memory by retrieval and extinction: a clue for memory deconsolidation
No full textAbstract
Memories are fragile and easily forgotten at first, but after a consolidation period of hours to weeks, are inscribed in our brains as stable traces, no longer vulnerable to conventional amnesic treatments. Retrieval of a memory renders it labile, akin to the early stages of consolidation. This phenomenon has been explored as memory reactivation, in the sense that the memory is temporarily ‘deconsolidated’, allowing a short time window for amnesic intervention. This window closes again after reconsolidation, which restores the stability of the memory. In contrast to this ‘transient deconsolidation’ and the short-spanned amnesic effects of consolidation blockers, some specific treatments can disrupt even consolidated memory, leading to apparent amnesia. We propose the term ‘amnesic deconsolidation’ to describe such processes that lead to disruption of consolidated memory and/or consolidated memory traces. We review studies of these ‘amnesic deconsolidation’ treatments that enhance memory extinction, alleviate relapse, and reverse learning-induced plasticity. The transient deconsolidation that memory retrieval induces and the amnesic deconsolidation that these regimes induce both seem to dislodge a component that stabilizes consolidated memory. Characterizing this component, at both molecular and network levels, will provide a key to developing clinical treatments for memory-related disorders and to defining the consolidated memory trace.</jats:p
Sound tuning of amygdala plasticity in auditory fear conditioning
No full textVarious auditory tones have been used as conditioned stimuli (CS) for fear conditioning, but researchers have largely neglected the effect that different types of auditory tones may have on fear memory processing. Here, we report that at lateral amygdala (LA) synapses (a storage site for fear memory), conditioning with different types of auditory CSs (2.8 kHz tone, white noise, FM tone) recruits distinct forms of long-term potentiation (LTP) and inserts calcium permeable AMPA receptor (CP-AMPAR) for variable periods. White noise or FM tone conditioning produced brief insertion (< 6 hr after conditioning) of CP-AMPARs, whereas 2.8 kHz tone conditioning induced more persistent insertion (>= 6 hr). Consistently, conditioned fear to 2.8 kHz tone but not to white noise or FM tones was erased by reconsolidation-update (which depends on the insertion of CP-AMPARs at LA synapses) when it was performed 6 hr after conditioning. Our data suggest that conditioning with different auditory CSs recruits distinct forms of LA synaptic plasticity, resulting in more malleable fear memory to some tones than to others.
The Singer or the Song? Developments in Performers' Rights from the Perspective of a Cultural Economist
No full textOver the last century, performers gradually acquired statutory protection of their economic and moral
rights. These rights are not copyright in the legal sense but neighboring rights and until recently, they
were mainly remuneration rights that are collectively administered. With the WPPT (WIPO
Performers and Phonograms Treaty), performers now have individual exclusive rights for digital
performances; this leads to the question: what has motivated this change – is it a change in the
perception of the value of performer or a change brought about by the changing technology of copying or,
indeed, a change that reflects different economic costs and benefits? The paper discusses the role of
copyright law as an incentive to performers and asks if the economic role of the performer is so different
from that of the author. The conclusion is that a complex interaction of the legal regulations, economic
conditions and institutional arrangements for administering these new rights will determine the outcome
Freemasons\u27 Song
No full textSong concerning pride in Freemasonryhttps://egrove.olemiss.edu/kgbsides_uk/1560/thumbnail.jp
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