Activity-Dependent Synaptic Plasticity in the Central Nucleus of the Amygdala

Samson, Rachel D.; Paré, Denis

doi:10.1523/jneurosci.3713-04.2005

Cited by 98 publications

(73 citation statements)

References 83 publications

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“…Recent studies suggest that the CeM is an essential site of plasticity in fear conditioning (Wilensky et al, 2001;Goosens and Maren, 2003;Paré et al, 2004). Long-term potentiation has been observed in the projections from the BA to the CeM (Fu and Shinnick-Gallagher, 2004) and from the MGm to the CeM (Samson and Paré, 2005). Thus, the CeM appears to be a site of convergence of plastic inputs from several structures involved in fear learning.…”

Section: Discussionmentioning

confidence: 99%

Lesions of the Basal Amygdala Block Expression of Conditioned Fear But Not Extinction

Anglada-Figueroa¹,

Quirk²

2005

J. Neurosci.

198

138

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Although the role of the amygdala in acquisition of conditioned fear is well established, there is debate concerning the intra-amygdala circuits involved. The lateral nucleus of the amygdala (LA) is thought to be an essential site of plasticity in fear conditioning. The LA has both direct and indirect [via the basal nuclei; basal amygdala (BA)] projections to the central nucleus (Ce) of the amygdala, an essential output for fear behaviors. Lesions of the LA or Ce prevent acquisition of conditioned freezing to a conditioned stimulus, but BA lesions do not, suggesting that the BA is not normally involved in fear conditioning. If true, posttraining BA lesions should also have no effect. Replicating previous studies, we found that rats given electrolytic BA lesions before training acquired conditioned fear normally. They also showed normal long-term retention and extinction of conditioned fear. Unexpectedly, BA lesions made after training completely blocked expression of conditioned fear. Despite this deficit, lesioned rats were able to learn a new tone-shock association. Thus, although the LA-Ce system is sufficient for fear acquisition in the absence of the BA, it is not sufficient when the BA is present, suggesting that the BA is an important site of plasticity in fear conditioning. The pattern of lesion deficits we observed (after but not before training) might be explained by homeostatic mechanisms that balance plasticity over multiple inputs, regulating the influence of the BA and LA onto Ce output neurons.

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Section: Discussionmentioning

confidence: 99%

Lesions of the Basal Amygdala Block Expression of Conditioned Fear But Not Extinction

Anglada-Figueroa¹,

Quirk²

2005

J. Neurosci.

198

138

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“…AMPA-EPSCs were isolated by holding the postsynaptic cell at Ϫ90 mV to block voltage-dependent postsynaptic NMDARs. In addition, postsynaptic NMDARs were blocked pharmacologically in most experiments by loading the postsynaptic cell internally with the NMDA channel blocker (ϩ)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801; 1 mM) via the recording pipette (Berretta and Jones, 1996;Woodhall et al, 2001;Humeau et al, 2003;Mameli et al, 2005;Samson and Pare, 2005;V. A. Bender et al, 2006;Corlew et al, 2007), which selectively blocks postsynaptic NMDA currents without affecting NMDA currents in neighboring cells (V. A. .…”

Section: Whole-cell Recordingmentioning

confidence: 99%

Synapse-Specific Expression of Functional Presynaptic NMDA Receptors in Rat Somatosensory Cortex

Brasier¹,

Feldman²

2008

J. Neurosci.

119

138

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Presynaptic NMDA receptors (NMDARs) modulate release and plasticity at many glutamatergic synapses, but the specificity of their expression across synapse classes has not been examined. We found that non-postsynaptic, likely presynaptic NR2B-containing NMDARs enhanced AMPA receptor-mediated synaptic transmission at layer 4 (L4) to L2/3 (L4 -L2/3) synapses in juvenile rat barrel cortex. This modulation was apparent at room temperature when presynaptic NMDARs were activated by elevation of extracellular glutamate or application of exogenous NMDAR agonists. At near physiological temperatures, modulation of transmission by presynaptic NMDARs occurred naturally, without the need for external activation. Blockade of presynaptic NMDARs depressed unitary and extracellularly evoked EPSCs at L4 -L2/3 synapses, accompanied by increases in paired-pulse ratio and coefficient of variation, indicative of a decrease in presynaptic release probability. NMDAR agonists increased the frequency of miniature EPSCs in L2/3 neurons, without altering their amplitude or kinetics. Focal application of NMDAR antagonist revealed that the NMDARs that modulate L4 -L2/3 transmission are located in L2/3, not L4, consistent with localization on terminals or axons of L4 -L2/3 synapses, rather than on the somatodendritic compartment of presynaptic L4 neurons. In contrast, presynaptic NMDARs did not modulate L4 -L4 synapses, which originate from the same presynaptic neurons as L4 -L2/3 synapses, or cross-columnar L2/3-L2/3 horizontal projections, which synapse onto the same postsynaptic target neurons. Thus, presynaptic NMDARs selectively modulate L4 -L2/3 synapses, relative to other synapses made by the same neurons. Existence of these receptors may support specialized processing or plasticity by L4 -L2/3 synapses.

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“…This DA-dependency is due in part to a DA modulation of the plastic synaptic events that underlie reinforcement and associative learning. Synaptic plasticity has indeed been shown to occur at target structures of the VTA, including the NAc (Kombian and Malenka 1994;Li and Kauer 2004;Pennartz et al 1993;Robbe et al 2002;Taverna and Pennartz 2003;Thomas et al 2001), PFC (Otani et al 2003) and amygdala (Bauer and LeDoux 2004;Bauer et al 2002;Fourcaudot et al 2009;Kandel 1998, 2007;Humeau et al 2003;Samson and Pare 2005). DA was shown to modulate plasticity in the striatum (Calabresi et al 2007;Centonze et al 2003;Kerr and Wickens 2001;Pawlak and Kerr 2008;Reynolds et al 2001), the amygdala (Bissière et al 2003), PFC Kolomiets et al 2009) and hippocampus (Frey et al 1989(Frey et al , 1990(Frey et al , 1991Lisman 1996, 1998;Gurden et al 1999) but not in the NAc.…”

Section: Models Of the Effects Of Dopamine Releasementioning

confidence: 99%

Computational models of reinforcement learning: the role of dopamine as a reward signal

2010

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Reinforcement learning is ubiquitous. Unlike other forms of learning, it involves the processing of fast yet content-poor feedback information to correct assumptions about the nature of a task or of a set of stimuli. This feedback information is often delivered as generic rewards or punishments, and has little to do with the stimulus features to be learned. How can such low-content feedback lead to such an efficient learning paradigm? Through a review of existing neuro-computational models of reinforcement learning, we suggest that the efficiency of this type of learning resides in the dynamic and synergistic cooperation of brain systems that use different levels of computations. The implementation of reward signals at the synaptic, cellular, network and system levels give the organism the necessary robustness, adaptability and processing speed required for evolutionary and behavioral success.

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Activity-Dependent Synaptic Plasticity in the Central Nucleus of the Amygdala

Cited by 98 publications

References 83 publications

Lesions of the Basal Amygdala Block Expression of Conditioned Fear But Not Extinction

Lesions of the Basal Amygdala Block Expression of Conditioned Fear But Not Extinction

Synapse-Specific Expression of Functional Presynaptic NMDA Receptors in Rat Somatosensory Cortex

Computational models of reinforcement learning: the role of dopamine as a reward signal

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