Hippocampal mossy fiber calcium transients are maintained during long-term potentiation and are inhibited by endogenous zinc

Quinta‐Ferreira, Mário; Matias, Carlos M.

doi:10.1016/j.brainres.2004.01.013

Cited by 37 publications

(17 citation statements)

References 44 publications

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“…2 C and D). TPEN, even in a significantly higher concentration than in our experiments, has no effect on glutamatergic EPSPs (22). When inhibition was eliminated by blocking the GABA A receptors (GABA A R) in the presence of TPEN with the selective antagonist picrotoxin (PTX) (100 M), LTP was restored.…”

Section: Expression Of Znt-3 Gene and Distribution Of Zn 2؉ -Containicontrasting

confidence: 57%

Synaptically released zinc gates long-term potentiation in fear conditioning pathways

Kodirov

Takizawa²,

Joseph³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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The functional role of releasable Zn 2؉ in the central nervous system remains unknown. Here we show that zinc transporter 3 (ZnT-3), which maintains a high concentration of Zn 2؉ in synaptic vesicles and serves as a marker for zinc-containing neurons, is enriched in the lateral nucleus of the amygdala and in the temporal area 3 of the auditory cortex, an area that conveys information about the auditory conditioned stimulus to the lateral nucleus of the amygdala, but not in other conditioned stimulus areas located in the auditory thalamus. Using whole-cell recordings from amygdala slices, we demonstrated that activity-dependent release of chelatable Zn 2؉ is required for the induction of spike timing-dependent long-term potentiation in cortical input to the amygdala implicated in fear learning. Our data indicate that synaptically released Zn 2؉ enables long-term potentiation at the cortico-amygdala synapses by depressing feed-forward GABAergic inhibition of principal neurons. This regulatory mechanism, implicating pathway-dependent release of Zn 2؉ , may serve an essential control function in assuring spatial specificity of long-lasting synaptic modifications in the neural circuit of a learned behavior.amygdala ͉ synapse ͉ synaptic plasticity ͉ glutamate ͉ GABA L ong-term potentiation (LTP) in afferent inputs to the amygdala is recruited during fear conditioning and used for retention of fear memory (1-5). A subset of glutamatergic neurons in fear conditioning pathways, including pyramidal neurons in the lateral nucleus of the amygdala (LA) where conditioned stimuli (CS) and unconditioned stimuli converge during fear learning (6-9), is enriched in zinc (Zn 2ϩ ) (4). Zn 2ϩ is found to be in a high concentration in synaptic vesicles at various synapses and to be colocalized with the neurotransmitters glutamate or GABA (10,11). Previous studies have demonstrated that this vesicular Zn 2ϩ can be released in a Ca 2ϩ -dependent manner in different regions of the brain, including the hippocampus, cortex, and amygdala, in response to synaptic stimulation at both glutamatergic and GABAergic synapses (11)(12)(13)(14)(15)(16)(17)(18)(19). This set of findings suggested to us the possibility that vesicular zinc may have a role in synaptic plasticity in the neural circuitry of fear learning.Zn 2ϩ has been implicated in a variety of neuronal functions in the mammalian brain both as a paracrine and as an autocrine mediator (20). However, despite intensive efforts the functional role of releasable zinc in synaptic transmission and plasticity remained elusive (10, 20). Here we report that chelatable zinc, released during synaptic activation, is critically involved in control of LTP in the cortico-amygdala pathway, which conveys auditory information about the CS to the amygdala during fear conditioning. We find that zinc acts by suppressing feed-forward inhibition of projection neurons by local circuit interneurons. The pathway-specific expression of zinc-containing cells suggests that this regulatory mechanism may define the spat...

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Section: Expression Of Znt-3 Gene and Distribution Of Zn 2؉ -Containicontrasting

confidence: 57%

Synaptically released zinc gates long-term potentiation in fear conditioning pathways

Kodirov

Takizawa²,

Joseph³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Studies have indicated that molecules related to Ca 2+ signaling are involved in the hippocampal synaptic plasticity and in learning and memory [26], [27], [28], [29]. Both VGCCs and NMDA receptors are known to be important sources of Ca 2+ influx for the induction of LTP in certain conditions [30], [31], [32]. Various L-type calcium channels have been demonstrated to be important in different forms of memories [33], [34], [35], [36], [37], [38].…”

Section: Introductionmentioning

confidence: 99%

Retrieval of Context-Associated Memory is Dependent on the Cav3.2 T-Type Calcium Channel

et al. 2012

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Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3.2 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of this channel in learning and memory, we subjected Cav3.2 homozygous and heterozygous knockout mice and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning, the Morris water-maze and passive avoidance. The Cav3.2 −/− mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2 +/− mice, whereas LTP persisted for only 120 minutes in Cav3.2 −/− mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes, we next performed experiments to knock down local function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil, a T-type channel blocker, exhibited similar behaviors as homozygous knockouts. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel.

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“…Another approach has shown that zinc labeled in situ in the vesicles is released (along with the label) over time (PerezClausell and Danscher, 1986) and more rapidly over time during stimulation (Kay et al, 1995;Budde et al, 1997;Varea et al, 2001;Quinta-Ferreira and Matias, 2004). Release of free zinc has been studied by microdialysis in the intact brain (Frederickson et al, 2005a) and by fluorimetric imaging of zinc release from brain or retinal slices (Thompson et al, 2000;Li et al, 2001;Ueno et al, 2002;Takeda et al, 2005;Qian and Noebels, 2005;Komatsu et al, 2005;Redenti and Chappell, 2005).…”

Section: Introductionmentioning

confidence: 99%

Synaptic release of zinc from brain slices: Factors governing release, imaging, and accurate calculation of concentration

Frederickson

Giblin

Balaji

et al. 2006

Journal of Neuroscience Methods

110

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Hippocampal mossy fiber calcium transients are maintained during long-term potentiation and are inhibited by endogenous zinc

Cited by 37 publications

References 44 publications

Synaptically released zinc gates long-term potentiation in fear conditioning pathways

Synaptically released zinc gates long-term potentiation in fear conditioning pathways

Retrieval of Context-Associated Memory is Dependent on the Cav3.2 T-Type Calcium Channel

Synaptic release of zinc from brain slices: Factors governing release, imaging, and accurate calculation of concentration

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