In particular, the actin network in neurons is extremely dynamic and neuronal activity can regulate a rapid turnover of actin. In this working model, the dynamic modulation of the cytoskeleton is a major candidate for an activity-dependent permissive state of synapses. Alternatively, one can consider the synaptic tag as a remodelling of the post-synaptic density (PSD), induced by LTP or LTD rendering synapses permissive to change. This may explain why several candidate molecules have been implicated in the setting of the synaptic tag and why particular molecules have been specifically implicated in the setting of LTP tags 13 or LTD tags 12, 14. One confounding aspect is that upon induction of plasticity, of either LTP or LTD, the setting of the synaptic tag is intrinsically indistinguishable from the expression of synaptic plasticity. This includes calcium/calmodulin dependent kinase II (CaMKII) for LTP tagging and capture 10, 11, 12 and mitogen-activated protein kinases (MAPKs) for LTD tagging and capture 12. Several molecules have been implicated in LTP and LTD maintenance by synaptic tagging and capture mechanisms 9. Although the nature of the synaptic tag remains unclear, it is generally accepted that it must be a local and transient molecular alteration caused by plasticity-inducing synaptic activation which can capture PRPs 8. The STC provides a cellular mechanism to associate transient and persistent forms of plasticity through the sharing and allocation of PRPs among independent sets of activated synapses. Since LTP and LTD are by large input-specific it was proposed that activated synapses are tagged so that synthesised PRPs are captured at modified synapses (synaptic tagging and capture hypothesis - STC) 6, 7. Classic work on synaptic plasticity has shown that persistent forms of LTP and LTD require de novo protein synthesis of plasticity-related proteins (PRPs) 4, 5. Our results support our hypothesis that modulation of the actin cytoskeleton provides an input-specific signal for synaptic protein capture.Īctivity-dependent plasticity of synaptic connections reflects a combination of functional and structural alterations at synapses and represents a cellular model of memory formation 1, 2, 3. Suspending synaptic activation also restricts the time window of synaptic capture, which can be restored by inhibiting actin polymerization. Moreover, inhibition of actin polymerisation mimics the setting of a synaptic tag, in an activity-dependent manner, allowing the expression of LTD in non-stimulated synapses. Interestingly, we found that actin depolymerisation and CaMKII activation are involved in LTD synaptic-tagging and capture. Inhibition of either actin depolymerisation or polymerization blocks LTD induction whereas only the inhibition of actin depolymerisation blocks LTD maintenance. We found that modulation of actin dynamics has different roles in the induction and maintenance of LTD. We propose that the synaptic tag represents a structural alteration that turns synapses permissive to change. SM-J700F, SM-J700H, SM-J700M, SM-J700T, J7, SM-J700T1, SM-J700K, SM-J700P, SM-j7008Ĭontrast ratio: Infinite (nominal), 3.Persistent forms of plasticity, such as long-term depression (LTD), are dependent on the interplay between activity-dependent synaptic tags and the capture of plasticity-related proteins. Wi-Fi 802.11 b/g/n, Wi-Fi Direct, hotspot Single SIM (Micro-SIM) or Dual SIM (Micro-SIM, dual stand-by)ĥ.5 inches, 83.4 cm 2 (~69.6% screen-to-body ratio)ħ20 x 1280 pixels, 16:9 ratio (~267 ppi density)Īndroid 5.1 (Lollipop), upgradable to 7.1.1 (Nougat) Versions: J700F (India, Thailand) J700M (LATAM) J700M/DS (Brazil) J700H with no LTE (South Africa, Pakistan, Vietnam, Philippines, Russia) J700T (T-Mobile, Metro PCS) J700P (Virgin Mobile, Boost).Īlso known as Samsung Galaxy J7 Duos with dual-SIM card slots Network