This Song Is 2 Seconds Long рџрџрџ [NEW]

Does this unit allow you to keep one track going and turn the other on and off? For instance, I loop percussion tracks, then play guitar over it. Using the RC-20XL, I record the guitar as an overdub for soloing, then hold the pedal to undo that last layer to go to the next song section. It works ok, but getting the timing right is tricky.

this song is 2 seconds long 😂😂😂

Whether it's smooth water or blazing light trails you're aiming for, extending the length of your exposure can give you a great creative buzz. Here's some practical advice on how to control long exposures and set a shutter speed longer than the default maximum of 30 seconds on your Canon EOS camera.

An extended exposure can even give water a misty appearance. When shooting in daylight, an ND filter is essential to achieve long shutter speeds. Canon EOS 5D Mark II, 148 seconds at f16. Billy Stock.

The manual claims you can record 10 loops, then cycle through them, one way forward only via footswitch, as you play, but I haven't tried this. These would NOT be on the fly loops, they would have to be pre-recorded. Perhaps if you have a few rhythm patterns you could pre-record these and use them in a song or maybe use 2 or 3 loops on 3 or 4 songs, otherwise I don't get how one would use this.

I soon became curious about looping, and devoured info on related gear. Bernhoft was using the RC-50 Loopstation, which was already discontinued, so I looked for a good alternative. A few more months of exposure to live looping and my curiosity got the better of me - I ended up getting the bigger Boss RC-300, and it quickly became central to my acoustic and live looping sets. Here I'll share what this looper is all about, along with its pros and cons based on years of use.

To accommodate different instruments and sound sources, the RC-300 comes with stereo 1/4" inputs, an XLR input with phantom power and an Aux input. Each one comes with dedicated input level knobs that can be blended to taste. Unfortunately, all these input ports are regarded by the looper as a single input signal. It doesn't allow routing of different inputs into dedicated tracks. This is a big letdown because sometimes I need to separately loop my vocals and guitars, much like how its done in recording. Thankfully, there are workarounds like using compact mixers and signal switchers on the input. If I want to record just the guitar part while singing, I just turn off the looped mic signal and use a second mic that goes straight to PA. Still, these work arounds are not perfect and often require more rounds of loop building - which ultimately prolongs song buildup.

This plays fine most of the time, but at some moments, I cannot figure out when it happens after I stop playing a song the amplifier switches back to silence. When I start a song again the internal DAC has to pick-up the signal again so you miss the first seconds of the song.8 out of 10 times this does not happen. It's audible by a click a few seconds after pressing stop. If it works good, it's good for the entire session.

The time parameter is issued in seconds, and will activate when the in-game clock reaches the specified time. So a time of 300 will activate when the clock hits 5:00. Multiple commands can be queued up in this way to activate at a set time. On servers with unlimited clocks, the time will never be reached so the command will activate immediately.

Given the diversity of the functions ascribed to synaptic plasticity, it is not surprising that many forms and mechanisms of synaptic plasticity have been described. Synaptic transmission can be either enhanced or depressed by activity, and these changes span temporal domains ranging from milliseconds to hours, days, and presumably even longer. Furthermore, virtually all excitatory synapses in the mammalian brain simultaneously express a number of different forms of synaptic plasticity. Here, we attempt to provide a broad overview of the mechanisms of the most prominent forms of plasticity observed at excitatory synapses in the mammalian brain. After briefly reviewing short-lasting forms of synaptic plasticity, we will emphasize current understanding of the cellular mechanisms and possible functions of the class of phenomena commonly termed long-term potentiation (LTP) and long-term depression (LTD).

At some synapses, repetitive activation leads to depression that can last for several seconds or even minutes (Betz, 1970; Zucker and Regehr, 2002). As in paired-pulse depression, this generally occurs in synapses that exhibit a high probability of release, and is thought to result, at least in part, from a transient depletion of the release-ready pool of synaptic vesicles. The decrease in synaptic strength can also arise from the release of modulatory substances from the activated presynaptic terminals, postsynaptic cells, or even neighboring cells, initiating a signaling cascade that leads to inhibition of the presynaptic release machinery. Finally, a postsynaptic mechanism of short-term plasticity may involve desensitization of ligand-gated receptors, making the target neuron less sensitive to neurotransmitter. A key characteristic of depression at many synapses is use dependence. Higher levels of transmission are associated with larger depression, and reduction of baseline transmission (eg, by reducing external calcium concentration) relieves depression.

Experimental support for the very existence of such long-lasting, activity-dependent changes in synaptic strength was lacking until the early 1970s when Bliss and colleagues (Bliss and Gardner-Medwin, 1973; Bliss and Lomo, 1973) reported that repetitive activation of excitatory synapses in the hippocampus caused a potentiation of synaptic strength that could last for hours or even days. Over the last three decades, this phenomenon, eventually termed LTP, has been the object of intense investigation because it is widely believed that it provides an important key to understanding some of the cellular and molecular mechanisms by which memories are formed (Martin et al, 2000; Pastalkova et al, 2006; Whitlock et al, 2006).

No form of plasticity has generated more interest, or been more extensively studied than LTP in the CA1 region of the hippocampus. The excitement surrounding this phenomenon is due to compelling evidence from rodents, primates, and humans associating the hippocampus with a neural system involved in various forms of long-term memory (Martin et al, 2000; Zola-Morgan and Squire, 1993). Furthermore, several basic properties of LTP make it an attractive cellular mechanism for rapid information storage. Similar to memory, LTP can be generated rapidly and is strengthened and prolonged by repetition. It also exhibits cooperativity, associativity, and input specificity. (Nicoll et al, 1988). Cooperativity means that LTP can be induced by the coincident activation of a critical number of synapses. Associativity is the capacity to potentiate a weak input (a small number of synapses) when it is activated in association with a strong input (a larger number of synapses). As such, associativity is a cellular analogue of classical conditioning and is an implicit property of the so-called Hebbian synapse. Input specificity indicates that LTP is elicited only at activated synapses and not at adjacent, inactive synapses on the same postsynaptic cell. This feature dramatically increases the storage capacity of individual neurons since different synapses on the same cell can be involved in separate circuits encoding different bits of information.

A current simplified view of the mechanisms underlying NMDAR-dependent LTD can be summarized as follows (Figure 2): a modest increase in postsynaptic calcium concentration within dendritic spines due to modest activation of NMDARs leads to preferential activation of protein phosphatases (as well as a few other key signaling proteins). This leads to the dissociation of AMPARs from their molecular scaffolds in the PSD and their lateral movement to endocytic zones on the periphery of the PSD, where they are endocytosed and potentially degraded. We have not discussed the maintenance of LTD because there is little work on this topic. There is evidence that LTD is accompanied by a shrinkage in the size of dendritic spines (Nagerl et al, 2004; Zhou et al, 2004) and that this may be due to the loss of AMPARs (Hsieh et al, 2006). Furthermore, similar to LTP, protein translation may be needed for the long-term stable expression of LTD (Pfeiffer and Huber, 2006). Thus, it is generally believed that the activity-dependent trafficking of AMPARs into and out of synapses during LTP and LTD, respectively, is the first critical step in the morphological growth or shrinkage of synapses and that these structural modifications are the mechanisms by which bidirectional changes in synaptic strength are maintained. Indeed, the size of individual synapses correlates closely with the number of AMPARs they contain (Matsuzaki et al, 2001; Nusser et al, 1998; Takumi et al, 1999).

In contrast to NMDAR-dependent LTP, the triggering and expression of this form of LTP is thought to be solely or predominantly presynaptic, thus we refer to it as presynaptic LTP. While somewhat controversial, most experimental evidence suggests that presynaptic LTP is triggered by high-frequency tetanic stimulation, which causes a large, activity-dependent increase in calcium concentration within presynaptic axon terminals (Nicoll and Malenka, 1995; Nicoll and Schmitz, 2005; Zalutsky and Nicoll, 1990). Presynaptic voltage-dependent calcium channels are the critical source of the calcium increase, although the triggering of this LTP at MF synapses can be facilitated by the activation of presynaptic kainate receptors, particularly GluR6 (Lauri et al, 2001; Schmitz et al, 2003). Results from pharmacological manipulations and knockout mice are all consistent with the hypothesis that the increase in presynaptic calcium activates a calcium/calmodulin-dependent adenylyl cyclase. This leads to a increase in presynaptic cAMP and activation of PKA, which phosphorylates critical presynaptic substrates to cause a long-lasting enhancement in transmitter release (Nicoll and Malenka, 1995; Nicoll and Schmitz, 2005). Although this sequence of events is consistent with most of the results from all of the synapses that have been reported to express presynaptic LTP, surprisingly, a very different postsynaptic induction mechanism has been proposed to occur at MF synapses. This involves trans-synaptic interactions between postsynaptic EphB receptor tyrosine kinases and presynaptic B-Ephrin ligands leading, via an unknown mechanism, to a long-lasting enhancement of transmitter release (Armstrong et al, 2006; Contractor et al, 2002). 041b061a72