[
J Neurophysiol,
2007]
The work of Clark et al. in this issue of J. Neurophysiology extends the analysis of thermotaxis in C. elegans by providing a detailed analysis of the adaptation of thermotactic behavior. Previous work indicates that thermotaxis in C. elegans involves a biased random walk in which changes in temperature alter the duration of the runs that an animal makes between turns. Interestingly, the authors find that although behavioral responses to increases and decreases in temperature have opposite effects on run length, the two responses are of similar magnitude and adapt with similar kinetics. These properties are predicted to allow the system act as a band-pass filter that would be less sensitive to temperature fluctuations occurring on a time-scale significantly faster or slower than the time needed for an average run. This analysis of C. elegans thermotaxis raises potential parallels to bacterial chemotaxis, with the kinetics of adaptation playing an important role in determining the ability of the organism to sense a stimulus gradient. This raises the possibility that diverse organisms may exploit similar system properties to solve similar problems, such as the problem of responding robustly to subtle gradations in an external stimulus.
[
Genetics,
2014]
Ca(2+)/calmodulin-dependent Kinase II (CaMKII) is a calcium-regulated serine threonine kinase whose functions include regulation of synaptic activity (Coultrap and Bayer 2012). A postsynaptic role for CaMKII in triggering long-lasting changes in synaptic activity at some synapses has been established, although the relevant downstream targets remain to be defined (Nicoll and Roche 2013). A presynaptic role for CaMKII in regulating synaptic activity is less clear with evidence for CaMKII either increasing or decreasing release of neurotransmitter from synaptic vesicles (SVs) (Wang 2008). In this issue Hoover et al. (2014) further expand upon the role of CaMKII in presynaptic cells by demonstrating a role in regulating another form of neuronal signaling, that of dense core vesicles (DCVs), whose contents can include neuropeptides and insulin-related peptides, as well as other neuromodulators such as serotonin and dopamine (Michael et al. 2006). Intriguingly, Hoover et al. (2014) demonstrate that active CaMKII is required cell autonomously to prevent premature release of DCVs after they bud from the Golgi in the soma and before they are trafficked to their release sites in the axon. This role of CaMKII requires it to have kinase activity as well as an activating calcium signal released from internal ER stores via the ryanodine receptor. Not only does this represent a novel function for CaMKII but also it offers new insights into how DCVs are regulated. Compared to SVs we know much less about how DCVs are trafficked, docked, and primed for release. This is despite the fact that neuropeptides are major regulators of human brain function, including mood, anxiety, and social interactions (Garrison et al. 2012; Kormos and Gaszner 2013; Walker and Mcglone 2013). This is supported by studies showing mutations in genes for DCV regulators or cargoes are associated with human mental disorders (Sadakata and Furuichi 2009; Alldredge 2010; Quinn 2013; Quinn et al. 2013). We lack even a basic understanding of DCV function, such as, are there defined DCV docking sites and, if so, how are DCVs delivered to these release sites? These results from Hoover et al. (2014) promise to be a starting point in answering some of these questions.