The role of T-type calcium channels in animals without nervous systems is unknown. Smith et al. characterize TCav3 from Trichoplax adhaerens, finding expression in neurosecretory-like cells and preference for Ca2+ over Na+ via strong extracellular Ca2+ block, despite low selectivity for Ca2+ in the pore.

Individuals vary in their responses to stroke and trauma, hampering predictions of outcomes. One reason might be that neural circuits contain hidden variability that becomes relevant only when those individuals are challenged by injury. We found that in the mollusc, Tritonia diomedea, subtle differences between animals within the neural circuit underlying swimming behavior had no behavioral relevance under normal conditions but caused differential vulnerability of the behavior to a particular brain lesion. The extent of motor impairment correlated with the site of spike initiation in a specific neuron in the neural circuit, which was determined by the strength of an inhibitory synapse onto this neuron. Artificially increasing or decreasing this inhibitory synaptic conductance with dynamic clamp correspondingly altered the extent of motor impairment by the lesion without affecting normal operation. The results suggest that neural circuit differences could serve as hidden phenotypes for predicting the behavioral outcome of neural damage.DOI: http://dx.doi.org/10.7554/eLife.02598.001

The sea slug Hermissenda crassicornis (Mollusca, Gastropoda, Nudibranchia) has been studied extensively in associative learning paradigms. However, lack of genetic information previously hindered molecular-level investigations. Here, the Hermissenda brain transcriptome was sequenced and assembled de novo, producing 165,743 total transcripts. Orthologs of 95 genes implicated in learning were identified. These included genes for a serotonin receptor and a GABA-B receptor subunit that had not been previously described in molluscs, as well as an adenylyl cyclase gene not previously described in gastropods. This study illustrates the Hermissenda transcriptome's potential as an important genetic tool in future learning and memory research.[Supplemental material is available for this article.]Nervous systems of molluscs have been a focus of neuroscience research for many decades, yet their study has been impeded by lack of genetic information. The nudibranch Hermissenda crassicornis exhibits a simple form of associative learning, which has been studied extensively: it can learn to associate light changes with vestibular stimulation (Crow and Alkon 1978). The neural correlates of Hermissenda's associative memories formed during lightmovement pairings have been uncovered (Alkon 1980;Crow and Alkon 1980;Britton and Farley 1999;Tamse et al. 2003;Cavallo et al. 2014). Hermissenda has also been the subject of investigations related to many other aspects of neuroscience, including sensory and motor neuron physiology (Crow and Tian 2004;Nesse and Clark 2010;Jin and Crow 2011;Crow et al. 2013) and the evolution of behaviors and neurotransmitter systems Newcomb et al. 2012;Lillvis and Katz 2013). A limited number of molecular-level studies have been performed on Hermissenda in these areas (Nelson and Alkon 1988;Crow et al. 1997). Broader-scale genetic experiments, such as identification of genes or specific genetic isoforms that produce proteins involved in Hermissenda associative learning, have been impossible without more extensive genetic information specifically from Hermissenda.Transcriptomes have been sequenced in a small number of other gastropod species, including neuronal transcriptomes from Aplysia californica (Moroz et al. 2006;Fiedler et al. 2010;Heyland et al. 2011), A. kurodai (Lee et al. 2008Choi et al. 2010), Lymnaea stagnalis (Bouetard et al. 2012;Sadamoto et al. 2012), and Tritonia diomedea (Senatore et al. 2015), which have been used in studies of learning and other aspects of neuroscience. The field of molluscan neurogenomics is growing thanks in large part to recent advances in sequencing technologies, which allow larger amounts of transcriptomic information to be sequenced at lower costs compared with technologies available a few years ago.In this study, we describe the brain transcriptome of the sea slug Hermissenda crassicornis. The transcriptome was sequenced from central nervous system tissue mRNA, which included the cerebropleural ganglia, pedal ganglia, optic ganglia, eyes, and statocyst hair cells. S...

The marine mollusc, varies daily in whether it swims and this correlates with whether serotonin (5-HT) enhances the strength of synapses made by the swim central pattern generator neuron, A1/C2. Another species,, reliably swims and does not vary in serotonergic neuromodulation. A third species, , never produces this behaviour and lacks the neuromodulation. We found that expression of particular 5-HT receptor subtype (5-HTR) genes in single neurons correlates with swimming. Orthologues to seven 5-HTR genes were identified from whole-brain transcriptomes. We isolated individual A1/C2 neurons and sequenced their RNA or measured 5-HTR gene expression using absolute quantitative PCR. A1/C2 neurons isolated from that produced a swim motor pattern just prior to isolation expressed 5-HT2a and 5-HT7 receptor genes, as did all samples. These subtypes were absent from A1/C2 isolated from that did not wim on that day and from A1/C2 neurons. Expression of other receptors was not correlated with swimming. This suggests that these 5-HTRs may mediate the modulation of A1/C2 synaptic strength and play an important role in swimming. Furthermore, it suggests that regulation of receptor expression could underlie daily changes in behaviour as well as evolution of behaviour.

The recruitment of additional neurons to neural circuits often occurs in accordance with changing functional demands. Here we found that synaptic recruitment plays a key role in functional recovery after neural injury. Disconnection of a brain commissure in the nudibranch mollusc, Tritonia diomedea, impairs swimming behavior by eliminating particular synapses in the central pattern generator (CPG) underlying the rhythmic swim motor pattern. However, the CPG functionally recovers within a day after the lesion. The strength of a spared inhibitory synapse within the CPG from Cerebral Neuron 2 (C2) to Ventral Swim Interneuron B (VSI) determines the level of impairment caused by the lesion, which varies among individuals. In addition to this direct synaptic connection, there are polysynaptic connections from C2 and Dorsal Swim Interneurons to VSI that provide indirect excitatory drive but play only minor roles under normal conditions. After disconnecting the pedal commissure (Pedal Nerve 6), the recruitment of polysynaptic excitation became a major source of the excitatory drive to VSI. Moreover, the amount of polysynaptic recruitment, which changed over time, differed among individuals and correlated with the degree of recovery of the swim motor pattern. Thus, functional recovery was mediated by an increase in the magnitude of polysynaptic excitatory drive, compensating for the loss of direct excitation. Since the degree of susceptibility to injury corresponds to existing individual variation in the C2 to VSI synapse, the recovery relied upon the extent to which the network reorganized to incorporate additional synapses.