Sleep scoring made easy-Semi-automated sleep analysis software and manual rescoring tools for basic sleep research in mice.

Studying sleep behavior in animal models demands clear separation of vigilance states. Pure manual scoring is time-consuming and commercial scoring software is costly. We present a LabVIEW-based, semi-automated scoring routine using recorded EEG and EMG signals. This scoring routine is •designed to reliably assign the vigilance/sleep states wakefulness (WAKE), non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) to defined EEG/EMG episodes.•straightforward to use even for beginners in the field of sleep research.•freely available upon request. Chronic recordings from mice were used to design and evaluate the scoring routine consisting of an artifact-removal, a scoring- and a rescoring routine. The scoring routine processes EMG and different EEG frequency bands. Amplitude-based thresholds for EEG and EMG parameters trigger a decision tree assigning each EEG episode to a defined vigilance/sleep state automatically. Using the rescoring routine individual episodes or particular state transitions can be re-evaluated manually. High agreements between auto-scored and manual sleep scoring could be shown for experienced scorers and for beginners quickly and reliably. With small modifications to the software, it can be easily adapted for sleep analysis in other animal models.

Altered synaptic plasticity and behavioral abnormalities in CNGA3-deficient mice.

The role of the cyclic nucleotide-gated (CNG) channel CNGA3 is well established in cone photoreceptors and guanylyl cyclase-D-expressing olfactory neurons. To assess a potential function of CNGA3 in the mouse amygdala and hippocampus, we examined synaptic plasticity and performed a comparative analysis of spatial learning, fear conditioning and step-down avoidance in wild-type mice and CNGA3 null mutants (CNGA3(-/-) ). CNGA3(-/-) mice showed normal basal synaptic transmission in the amygdala and the hippocampus. However, cornu Ammonis (CA1) hippocampal long-term potentiation (LTP) induced by a strong tetanus was significantly enhanced in CNGA3(-/-) mice as compared with their wild-type littermates. Unlike in the hippocampus, LTP was not significantly altered in the amygdala of CNGA3(-/-) mice. Enhanced hippocampal LTP did not coincide with changes in hippocampus-dependent learning, as both wild-type and mutant mice showed a similar performance in water maze tasks and contextual fear conditioning, except for a trend toward higher step-down latencies in a passive avoidance task. In contrast, CNGA3(-/-) mice showed markedly reduced freezing to the conditioned tone in the amygdala-dependent cued fear conditioning task. In conclusion, our study adds a new entry on the list of physiological functions of the CNGA3 channel. Despite the dissociation between physiological and behavioral parameters, our data describe a so far unrecognized role of CNGA3 in modulation of hippocampal plasticity and amygdala-dependent fear memory.