The HITS-CLIP sequencing method is used to demonstrate that cryptic exons can detect messenger RNA that contains nonsense mutations, and then cause this RNA to decay, which shows that these exons are involved in maintaining the electrical balance of neurons and, possibly, preventing epilepsy.

Optogenetic techniques, whereby light is used to activate neuronal cells, are quickly becoming widely used in neuroscience; but excessive exposure to light can actually silence certain types of neuronal cells.

The mRNA that encodes a Drosophila sodium channel enables neurons to adapt to acute temperature changes, via a mechanism independent of its protein-coding role.

No single molecular change is uniquely necessary to cause neuropathic changes in primary afferent excitability; multiple different changes are sufficient.

A protein called SIR-2.1 helps to protect worms from the effects of aging by regulating metabolic processes that would otherwise generate damaging reactive oxygen species.

Contrary to a long-standing hypothesis, the neuronal death that leads to muscle wastage in amyotrophic lateral sclerosis does not result from overactivity of those neurons during development.

The pain mediator bradykinin was found to sensitize spinal motoneurons by a direct postsynaptic action, questioning the role of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model.

Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.

Comprehensive gene profiling of the hypothalamic hypocretin neurons, high resolution imaging and behavioral assays have revealed the molecular signature of these versatile neurons and identified a potassium channel that is required for nighttime sleep.