Non-technical summary
Small diameter nerve fibres provide sensory input that is perceived as pain. Periods of raised impulse traffic slow the rate of impulse travel, although not all nerve fibres are affected equally, and the mechanism of slowing is still the subject of debate. We describe a novel way of pharmacologically discriminating two sub-sets of neurones that are the parent cell bodies of small diameter sensory nerves. We show that the excitability properties of these populations differ from one another and also report that repeated impulse generation can depress the excitation mechanism. These findings might explain the slowing of the rate of impulse travel in nerve fibres during periods of raised activity, and offer insights into the molecular mechanisms of pain.

Non-technical summary
Spinal motor networks can generate complex locomotor patterns at early stages of development. In this work we examine the modulatory effects of serotonin on spinal locomotor circuits in the neonatal mouse. We manipulate the concentration of serotonin within the spinal cord by applying a serotonin reuptake inhibitor. Our results lead us to suggest that endogenous serotonin is capable of modulating spinal locomotor circuits during early neonatal development in the mouse. Furthermore, we demonstrate that serotonin has both inhibitory and excitatory effects on the locomotor rhythm which are dependent on the class of receptor activated.

Non-technical summary
Every thought we have or action we perform is the result of electrical activity in the neurones (nerve cells) that make up our nervous system. It is therefore essential that the correct amount of activity is maintained. This study examines a process called ‘homeostasis’ through which neurones monitor and control their electrical activity so as to prevent an ‘overload’ which would make the cells malfunction and could even kill them. Our results help us understand how well cells are able to adjust their electrical properties and how homeostasis works inside individual cells. This is important for understanding how the nervous system works and for understanding diseases such as epilepsy that may be caused by a loss of proper homeostatic control.

Non-technical summary
Mechanical sensation (e.g. from touch or limb movement) begins when proteins that act as stretch-sensitive ion channels open in the membranes of nerve endings, allowing ionic fluxes to generate electrical signals. However, the specific channel subtype responsible in many endings is unknown. We show that one channel type (ENaC/degenerins) is present in sensory endings in muscle and that channel blockers inhibit movement-induced electrical responses. Identifying the channels involved helps our understanding of normal and abnormal processes affecting all mechanical senses, from motor co-ordination and touch to blood pressure, hearing and balance.

Non-technical summary
Immature cochlear hair cells relay signals to the developing auditory pathway via the release of chemicals (neurotransmitters) at specialised junctions (synapses) with nerve fibres. Synaptic transmission requires the fusion of small vesicles containing neurotransmitter molecules with the presynaptic cell membrane. Vesicle fusion is finely controlled by calcium ions flowing through protein channels spanning the hair cell membrane. Alteration in the function (i.e. due to genetic defects) of such ion channels can cause deafness. We show that the fusion of each vesicle is controlled by a few calcium channels. This finding represents an important step towards an understanding of how hair cells are able to transmit information with temporal precision.

Non-technical summary
Although it has long been known that practice of a motor task with one limb improves performance with the opposite limb, the underlying mechanisms are poorly understood. Here we show that cross-limb transfer of ballistic motor performance (i.e. fastest possible movement) depends partly on changes in the cerebral hemisphere that controls movements of the untrained limb. We speculate that these ‘crossed’ adaptations occur because both sides of the brain are activated when ballistic tasks are performed with one limb. The data may have practical applications if crossed effects can be exploited to enhance movement capacity in disorders of movement that affect predominantly one side of the body.

Non-technical summary
The influx of Ca²⁺ ions through L-type Ca²⁺ channels (LCCs) triggers numerous critical cellular functions, including excitation–contraction coupling in cardiac muscle, excitation–secretion coupling in neurons, and excitation–transcription coupling in gene expression. A Ca²⁺-dependent inactivation of LCCs limits the amount and defines the timing of Ca²⁺ ion entry during depolarization. However, at the single channel level the gating properties of individual LCCs have not yet been defined under physiological conditions. In the present study we have identified the Ca²⁺-dependent gating parameters that underlie LCC inactivation. The present results help to clarify the physiological role of Ca²⁺ and voltage in producing unitary LCC inactivation, and support an emerging picture of the molecular mechanisms underlying this critical process.

Non-technical summary
Exercise and stress increase the demands of the body, requiring stronger heartbeats. Transient calcium elevations inside cardiac muscle cells underlie each beat, and are regulated by molecular mechanisms during exercise and stress. In the present study, a mechanism leading to better synchronization of these calcium elevations during exercise and stress has been characterized, and results from modifications of calcium release channels inside cardiac muscle cells. A side-effect of optimized coordination of calcium release is spurious calcium signals, accidentally produced when these cells should be at rest, i.e. between heartbeats, which could disturb the normally regular heart rhythm. These findings improve our understanding of stress-induced heart rhythm disturbances, for example in patients harbouring mutations in these calcium release channels.

Non-technical summary
Blood microvessels are permeable to protein, water, sugars and gases, which enables blood–tissue exchange of nutrients and wastes. The smallest veins, the venules, are a major site for blood–tissue exchange. Whether lymphatic vessels, responsible for returning excess protein and water to the blood, possess a similar permeability to protein is unknown. We demonstrate that lymphatic vessels are permeable to the major protein in plasma, albumin, not differing from that of the venules. Further, when lymphatic vessel permeability to water was estimated, it too resembled the water permeability of venules. As lymphatic vessels possess permeability properties similar to the venules, we demonstrated their capability of performing exchange, a novel lymphatic function, with important implications for protein and fluid balance.

Non-technical summary
Acute exposure to intermittent hypoxia elicits a serotonin-dependent form a respiratory plasticity called phrenic long term facilitation (pLTF). We hypothesized that adenosine released during hypoxia may contribute to mechanisms of pLTF potentially via activation of spinal adenosine 2A (A_2A) receptors. However, we demonstrate that inhibition of spinal A_2A receptors greatly enhances the magnitude of pLTF, suggesting A_2A receptor activation constrains (versus contributes) mechanisms of pLTF. These findings further our understanding of cellular signaling events involved in hypoxia-induced respiratory neuroplasticity.