Sensory Processing of Cutaneous Temperature in the Peripheral and Central Nervous System.

Thermal perception is critical for sensing environmental temperature, keeping body temperature consistent, and avoiding thermal danger. Central to thermal perception is the detection of cutaneous (skin) temperature information by the peripheral nerves and its transmission to the spinal cord, thalamus, and downstream cortical areas including the insular cortex, primary somatosensory cortex, and secondary somatosensory cortex. Although much is still unknown about this process, advances in technology have enabled significant progress to be made in recent years.

KCC2 downregulation after sciatic nerve injury enhances motor function recovery.

Injury to mature neurons induces downregulated KCC2 expression and activity, resulting in elevated intracellular [Cl] and depolarized GABAergic signaling. This phenotype mirrors immature neurons wherein GABA-evoked depolarizations facilitate neuronal circuit maturation. Thus, injury-induced KCC2 downregulation is broadly speculated to similarly facilitate neuronal circuit repair.

Spatiotemporal Analysis of Microglial Ca2+ Activity at Single-Cell Resolution.

Microglia are the sole resident immune cells in the central nervous system. Their morphology is highly plastic, changing depending on their activity. Under homeostatic conditions, microglia possess a highly ramified morphology.

Controlled activation of cortical astrocytes modulates neuropathic pain-like behaviour.

Chronic pain is a major public health problem that currently lacks effective treatment options. Here, a method that can modulate chronic pain-like behaviour induced by nerve injury in mice is described. By combining a transient nerve block to inhibit noxious afferent input from injured peripheral nerves, with concurrent activation of astrocytes in the somatosensory cortex (S1) by either low intensity transcranial direct current stimulation (tDCS) or via the chemogenetic DREADD system, we could reverse allodynia-like behaviour previously established by partial sciatic nerve ligation (PSL).

Global transgenic upregulation of KCC2 confers enhanced diazepam efficacy in treating sustained seizures.

Reduced anticonvulsant efficacy of benzodiazepines is a problem in the treatment of status epilepticus, with up to 50% of patients failing to respond to their first dose. KCC2 is a neuronal K -Cl co-transporter that helps set and maintain intracellular Cl concentrations. KCC2 functional downregulation is a potential contributor to benzodiazepine resistance.

Reactive astrocyte-driven epileptogenesis is induced by microglia initially activated following status epilepticus.

Extensive activation of glial cells during a latent period has been well documented in various animal models of epilepsy. However, it remains unclear whether activated glial cells contribute to epileptogenesis, i.e.

Histamine depolarizes rat intracardiac ganglion neurons through the activation of TRPC non-selective cation channels.

The cardiac plexus, which contains parasympathetic ganglia, plays an important role in regulating cardiac function. Histamine is known to excite intracardiac ganglion neurons, but the underlying mechanism is obscure. In the present study, therefore, the effect of histamine on rat intracardiac ganglion neurons was investigated using perforated patch-clamp recordings.

Overexpression of neuronal K-Cl co-transporter enhances dendritic spine plasticity and motor learning.

The neuronal K-Cl cotransporter KCC2 maintains a low intracellular Cl concentration and facilitates hyperpolarizing GABA receptor responses. KCC2 also plays a separate role in stabilizing and enhancing dendritic spines in the developing nervous system. Using a conditional transgenic mouse strategy, we examined whether overexpression of KCC2 enhances dendritic spines in the adult nervous system and characterized the effects on spine dynamics in the motor cortex in vivo during rotarod training.