Separate anterior paraventricular thalamus projections differentially regulate sensory and affective aspects of pain.

The experience of pain is complex, involving both sensory and affective components, yet the underlying neural mechanisms remain elusive. Here, we show that formalin-induced pain behaviors coincide with increased responses in glutamatergic neurons within the anterior paraventricular nucleus of the thalamus (PVA). Furthermore, we describe non-overlapping subpopulations of PVAVgluT2 neurons involved in sensory and affective pain processing, whose activity varies across different pain states.

Identification of Novel Targeting Sites of Calcineurin and CaMKII in Human Ca3.2 T-Type Calcium Channel.

The Cav3.2 T-type calcium channel is implicated in various pathological conditions, including cardiac hypertrophy, epilepsy, autism, and chronic pain. Phosphorylation of Cav3.

The Tarantula Toxin ω-Avsp1a Specifically Inhibits Human Ca3.1 and Ca3.3 via the Extracellular S3-S4 Loop of the Domain 1 Voltage-Sensor.

Inhibition of T-type calcium channels (Ca3) prevents development of diseases related to cardiovascular and nerve systems. Further, knockout animal studies have revealed that some diseases are mediated by specific subtypes of Ca3. However, subtype-specific Ca3 inhibitors for therapeutic purposes or for studying the physiological roles of Ca3 subtypes are missing.

Permissive Modulation of Sphingosine-1-Phosphate-Enhanced Intracellular Calcium on BK Channel of Chromaffin Cells.

Sphingosine-1-phosphate (S1P), is a signaling sphingolipid which acts as a bioactive lipid mediator. We assessed whether S1P had multiplex effects in regulating the large-conductance Ca-activated K channel (BK) in catecholamine-secreting chromaffin cells. Using multiple patch-clamp modes, Ca imaging, and computational modeling, we evaluated the effects of S1P on the Ca-activated K currents () in bovine adrenal chromaffin cells and in a pheochromocytoma cell line (PC12).

Spinal protein kinase C/extracellular signal-regulated kinase signal pathway mediates hyperalgesia priming.

Chronic pain can be initiated by one or more acute stimulations to sensitize neurons into the primed state. In the primed state, the basal nociceptive thresholds of the animal are normal, but, in response to another hyperalgesic stimulus, the animal develops enhanced and prolonged hyperalgesia. The exact mechanism of how primed state is formed is not completely understood.

The type VI adenylyl cyclase protects cardiomyocytes from β-adrenergic stress by a PKA/STAT3-dependent pathway.

Background: The type VI adenylyl cyclase (AC6) is a main contributor of cAMP production in the heart. The amino acid (aa) sequence of AC6 is highly homologous to that of another major cardiac adenylyl cyclase, AC5, except for its N-terminus (AC6-N, aa 1-86). Activation of AC6, rather than AC5, produces cardioprotective effects against heart failure, while the underlying mechanism remains to be unveiled.

Physical interaction between calcineurin and Cav3.2 T-type Ca2+ channel modulates their functions.

Cav3.2 T-type Ca(2+) channel is required for the activation of calcineurin/NFAT signaling in cardiac hypertrophy. We aimed to investigate how Cav3.

Ca(v)3.2 T-type Ca2+ channel-dependent activation of ERK in paraventricular thalamus modulates acid-induced chronic muscle pain.

Treatments for chronic musculoskeletal pain, such as lower back pain, fibromyalgia, and myofascial pain syndrome, remain inadequate because of our poor understanding of the mechanisms that underlie these conditions. Although T-type Ca2+ channels (T-channels) have been implicated in peripheral and central pain sensory pathways, their role in chronic musculoskeletal pain is still unclear. Here, we show that acid-induced chronic mechanical hyperalgesia develops in Ca(v)3.

The Ca(v)3.2 T-type Ca(2+) channel is required for pressure overload-induced cardiac hypertrophy in mice.

Voltage-gated T-type Ca(2+) channels (T-channels) are normally expressed during embryonic development in ventricular myocytes but are undetectable in adult ventricular myocytes. Interestingly, T-channels are reexpressed in hypertrophied or failing hearts. It is unclear whether T-channels play a role in the pathogenesis of cardiomyopathy and what the mechanism might be.

Ca2+ binding protein-1 inhibits Ca2+ currents and exocytosis in bovine chromaffin cells.

Calcium binding protein-1 (CaBP1) is a calmodulin like protein shown to modulate Ca2+ channel activities. Here, we explored the functions of long and short spliced CaBP1 variants (L- and S-CaBP1) in modulating stimulus-secretion coupling in primary cultured bovine chromaffin cells. L- and S-CaBP1 were cloned from rat brain and fused with yellow fluorescent protein at the C-terminal.