Animals perform or terminate particular behaviors by integrating external cues and internal states through neural circuits. Identifying neural substrates and their molecular modulators promoting or inhibiting animal behaviors are key steps to understand how neural circuits control behaviors. Here, we identify the Cholecystokinin-like peptide Drosulfakinin (DSK) that functions at single-neuron resolution to suppress male sexual behavior in Drosophila. We found that Dsk neurons physiologically interact with male-specific P1 neurons, part of a command center for male sexual behaviors, and function oppositely to regulate multiple arousal-related behaviors including sex, sleep and spontaneous walking. We further found that the DSK-2 peptide functions through its receptor CCKLR-17D3 to suppress sexual behaviors in flies. Such a neuropeptide circuit largely overlaps with the fruitless-expressing neural circuit that governs most aspects of male sexual behaviors. Thus DSK/CCKLR signaling in the sex circuitry functions antagonistically with P1 neurons to balance arousal levels and modulate sexual behaviors.

Highlights Perceived risk of COVID-19 was higher as compared to other potential threats. Knowledge gaps existed regarding transmission and prevention of COVID-19. Depressive states were positively related to risk perception. Risk communicators need to understand specific knowledge needs of vulnerable groups. Popular media platforms can be adopted by health professionals in risk communication.

Low-temperature pyrolysis offers a potential way of upgrading lignite and producing chars to replace thermal or pulverized coal injection (PCI) coals in combustion or being used as inert components in a blend for coking. In this study, the characteristics of chars from low-temperature pyrolysis of two lignite coals have been investigated. The changes in char morphology and chemical structures were investigated using scanning electron microscopy (SEM) and Fourier transform infrared spectroscopy (FTIR). The combustion reactivity of chars was analyzed in a thermogravimetric analyer (TGA) using non-isothermal techniques. The results show that chars from low-temperature pyrolysis of lignite coal below 450 °C were more reactive than higher temperature chars. Higher reactivity of low-temperature chars was attributed to the higher concentration of active sites and lower degree of structural order compared to that of high-temperature chars. Indonesian (YN) lignite showed a higher weight loss rate compared to Hulunbeier (HL) coal, which was attributed to a higher concentration of liptinite and vitrinite in YN coal. FTIR analysis indicated that the aliphatic structures and oxygen-containing functional groups decreased with an increasing pyrolysis temperature. The intensity of tightly bound cyclic OH tetramers and OH−ether O hydrogen bonds were higher than other hydrogen bonds in the 3700−3600 cm −1 region of infrared (IR) spectra. The density of alkyl chains and crosslinking reactions affected the yield of tar. The aromaticity of char increased with an increasing pyrolysis temperature. The abundance of CO and COOH structures decreased drastically with increasing temperature. A lower concentration of active sites on high-temperature chars resulted in lower combustion reactivity compared to low-temperature chars. The C−O and C C groups decreased as the temperature increased possibly because of the aromatic condensation. The extent of aromatic substitution decreased up to 650 °C. At temperatures above 650 °C, the degree of aromaticity was strengthened and larger condensed aromatic nuclei were formed. Brunauer−Emmett−Teller (BET) surface area analysis revealed that high-temperature chars have significantly higher surface area compared to chars produced at low temperatures. However, the concentration of active sites was lower in high-temperature chars. Therefore, it can be concluded that diffusion was the main reaction mechanism in high-temperature chars.

An increasing body of neuroimaging and electrophysiological studies of the brain suggest that the insular cortex (IC) integrates multimodal salient information ranging from sensation to cognitive-affective events to create conscious interoception. Especially with regard to pain experience, the IC has been supposed to participate in both sensory-discriminative and affective-motivational aspects of pain. In this review, we discuss the latest data proposing that subregions of the IC are involved in isolated pain networks: the posterior sensory circuit and the anterior emotional network. Due to abundant connections with other brain areas, the IC is likely to serve as an interface where cross-modal shaping of pain occurs. In chronic pain, however, this mode of emotional awareness and the modulation of pain are disrupted. We highlight some of the molecular mechanisms underlying the changes of the pain modulation system that contribute to the transition from acute to chronic pain in the IC.

Long-term potentiation of glutamatergic transmission has been observed after physiological learning or pathological injuries in different brain regions, including the spinal cord, hippocampus, amygdala, and cortices. The insular cortex is a key cortical region that plays important roles in aversive learning and neuropathic pain. However, little is known about whether excitatory transmission in the insular cortex undergoes plastic changes after peripheral nerve injury. Here, we found that peripheral nerve ligation triggered the enhancement of AMPA receptor (AMPAR)-mediated excitatory synaptic transmission in the insular cortex. The synaptic GluA1 subunit of AMPAR, but not the GluA2/3 subunit, was increased after nerve ligation. Genetic knock-in mice lacking phosphorylation of the Ser845 site, but not that of the Ser831 site, blocked the enhancement of the synaptic GluA1 subunit, indicating that GluA1 phosphorylation at the Ser845 site by protein kinase A (PKA) was critical for this upregulation after nerve injury. Furthermore, A-kinase anchoring protein 79/150 (AKAP79/ 150) and PKA were translocated to the synapses after nerve injury. Genetic deletion of adenylyl cyclase subtype 1 (AC1) prevented the translocation of AKAP79/150 and PKA, as well as the upregulation of synaptic GluA1-containing AMPARs. Pharmacological inhibition of calcium-permeable AMPAR function in the insular cortex reduced behavioral sensitization caused by nerve injury. Our results suggest that the expression of AMPARs is enhanced in the insular cortex after nerve injury by a pathway involving AC1, AKAP79/150, and PKA, and such enhancement may at least in part contribute to behavioral sensitization together with other cortical regions, such as the anterior cingulate and the prefrontal cortices.

Vagal afferent neurons relay important information regarding the control of the gastrointestinal system. However, the ionic mechanisms that underlie vagal activation induced by sensory inputs are not completely understood. We postulate that transient receptor potential (TRP) channels and/or two-pore potassium (K2p) channels are targets for activating vagal afferents. In this study we explored the distribution of these channels in vagal afferents by quantitative PCR after a capsaicin treatment to eliminate capsaicin-sensitive neurons, and by single-cell PCR measurements in vagal afferent neurons cultured after retrograde labeling from the stomach or duodenum. We found that TRPC1/3/5/6, TRPV1-4, TRPM8, TRPA1, TWIK2, TRAAK, TREK1, and TASK1/2 were all present in rat nodose ganglia. Both lesion results and single-cell PCR results suggested that TRPA1 and TRPC1 were preferentially expressed in neurons that were either capsaicin sensitive or TRPV1 positive. Expression of TRPM8 varied dynamically after various manipulations, which perhaps explains the disparate results obtained by different investigators. Last, we also examined ion channel distribution with the A-type CCK receptor (CCK-R(A)) and found there was a significant preference for neurons that express TRAAK to also express CCK-R(A), especially in gut-innervating neurons. These findings, combined with findings from prior studies, demonstrated that background conductances such as TRPC1, TRPA1, and TRAAK are indeed differentially distributed in the nodose ganglia, and not only do they segregate with specific markers, but the degree of overlap is also dependent on the innervation target.

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