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Spinal neuropeptide Y1 receptor-expressing neurons form an essential excitatory pathway for mechanical itch.
Acton D, Ren X, DiCostanzo S, Dalet A, Bourane S, Bertocchi I, Eva C, Goulding M (2019) Spinal neuropeptide Y1 receptor-expressing neurons form an essential excitatory pathway for mechanical itch. Cell Reports 28(3):625-639.e6 . doi: 10.1016/j.celrep.2019.06.033
Objective: To determine the central pathway for mechanical itch.
Summary: NPY-Y1 signaling regulates the transmission of innocuous tactile information by establishing biologically relevant thresholds for touch discrimination and mechanical itch reflexes. Neither the evoked nor spontaneous scratching seen following activation of Y1Cre neurons was affected by ablation of the GRPR+ neurons. NK1R+ neuron ablation failed to modulate mechanically evoked itch.
Usage: P28 mice were given a single intrathecal (i.t.) injection of either Bombesin-SAP (400 ng in 5 mL 0.9% sterile saline) to ablate GRPR+ cells or SSP-SAP to ablate NK1r+ neurons (100 ng in 5 mL 0.9% sterile saline). Littermate controls received Blank-SAP (equal mass in 5 mL 0.9% sterile saline).
Related Products: Bombesin-SAP (Cat. #IT-40), SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)
Tac1-expressing neurons in the periaqueductal gray facilitate the itch-scratching cycle via descending regulation
Gao ZR, Chen WZ, Liu MZ, Chen XJ, Wan L, Zhang XY, Yuan L, Lin JK, Wang M, Zhou L, Xu XH, Sun YG (2019) Tac1-expressing neurons in the periaqueductal gray facilitate the itch-scratching cycle via descending regulation. Neuron 101(1):45-59.e9. doi: 10.1016/j.neuron.2018.11.010
Objective: To determine the neural mechanism promoting the itch-scratching cycle.
Summary: Ablation of Tac1+ but not SST+ neurons decreases itch-induced scratching behavior. l/vlPAG Tac1+ neurons Induce Scratching Behavior via a Descending Pathway.
Usage: To ablate the spinal GRPR+ neurons, mice were intrathecally injected with Bombesin-SAP or Control Blank-SAP (400 ng/5 mL).
Related Products: Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)
Circuit dissection of the role of somatostatin in itch and pain
Huang J, Polgár E, Solinski HJ, Mishra SK, Tseng PY, Iwagaki N, Boyle KA, Dickie AC, Kriegbaum MC, Wildner H, Zeilhofer HU, Watanabe M, Riddell JS, Todd AJ, Hoon MA (2018) Circuit dissection of the role of somatostatin in itch and pain. Nat Neurosci 21(5):707-716. doi: 10.1038/s41593-018-0119-z
Objective: To determine the role of somatostatin in itch and pain.
Summary: Results define the neural circuit underlying somatostatin-induced itch and characterize a contrasting antinociceptive role for the peptide.
Usage: Ablation of Npr1- and GRPR-expressing spinal cord interneurons was accomplished by intrathecal (segment L3/4) injection of Nppb-SAP (4 μg/10 μL) and Bombesin-SAP (2.5 μg) respectively.
Related Products: Bombesin-SAP (Cat. #IT-40), Nppb-SAP (Cat. #IT-69)
Itch induces conditioned place aversion in mice
Mu D, Sun Y-G (2017) Itch induces conditioned place aversion in mice. Neuroscience Letters 658:91-96.. doi: 10.1016/j.neulet.2017.08.046
Summary: Consistently, ablation of itch‐specific neurons that express gastrin‐releasing peptide receptor in the spinal cord also abolished itch‐induced Conditioned Place Aversion (CPA), confirming that itch‐induced CPA is dependent on the spinal itch circuit.
Usage: Mice were given a single intrathecal injection (400 ng/5 μl each) of Bombesin-SAP (Cat. #IT-40) or Control Blank-SAP (Cat. #IT-21).
Related Products: Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)
Spinal mechanisms of itch transmission
Barry DM, Munanairi A, Chen Z-F (2018) Spinal mechanisms of itch transmission. Neurosci Bull 34:156-164. doi: 10.1007/s12264-017-0125-2
Related Products: Bombesin-SAP (Cat. #IT-40)
Molecular and neural basis of contagious itch behavior in mice
Yu Y-Q, Barry DM, Hao Y, Liu X-T, Chen Z-F (2017) Molecular and neural basis of contagious itch behavior in mice. Science 355:1072. doi: 10.1126/science.aak9748
Summary: The authors selectively ablated the SCN gastrin-releasing peptide receptor (GRPR) neurons using Bombesin-SAP (Cat. #IT-40), a peptide-conjugated toxin that kills GRPR neurons in the spinal cord. After bilateral injection of Bombesin-SAP into the SCN, immunohistochemistry showed that Bombesin-SAP injection resulted in ablation of SCN GRPR+ neurons.
Related Products: Bombesin-SAP (Cat. #IT-40)
The peptidergic control circuit for sighing.
Li P, Janczewski W, Yackle K, Kam K, Pagliardini S, Krasnow M, Feldman J (2016) The peptidergic control circuit for sighing. Nature 530:293-297. doi: 10.1038/nature16964
Summary: Sighs are often associated with relief or sadness, but rodents sigh spontaneously dozens of times per hour. There are physiological benefits to sighing, including enhancement of gas exchange and preservation of lung integrity. The authors identify a peptidergic sigh control circuit in the retrotrapezoid nucleus/parafacial respiratory group of the mouse brain that projects to the pre-Bötzinger complex. Mice received bilateral 6.2-ng injections of Bombesin-SAP (Cat. #IT-40) into the pre-Bötzinger complex. Blank-SAP (Cat. #IT-21) was used as control. Elimination of the bombesin receptor-expressing neurons or inhibition of neuromedin B receptor-expressing neurons suppressed sighing. Interfering with the activity of both receptors abolished sigh activity while leaving normal breathing intact. The data suggest that overlapping peptidergic pathways are the core of a sigh control circuit.
Related Products: Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)
Gate control of mechanical itch by a subpopulation of spinal cord interneurons.
Bourane S, Duan B, Koch S, Dalet A, Britz O, Garcia-Campmany L, Kim E, Cheng L, Ghosh A, Ma Q, Goulding M (2015) Gate control of mechanical itch by a subpopulation of spinal cord interneurons. Science 350:550-554. doi: 10.1126/science.aac8653
Summary: Light mechanical stimulation of the hairy skin can induce a form of itch known as mechanical itch. This itch sensation is normally suppressed by inputs from mechanoreceptors, however, in many forms of chronic itch, including alloknesis, this gating mechanism is lost. Scientists demonstrated that a population of spinal inhibitory interneurons (INs), that are defined by the expression of neuropeptide Y::Cre (NPY::Cre), act to gate mechanical itch. Mice in which dorsal NPY::Cre-derived neurons are selectively ablated or silenced develop mechanical itch without an increase in sensitivity to chemical itch or pain. This chronic itch state is histamine-independent and is transmitted independently of the GRP-GRPR signaling pathway. The scientists thereby revealed a dedicated spinal cord inhibitory pathway that gates the transmission of mechanical itch. Mice were given an intrathecal injection of 400 ng of Bombesin-SAP (Cat. #IT-40) in 10 ml of sterile saline to ablate GRPR-expressing neurons.
Related Products: Bombesin-SAP (Cat. #IT-40)
A central role for spinal dorsal horn neurons that express neurokinin-1 receptors in chronic itch.
Akiyama T, Nguyen T, Curtis E, Nishida K, Devireddy J, Delahanty J, Carstens M, Carstens E (2015) A central role for spinal dorsal horn neurons that express neurokinin-1 receptors in chronic itch. Pain 156:1240-1246. doi: 10.1097/j.pain.0000000000000172
Summary: Chronic itch is caused by increased sensitivity of itch-signaling pathways. It can be generated by normally itchy stimuli (hyperknesis) and by normally non-itchy light touch (alloknesis). The authors used an ovalbumin-induced atopic dermatitis model to study chronic itch in mice. The mice received 400-ng intrathecal injections of Bombesin-SAP (Cat. #IT-40), SSP-SAP (Cat. #IT-11), or the control Blank-SAP (Cat. #IT-21). While Bombesin-SAP significantly attenuated hyperknesis, it had no effect on spontaneous scratching or alloknesis. SSP-SAP reduced all behavioral signs of chronic itch.
Related Products: Bombesin-SAP (Cat. #IT-40), SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)
Spinal antinociceptive effect of gastrin releasing peptide (GRP) via GABAergic inhibitory interneurons expressing the GRP receptor (GRPR)
Akiyama T, Tominaga M, Davoodi A, Nagamine M, Takamori K, Carstens MI, Carstens E (2014) Spinal antinociceptive effect of gastrin releasing peptide (GRP) via GABAergic inhibitory interneurons expressing the GRP receptor (GRPR). Neuroscience 2014 Abstracts 158.02. Society for Neuroscience, Washington, DC.
Summary: GRPR-expressing dorsal horn neurons signal itch. We investigated a role for such neurons in modulating the spinal neurotransmission of mechanical and heat pain in mice. In behavioral studies, we measured heat and mechanical paw withdrawal thresholds using Hargreaves and von Frey assays, respectively. Mice received intrathecal (it) administration of one of following (5 µL volume); bombesin (6.2 pmol), GRP (0.1 nmol), and GRPR antagonists RC-3095 (0.03 nmol) and BW2258U89 (1.5 nmol). It administration of bombesin or GRP significantly reduced both heat and mechanical withdrawal thresholds with a maximal effect 10 min post-administration. In contrast, it administration of RC-3095 and BW2258U89 significantly increased both heat and mechanical withdrawal thresholds with a maximal effect 10 min post-administration. Mice treated with it bombesin-saporin to ablate GRPR-expressing spinal neurons exhibited reduced heat and mechanical withdrawal thresholds. It GRP failed to elicit heat and mechanical hyperalgesia in these mice. In electrophysiological recordings from superficial lumbar dorsal horn neurons, either bombesin or RC-3095 was spinally applied during responses elicited by noxious mechanical or heat stimulation of the cutaneous receptive field on the hindpaw. Bombesin increased both noxious mechanical- and heat-evoked activity in bombesin-sensitive neurons, while RC-3095 decreased noxious heat-evoked activity. In bombesin-insensitive neurons, bombesin decreased both noxious mechanical- and heat-evoked activity, while RC-3095 increased both. We additionally employed a double-label strategy to investigate if GRPR-expressing dorsal horn neurons coexpressed GABA, a molecular marker of inhibitory interneurons. Approximately 10% of GRPR-positive neurons were immunopositive for GABA. These results indicate that a subset of GRPR-expressing neurons function as interneurons in a circuit that suppresses nociceptive transmission in the dorsal horn. Noxious mechanical and heat stimuli activate GRPR-expressing dorsal horn neurons. A GABAergic subset of these may serve as inhibitory interneurons that contribute to inhibition of spinal neurons signaling heat and mechanical pain. Alternatively, GRPR-expressing neurons may drive other subsets of inhibitory interneurons. The antinociceptive circuit described here can be activated by pruritogens. We propose that the relative activity in antinociceptive and antipruritic circuits within the dorsal horn modulates itch- and pain-signaling ascending neurons to result in the perception of itch or pain.
Related Products: Bombesin-SAP (Cat. #IT-40)