References

Ueda H (2019) Systems pathology of neuropathic pain and fibromyalgia. Biol Pharm Bull 42(11):1773-1782. doi: 10.1248/bpb.b19-00535

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Kiuchi MG, Chen S, Carnagarin R, Matthews VB, Schlaich MP (2019) Renal denervation for treating congenital long QT syndrome: Shortening the QT interval or modulating sympathetic tone?. Europace 21(11):1755-1756. doi: 10.1093/europace/euz251

Summary: Targeted ablation of cardiac sympathetic neurons (TACSN) through CTB-SAP injection in the left stellate ganglion (LSG), inhibited its activation, improved sympathetic remodelling, and restored cardiac autonomic balance.

See: Xiong L et al. Targeted ablation of cardiac sympathetic neurons improves ventricular electrical remodelling in a canine model of chronic myocardial infarction. Europace 20(12):2036-2044, 2018.

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Herman JP (2020) Corticolimbic stress regulatory circuits, hypothalamo–pituitary–adrenocortical adaptation, and resilience. Chen A (Ed.): Stress Resilience 291-309. Academic Press doi: 10.1016/B978-0-12-813983-7.00019-7

Summary: Review. Immunolesion of paraventricular nucleus (PVN)-projecting norepinephrine (NE) neurons with Anti-DBH-SAP attenuates acute stress reactivity (interestingly, to restraint), but it does not inhibit somatic or HPA axis responses to stress in any simple way (Flak et al.). PVN-projecting NE neurons appear to be responsible for acute responses to systemic stressors, but they do not appear to be important in mediating effects of chronic stress (Ritter et al.).

Usage: Flak et al. injected 8.82 ng of Anti-DBH-SAP into the PVN. Ritter et al. injected 42 ng into the PVN.

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See Also:

• Flak J et al. Role of paraventricular nucleus-projecting norepinephrine/epinephrine neurons in acute and chronic stress. Eur J Neurosci 39:1903-1911, 2014.
• Ritter S et al. Immunotoxin lesion of hypothalamically projecting norepinephrine and epinephrine neurons differentially affects circadian and stressor-stimulated corticosterone secretion. Endocrinology 144(4):1357-1367, 2003.

Li X (2019) Light stimulation into dorsal raphe nucleus contributes to antidepressant effect for a stressed rat model. bioRxiv 821421. doi: 10.1101/821421 PMID: 0

Usage: immunohisochemistry (1:500)

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Abd El‐Rahman SS, Fayed HM (2019) Targeting AngII/AT1R signaling pathway by perindopril inhibits ongoing liver fibrosis in rat. J Tissue Eng Regen Med 13:2131-2141. doi: 10.1002/term.2940 PMID: 31348596

Usage: IHC (1:100)

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Cunningham C, Lowry JP (2019) In vivo monitoring of cholinergic neurotransmission with a microelectrochemical choline biosensor. Neuroscience 2019 Abstracts 614.03. Society for Neuroscience, Chicago, IL.

Summary: Acetylcholine acts as a key neuromodulator within the central nervous system, capable of altering neuronal excitability and coordinating neuronal firing patterns. Conversely, cholinergic neurotransmission plays a crucial role in a variety of cognitive functions, including the encoding of new memories. Cholinergic neuronal loss, and the resulting drop in cholinergic neurotransmission (collectively referred to as hypocholinergia), is closely associated with cognitive dysfunction in a number of chronic neurodegenerative disorders including Alzheimer’s disease. However, conventional analytical techniques for monitoring in vivo cholinergic neurotransmission lack the spatiotemporal resolution required to accurately detect endogenous cholinergic dynamics. Here we validate in mice a Pt-based electrochemical biosensor for selective monitoring of choline, a verified marker of cholinergic transmission. Enzymatic choline biosensors (modified with choline oxidase) were sterotaxically implanted in the medial prefrontal cortex (mPFC) and contralateral dorsal hippocampus (dHPC) of female C57Bl6J mice. Real-time choline current recordings over a period of several days revealed circadian fluctuations in both regions, with extracellular choline levels highest during light phases. Administration of pharmacological compounds known to induce central acetylcholine release, scopolamine (1mg/kg) and amphetamine (4mg/kg), evoked a robust increase in choline current. In contrast, peripheral injection of the reversible acetylcholinesterase inhibitor, donepezil (3mg/kg), produced a marked decrease in recorded choline current. The induction of systemic infammation with bacterial lipopolysaccharide (LPS; 500µg/kg) produced characteristic ‘sickness behaviour’ in mice and evoked a tonic rise in central choline levels in both the mPFC and dHPC. Furthermore, the induction of hypocholinergia in selected mice was preformed via intracerebroventricular injections of murine-p75-saporin immunotoxin (1.2µg). Evoked cholinergic neurotransmission was dramatically attenuated in lesioned (hypocholinergic) mice. Collectively, the data suggests that microelectrochemical choline biosensors may serve as a powerful tool for monitoring cholinergic neurotransmission across a number of behavioural and disease states.

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Lee J, Seo Y, Shin J, Kong C, Na Y, Chang W, Chang J (2019) Increased transplantation efficacy of mesenchymal stem cell by focused ultrasound and improvement of the spatial memory in the 192 IgG-saporin rat model. Neuroscience 2019 Abstracts 048.01. Society for Neuroscience, Chicago, IL.

Summary: Introduction: Stem cell therapy has been found to have therapeutic effects in neurodegenerative disease, but traditional transplant methods, such as parenchymal or intravenous injection, possess limitations like secondary injuries, infection, and low survival rate of stem cells in the brain. Meanwhile, recently the focused ultrasound(FUS) was found to have promising results regarding transplantation of stem cells into the rat brain. However, the mechanism of stem cell transplantation with FUS and possibility of cognitive recovery remain elusive. Therefore, this study investigates a possibility for non-invasive focused ultrasound use in stem cell transplantation into the brain of dementia rat model. Materials & methods: We divided rats into five groups: Normal, Lesion, Cell only, FUS + Cell, and FUS only. We used 192 IgG-saporin for degeneration of basal forebrain cholinergic neuron and it was injected into all rats except for the normal group. After a week, 5p mesenchymal stem cells (MSC: 3*106/200ul) were injected in the tail vein of all rats of the cell only and FUS + Cell group, and the FUS + Cell group received the FUS three hours before cell transplantation. FUS was applied with parameters of 0.25Mpa, 300s (Targeted hippocampal region: AP -3.5, ML ±2). And last, FUS only group was received only FUS without any treatment. Five weeks after transplantation, rats performed the Morris water maze test. Results: MSC were detected in both cell only and FUS + Cell group of the hippocampus region. After comparing FUS+MSC & cell only rats, it was confirmed that FUS increases MSC homing in the sonicated rat’s brain. In addition, the most effective memory restoration occurred in the FUS + Cell group. Moreover, the FUS + Cell group exhibited better recall of the platform position than the other groups. And FUS only group did not recover. Conclusion: Noninvasive FUS can increase the efficacy of stem cell delivery. And memory impairment due to cholinergic denervation can be effectively improved by cell transplantation with FUS. The results of this study suggest possibility of stem cell homing and therapeutic effects of the FUS in dementia rat model. However, further study regarding the function of stem cells transplanted in the brain and a more detailed mechanism of stem cell homing by FUS is needed.

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Grayson VS, Han Y, Guedea AL, Jovasevic V, Gao C, Apkarian A, Radulovic JM (2019) The role of subcortical hippocampal inputs in contextual memory formation. Neuroscience 2019 Abstracts 786.03. Society for Neuroscience, Chicago, IL.

Summary: The role of cortical efferents to the hippocampus in the formation of episodic-like memory is well established, however, less is known about the contribution of subcortical memory circuits to memory. In the present study, we studied the roles of several subcortical inputs into the dorsal hippocampus in mouse models of contextual fear conditioning, extinction, and reinstatement. Fear conditioning was induced by a single exposure of mice to a context followed by foot shock. Subsequently, mice were exposed to daily extinction trials. After significant reduction of freezing, indicating successful extinction, mice were exposed to a brief reminder shock and re-tested in the conditioning context. Circuit manipulations were performed by chemogenetic silencing with the inhibitory designer receptor exclusively activated by designer drugs (DREADD) hM4(Gi) or targeted cholinergic depletion induced by 192 IgG-saporin, at different stages of fear conditioning, extinction, and reinstatement. We identified projection- and neurotransmitter-specific roles of discrete circuits, indicating complex regulation of fear-inducing memories by subcortical afferents.

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Wang S, Kim M, Ong K, Pae E-K, Chung M-K (2019) Nociceptors expressing TRPV1 and trigeminal nucleus neurons expressing NK1 mediate orthodontic pain. Neuroscience 2019 Abstracts 052.10. Society for Neuroscience, Chicago, IL.

Summary: Orthodontic force produces mechanical irritation and inflammation in periodontium, which inevitably accompanies pain. Despite its high prevalence, treatment of orthodontic pain is not effective. Determining detailed neural mechanisms involving peripheral and central nervous system should be critical to improve the management of orthodontic pain. Periodontal ligament is projected by peptidergic nociceptors, which is enriched with transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin. Trigeminal subnucleus caudalis (Vc), is critical for relaying orofacial nociceptive signal into brain. A group of second- order neurons in the superficial dorsal horn of Vc express neurokinin 1 receptor (NK1), a receptor for substance P, and receive inputs from peptidergic nociceptors. However, the contribution of these nociceptive neurons to orthodontic pain has not been determined. Orthodontic force of 10g produced reliable tooth movement in mice. Orthodontic pain was evaluated by measuring mouse grimace scale (MGS) and bite force (BF), which could represent spontaneous pain and chewing-evoked pain, respectively. Orthodontic force increased MGS and decreased BF, which peaked at 1d and returned near to sham level at 7d. Using targeted chemical ablation of specific subsets of neurons, we determined the contribution of TRPV1+ nociceptors and NK1+ Vc neurons to orthodontic pain behaviors in mice. Ablation of TRPV1+ nociceptors by injecting resiniferatoxin into trigeminal ganglia significantly attenuated orthodontic force assessed by MGS and BF. Chemical ablation of NK1+ Vc neurons by injecting saporin conjugated with substance P into Vc also significantly reduced the extent of changes in MGS and BF by orthodontic force. These results suggest that TRPV1+ trigeminal nociceptors and NK1+ Vc neurons constitute a major neural pathway for transmission of orthodontic pain, which is a fundamental neural mechanism of orthodontic pain transmission. The new mouse model of orthodontic pain will be useful for mechanistic study to develop novel approaches for painless orthodontics.

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Osterlund JR, BLackwell AA, Lipton M, Castillo V, Kartje GL, Tsai S-Y, Wallace DG (2019) Selective loss of septohippocampal cholinergic projections is associated with more circuitous homeward progressions. Neuroscience 2019 Abstracts 789.11. Society for Neuroscience, Chicago, IL.

Summary: Rodents rely on self-movement cues as a source of information to maintain spatial orientation during exploration. The vestibular system provides a source of self-movement cues that are processed by the septohippocampal cholinergic system, and when damaged, disruptions in movement organization are observed. The current study examined the effects of medial septum infusion of 192 IgG-saporin on movement organization during a single exploratory session that limited rats to using only self-movement cues. Rats organize their exploratory behavior into stops and progression. Although stops occur throughout the environment, they tend to cluster within a restricted area indicative of home base establishment. In the current study, movement organization characteristics and home base stability were similar between the lesion and sham groups. However, the lesion group exhibited greater path circuity during progressions returning to the home base. Increases in path circuitry have been implicated in spatial disorientation, indicating a role for medial septum cholinergic projections in processing self-movement cues to maintain spatial orientation. These results provide a foundation for future work to investigate the efficacy of interventions that enhance neuroplasticity within the septohippocampal cholinergic system.

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