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PARVing the way to cap translation for seizure control
Gross C (2021) PARVing the way to cap translation for seizure control. Epilepsy Curr 21(5):360-362. doi: 10.1177/15357597211027010
Summary: Loss of GABAergic interneurons leads to spontaneous recurrent seizures that persist over months if the amount and spatial spread of initial inhibitory neuron loss is sufficient.
Usage: Intrahippocampal injections of SSP-SAP (0.4 ng/10 nL) were performed using a 0.5-μL Neuros Syringe lowered into four hippocampal sites along both the transverse and longitudinal hippocampal axes bilaterally.
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Possible contribution of cerebellar disinhibition in epilepsy
Ming X, Prasad N, Thulasi V, Elkins K, Shivamurthy VKN (2021) Possible contribution of cerebellar disinhibition in epilepsy. Epilepsy Behav 118:107944. doi: 10.1016/j.yebeh.2021.107944
Summary: The authors hypothesize that loss of inhibition from the cerebellum can lead to cortical activation and seizures. An animal study showed microinjection of SSP-SAP produced a selective ablation of hippocampal inhibitory interneurons in vivo and a highly focal disinhibition. These results also demonstrate that the ‘‘epileptic” pathophysiology produced by experimental status epilepticus or head trauma can be replicated by focal interneuron loss, without involving principal cell loss and other interpretive confounds inherent in the use of global neurologic injury models.
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See Also:
- Martin JL et al. Focal inhibitory interneuron loss and principal cell hyperexcitability in the rat hippocampus after microinjection of a neurotoxic conjugate of saporin and a peptidase-resistant analog of substance P. J Comp Neurol 436:127-152, 2001.
- Chun E et al. Targeted hippocampal GABA neuron ablation by stable substance P-saporin causes hippocampal sclerosis and chronic epilepsy in rats. Epilepsia 60(5):e52-e57, 2019.
Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats
Chun E (2020) Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats. Morehouse School of Medicine Thesis.
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Featured Article: Targeted hippocampal GABA neuron ablation produces hippocampal sclerosis, epilepsy, and dissociable effects on the Morris water maze and object-place paired association tasks
Bumanglag AV, Truckenbrod LM, Chun E, Hernandez AR, Federico QP, Maurer AP, Sloviter RS, Burke SN (2019) Featured Article: Targeted hippocampal GABA neuron ablation produces hippocampal sclerosis, epilepsy, and dissociable effects on the Morris water maze and object-place paired association tasks. Targeting Trends 20
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Read the featured article in Targeting Trends.
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Central circuit mechanisms of itch.
Chen XJ, Sun YG (2020) Central circuit mechanisms of itch. Nat Commun 11:3052. doi: 10.1038/s41467-020-16859-5
Summary: The authors summarize the progress in elucidating the neural circuit mechanism of itch at spinal and supraspinal levels.
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A role for neurokinin 1 receptor expressing neurons in the paratrigeminal nucleus in bradykinin-evoked cough in guinea-pigs.
Driessen AK, McGovern AE, Behrens R, Moe AAK, Farrell MJ, Mazzone SB (2020) A role for neurokinin 1 receptor expressing neurons in the paratrigeminal nucleus in bradykinin-evoked cough in guinea-pigs. J Physiol 598(11):2257-2275. doi: 10.1113/JP279644
Objective: This study aimed to assess the involvement of paratrigeminal neurokinin 1 receptor neurons in the regulation of cough, breathing and airway defensive responses.
Summary: These findings warrant further investigations into targeting the jugular ganglia and paratrigeminal nucleus as a therapy for treating cough in disease.
Usage: Targeted toxin lesions across three sites of the paratrigeminal nucleus (200nl per injection site).
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Episodic stimulation of central chemoreceptor neurons elicits disordered breathing and autonomic dysfunction in volume overload heart failure.
Díaz HS, Andrade DC, Toledo C, Pereyra KV, Schwarz KG, Díaz-Jara E, Lucero C, Arce-Álvarez A, Schultz HD, Silva JN, Takakura AC, Moreira TS, Marcus NJ, Del Rio R (2020) Episodic stimulation of central chemoreceptor neurons elicits disordered breathing and autonomic dysfunction in volume overload heart failure. Am J Physiol Lung Cell Mol Physiol 318(1):L27-L40. doi: 10.1152/ajplung.00007.2019
Objective: To determine the role of the central chemoreflex in the development of respiratory and autonomic dysfunction in volume overload heart failure (HF).
Summary: Episodic hypercapnic stimulation triggers ventilatory plasticity and elicits cardiorespiratory abnormalities in HF that are largely dependent on retrotrapezoid nucleus (RTN) chemoreceptor neurons.
Usage: Bilateral injections of SSP-SAP, 0.6 ng/30 nL, into the RTN were administered to destroy chemoreceptor neurons.
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Contribution of the retrotrapezoid nucleus and carotid bodies to hypercapnia- and hypoxia-induced arousal from sleep.
Souza GMPR, Stornetta RL, Stornetta DS, Abbott SBG, Guyenet PG (2019) Contribution of the retrotrapezoid nucleus and carotid bodies to hypercapnia- and hypoxia-induced arousal from sleep. J Neurosci 39(49):9725-9737. doi: 10.1523/JNEUROSCI.1268-19.2019
Objective: To examine the contribution of two lower brainstem nuclei that could be implicated in CO2 and hypoxia-induced arousal.
Summary: RTN, a brainstem nucleus that mediates the effect of brain acidification on breathing, also contributes to arousal elicited by CO2 but not hypoxia.
Usage: To ablate the retrotrapezoid nucleus (RTN), SSP-SAP was administered (2.4 ng) through bilateral injections via a dorsal craniotomy.
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Episodic stimulation of central chemoreflex elicits long-term breathing disorders and autonomic imbalance in heart failure rats.
Díaz HS, Andrade DC, Toledo C, Lucero C, Arce-Álvarez A, Del Rio R (2019) Episodic stimulation of central chemoreflex elicits long-term breathing disorders and autonomic imbalance in heart failure rats. Eur Respir J 54(suppl 63):OA4936. doi: 10.1183/13993003.congress-2019.OA4936
Objective: To determine the role of CC in the development of cardiorespiratory dysfunction in a HF model.
Summary: Rats were exposed to pisodic hypercapnic stimulation (EHS) The effects of EHS in rats with heart failure were attenuated by SSP-SAP treatment.
Usage: Selective destruction of chemoreceptor neurons within the retrotapezoid nucleus (RTN) was performed via SSP-SAP injections (0.6 ng/30 nL).
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Nociceptors expressing TRPV1 and trigeminal nucleus neurons expressing NK1 mediate orthodontic pain
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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