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Riley, Jonathan P., Bethwel Raore, Jason S. Taub, Thais Federici, and Nicholas M. Boulis. "Platform and Cannula Design Improvements for Spinal Cord Therapeutics Delivery." Operative Neurosurgery 69, suppl_2 (April 5, 2011): ons147—ons155. http://dx.doi.org/10.1227/neu.0b013e3182195680.
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Abstract BACKGROUND Only recently have data been published attempting to validate a technology and technique suitable for targeted delivery of biological payloads to the human spinal cord. OBJECTIVE To characterize the development and evolution of a spine-stabilized microinjection platform as a vehicle for biologics delivery to the cervical and thoracolumbar spine on the basis of preclinical experience in both non–Good Laboratory Practice (GLP) experimental series and GLP studies. METHODS Our laboratory completed > 100 cervical and lumbar porcine microinjection procedures between July 2004 and June 2010. This included both non–GLP- and GLP-adherent survival series to validate the safety and accuracy achievable with intraspinal microinjection. During this time, 3 different microinjection platforms, injection stages, and cannula designs were tested. RESULTS Repetitive technological improvements reduced incision length, decreased procedural complexity, and simplified ventral horn targeting and accuracy. These changes reduced procedural invasiveness and the likelihood of neurological morbidity while improving targeting accuracy. In part as a result of these technological improvements and procedural modifications, we have safely progressed from single unilateral microinjections to multiple bilateral injections without long-term neurological sequelae. CONCLUSION Technological and procedural refinements have significantly enhanced the capabilities of intraspinal microinjection-based biologics delivery. Reductions in procedural invasiveness and the capability to deliver sequential biological payloads effectively have broadened the flexibility of intraspinal microinjection to a widened array of intrinsic spinal cord pathologies. These advances have laid the groundwork for clinical translation of spinal cord microinjections.
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Willette, R. N., and C. F. Sauermelch. "Abluminal effects of endothelin in cerebral microvasculature assessed by laser-Doppler flowmetry." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 6 (December 1, 1990): H1688—H1693. http://dx.doi.org/10.1152/ajpheart.1990.259.6.h1688.
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Laser-Doppler flowmetry was used to assess the intraparenchymal effects of endothelin 1 (ET-1) on cortical microvascular perfusion (CP). The initial part of this study examined effects of the intraparenchymal microinjection technique on local cortical microvascular responsivity. In anesthetized rats, the microinjection of vehicle (saline) beneath the cortical surface did not alter CO2 responsivity or autoregulation of the cortical microvasculature. In addition, predictable monophasic changes in local CP were elicited by the intraparenchymal microinjection of known vasodilators and vasoconstrictors, i.e., nitroprusside and prostaglandin F2 alpha, respectively. These experiments demonstrate normal responsivity of the cortical microvasculature after intraparenchymal microinjection. In the second part of this study, intraparenchymal microinjections (100 nl) of ET-1 (1-1,000 fmol) were evaluated. Microinjections of less than 10 fmol of ET-1 did not alter CP. However, doses between 10 and 1,000 fmol of ET-1 elicited monophasic dose-related reductions in CP. At 1,000 fmol, the highest dose studied, ET-1 produced a complex microvascular response consisting of an initial profound reduction in CP followed by alternating cycles of increased perfusion ultimately lapsing back to a prolonged period of hypoperfusion. No significant changes in blood pressure were observed after ET-1 administration, and no significant changes in any of the hemodynamic variables were observed after vehicle microinjection. These results suggest that abluminal microvascular actions of ET-1 mediate cerebral vasoconstriction and hypoperfusion.
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Pokrovskiy, V. M., E. A. Patrakhanov, A. Yu Karagodina, Yu V. Stepenko, N. E. Kazban, A. V. Turpakova, O. B. Altukhova, P. R. Lebedev, and A. V. Deykin. "METHODOLOGICAL RECOMMENDATIONS FOR THE USE OF REPRODUCTIVE TECHNOLOGIES TO CREATE GENETICALLY MODIFIED RABBITS." Bulletin of Udmurt University. Series Biology. Earth Sciences 32, no. 4 (December 27, 2022): 439–48. http://dx.doi.org/10.35634/2412-9518-2022-32-4-439-448.
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In this article, we present some practical recommendations that we developed in the course of two years of work on obtaining several lines of rabbits with an artificially modified genome. The technology of obtaining genetically modified rabbits, based on obtaining dated fertilized eggs with further microinjection of genetic constructs, assessment of survival and embryo transfer by laparoscopic and laparotomic methods. The following regimen demonstrated the greatest efficiency: administration of serum gonadotropin (Follimag, MOSAGROGEN, Russia) at a dose of 4ME/kg subcutaneously and intravenous administration of human chorionic gonadotropin (Chorulon, Merck Animal Health, USA) at a dose of 60ME/kg. Thus, the resulting operating procedure allows the operator to perform microinjections with high transfer efficiency and maximum cell survival. Microinjection is carried out through an Eppendorf FemtoJet 4i pneumatic microinjector using hydraulic micromanipulators under visual control through a NIKON ECLIPSE TS2R inverted research microscope. The described results may be useful in the compilation of standard operating procedures used in laboratories that are engaged in the production of genetically modified rabbit animals.
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Riley, Jonathan, Jonathan Glass, Eva L. Feldman, Meraida Polak, Jane Bordeau, Thais Federici, Karl Johe, and Nicholas M. Boulis. "Intraspinal Stem Cell Transplantation in Amyotrophic Lateral Sclerosis." Neurosurgery 74, no. 1 (September 5, 2013): 77–87. http://dx.doi.org/10.1227/neu.0000000000000156.
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Abstract BACKGROUND: The first US Food and Drug Administration approved clinical trial for a stem cell-based treatment of amyotrophic lateral sclerosis has now been completed. OBJECTIVE: Primary aims assessed the safety of a direct microinjection-based technique and the toxicity of neural stem cell transplantation to the ventral horn of the cervical and thoracolumbar spinal cord. Results from thoracolumbar-only microinjection groups have been previously published. Cervical and cervical plus thoracolumbar microinjection group perioperative morbidity results are presented. METHODS: Eighteen microinjection procedures (n = 12 thoracolumbar [T10/11], n = 6 cervical [C3-5]) delivered NSI-566RSC (Neuralstem, Inc), a human neural stem cell, to 15 patients in 5 cohorts. Each injection series comprised 5 injections of 10 μL at 4-mm intervals. The patients in group A (n = 6) were nonambulatory and received unilateral (n = 3) or bilateral (n = 3) thoracolumbar microinjections. The patients in groups B to E were ambulatory and received either unilateral (group B, n = 3) or bilateral (group C, n = 3) thoracolumbar microinjection. Group D and E patients received unilateral cervical (group D, n = 3) or cervical plus bilateral thoracolumbar microinjection (group E, n = 3). RESULTS: Unilateral cervical (group D, n = 3) and cervical plus thoracolumbar (group E, n = 3) microinjections to the ventral horn have been completed in ambulatory patients. One patient developed a postoperative kyphotic deformity prompting completion of a laminoplasty in subsequent patients. Another required reoperation for wound dehiscence and infection. The solitary patient with bulbar amyotrophic lateral sclerosis required perioperative reintubation. CONCLUSION: Delivery of a cellular payload to the cervical or thoracolumbar spinal cord was well tolerated by the spinal cord in this vulnerable population. This encouraging finding supports consideration of this delivery approach for neurodegenerative, oncologic, and traumatic spinal cord afflictions.
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Dean, David A., and Joshua Z. Gasiorowski. "Microinjecting Cells Using a Pulsed-Flow Microinjection System." Cold Spring Harbor Protocols 2011, no. 3 (March 2011): prot5589. http://dx.doi.org/10.1101/pdb.prot5589.
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Dean, David A., and Joshua Z. Gasiorowski. "Microinjecting Cells Using a Constant-Flow Microinjection System." Cold Spring Harbor Protocols 2011, no. 3 (March 2011): prot5590. http://dx.doi.org/10.1101/pdb.prot5590.
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Colombari, Eduardo, Robin L. Davisson, Richard A. Shaffer, William T. Talman, and Stephen J. Lewis. "Hemodynamic effects ofl-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (April 1, 1998): H1066—H1074. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1066.
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This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of l-glutamate (l-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection ofl-Glu produced an initial pressor response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, l-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of l-Glu after administration of prazosin and N G-nitro-l-arginine methyl ester (l-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections ofl-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of l-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.
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Avanzino, G. L., P. Ruggeri, D. Blanchi, C. E. Cogo, R. Ermirio, and L. C. Weaver. "GABAB receptor-mediated mechanisms in the RVLM studied by microinjections of two GABAB receptor antagonists." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 5 (May 1, 1994): H1722—H1728. http://dx.doi.org/10.1152/ajpheart.1994.266.5.h1722.
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The cardiovascular effects of microinjections of two gamma-aminobutyric acid (GABA) antagonists specifically acting on GABAB receptors, 2-hydroxy-saclofen (2-OH-S) and CGP-35348, into vasopressor sites of rostral ventrolateral medulla (RVLM) were studied in rats anesthetized with urethan. Bilateral microinjection of 2-OH-S induced significant increases in mean arterial pressure (MAP) and heart rate (HR) in 21 of 26 RVLM vasopressor sites (81%); average increases obtained in the 26 sites studied were +25.2 +/- 3.0 mmHg and +12.7 +/- 2.1 beats/min. Bilateral microinjection of CGP-35348 induced significant increases in MAP and HR in 10 of 12 RVLM sites (83%). Average increases in the 12 sites studied were +27.6 +/- 3.9 mmHg and +14.6 +/- 2.5 beats/min. Sixteen rats received unilateral electrolytic lesions of one RVLM. Microinjections of either 2-OH-S or CGP-35348 into vasopressor sites within the intact RVLM significantly antagonized the depressor responses observed after injections of baclofen (20 pmol) into the same sites, whereas both GABAB antagonists did not affect the depressor response induced by microinjection of muscimol (5 pmol). These results suggest a tonic inhibitory mechanism within the RVLM mediated by GABAB receptors involved in central cardiovascular regulation.
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Nason, Malcolm W., and Peggy Mason. "Modulation of Sympathetic and Somatomotor Function by the Ventromedial Medulla." Journal of Neurophysiology 92, no. 1 (July 2004): 510–22. http://dx.doi.org/10.1152/jn.00089.2004.
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The ventromedial medulla is implicated in a variety of functions including nociceptive and cardiovascular modulation and the control of thermoregulation. To determine whether single microinjections into the ventromedial medulla elicit changes in one or multiple functional systems, the GABAA receptor antagonist bicuculline was microinjected (70 nl, 5–50 ng) into the ventromedial medulla of lightly anesthetized rats, and cardiovascular, respiratory, and nociceptive measures were recorded. Bicuculline microinjection into either the midline raphe or the laterally adjacent reticular nucleus simultaneously increased interscapular brown adipose tissue temperature, heart rate, blood pressure, expired [CO2], and respiration rate and elicited shivering. Bicuculline microinjection also decreased the noxious stimulus-evoked changes in heart rate and blood pressure, decreased the frequency of heat-evoked sighs, and suppressed the cortical desynchronization evoked by noxious stimulation. Although bicuculline suppressed the motor withdrawal evoked by noxious tail heat, it enhanced the motor withdrawal evoked by noxious paw heat, evidence for specifically patterned nociceptive modulation. Saline microinjections into midline or lateral sites had no effect on any measured variable. All bicuculline microinjections, midline or lateral, evoked the same set of physiological effects, consistent with the lack of a topographical organization within the ventromedial medulla. Furthermore, as predicted by the isodendritic morphology of cells in the ventromedial medulla, midline bicuculline microinjection increased the number of c-fos immunoreactive cells in both midline raphe and lateral reticular nuclei. In summary, 70-nl microinjections into ventromedial medulla activate cells in multiple nuclei and elicit increases in sympathetic and somatomotor tone and a novel pattern of nociceptive modulation.
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Carstens, E. "Responses of Rat Spinal Dorsal Horn Neurons to Intracutaneous Microinjection of Histamine, Capsaicin, and Other Irritants." Journal of Neurophysiology 77, no. 5 (May 1, 1997): 2499–514. http://dx.doi.org/10.1152/jn.1997.77.5.2499.
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Carstens, E. Responses of rat spinal dorsal horn neurons to intracutaneous microinjection of histamine, capsaicin, and other irritants. J. Neurophysiol. 77: 2499–2514, 1997. To investigate the spinal processing of cutaneous pruritic and algesic stimuli, single-unit recordings were made from wide-dynamic-range-type lumbar spinal dorsal horn neurons in pentobarbital-sodium-anesthetized rats. Neuronal responses were recorded to mechanical and noxious thermal stimuli, as well as to microinjection (1 μl) of histamine (0.01–10% = 9 × 10−1–9 × 10−4 M), capsaicin (0.1% = 3.3 × 10−3 M), or other algesic chemicals into skin within the receptive field via intracutaneously placed needles. Most (84%) of the 89 neurons responded to intracutaneous (ic) microinjection of histamine with a brief phasic discharge followed by an afterdischarge of variable (s to min) duration. Ten minutes after ic microinjection of histamine (but not NaCl), there was a significant increase in the mean area of the low-threshold (but not high-threshold) portion of unit mechanical receptive fields. However, responses to graded pressure stimuli were not significantly affected after histamine. Responses did not exhibit significant tachyphylaxis when histamine microinjections were repeated at 5- or 10-min intervals. Unit responses significantly increased in a dose-related manner to microinjection of histamine at concentrations ranging across 4 orders of magnitude. Within 30 s after ic microinjection of the H1 antagonist cetirizine, unit responses to ic histamine delivered at the same skin site were significantly attenuated. Unit responses to histamine, as well as to noxious thermal stimulation, were significantly reduced after systemic administration of morphine (3.5 mg/kg ip) in a naloxone-reversible manner. Application of a mechanical rub, scratch, or a noxious heat stimulus during the unit's ongoing response to ic histamine produced a brief and marked excitation, often followed by a period of reduced ongoing discharge. Unit responses to histamine were markedly suppressed by electrical stimulation in the midbrain periaqueductal gray. Most (79%) histamine-responsive units tested also responded to ic microinjection of capsaicin. After the initial microinjection of capsaicin, subsequent responses to histamine and capsaicin microinjections were significantly reduced. Units also responded to ic ethanol (capsaicin vehicle) in a dose-related manner, and showed tachyphylaxis to repeated ic ethanol at 80% but not at 8%. The mean response to 80% ethanol was significantly smaller than to 0.1% capsaicin. All units tested also responded to topical application of mustard oil (50%) and ic serotonin (30 μg). The results are discussed in terms of theories that attempt to reconcile psychophysical and clinical observations of pain and itch sensation.
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Wheatley, S. "Microinjection." Cell Biology International 24, no. 5 (May 2000): 326. http://dx.doi.org/10.1006/cbir.1999.0549.
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Ghaemi, Reza, Justin Tong, Bhagwati P. Gupta, and P. Ravi Selvaganapathy. "Microfluidic Device for Microinjection of Caenorhabditis elegans." Micromachines 11, no. 3 (March 11, 2020): 295. http://dx.doi.org/10.3390/mi11030295.
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Microinjection is an established and reliable method to deliver transgenic constructs and other reagents to specific locations in C. elegans worms. Specifically, microinjection of a desired DNA construct into the distal gonad is the most widely used method to generate germ-line transformation of C. elegans. Although, current C. elegans microinjection method is effective to produce transgenic worms, it requires expensive multi degree of freedom (DOF) micromanipulator, careful injection alignment procedure and skilled operator, all of which make it slow and not suitable for scaling to high throughput. A few microfabricated microinjectors have been developed recently to address these issues. However, none of them are capable of immobilizing a freely mobile animal such as C. elegans worm using a passive immobilization mechanism. Here, a microfluidic microinjector was developed to passively immobilize a freely mobile animal such as C. elegans and simultaneously perform microinjection by using a simple and fast mechanism for needle actuation. The entire process of the microinjection takes ~30 s which includes 10 s for worm loading and aligning, 5 s needle penetration, 5 s reagent injection and 5 s worm unloading. The device is suitable for high-throughput and can be potentially used for creating transgenic C. elegans.
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Czaban, B. Barbara, Arthur Forer, and Dwayne A. Wise. "Microinjection into crane-fly spermatocytes." Biochemistry and Cell Biology 71, no. 3-4 (March 1, 1993): 222–28. http://dx.doi.org/10.1139/o93-034.
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We were successful in microinjecting fluorescently labelled material into crane-fly spermatocytes. In our experiments, we obtained four results. (i) In most attempts, the membrane stretched around the micropipette and prevented entry of fluorescent material, even when the micropipette appeared to be pushed completely through the cell. This confirms suppositions from earlier micromanipulation experiments that the elastic membrane prevents the micropipette needle from entering the cell, (ii) In some attempts, cells lysed upon contact with the micropipette, (iii) In other attempts, we successfully injected fluorescent material into cells. (iv) Fluorescent material left the cells after injection, often passing into adjacent cells. Although our success rate is low, microinjection into crane-fly spermatocytes is indeed possible.Key words: microinjection, crane-fly spermatocytes.
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Callera, J. C., L. G. Bonagamba, C. Sevoz, R. Laguzzi, and B. H. Machado. "Cardiovascular effects of microinjection of low doses of serotonin into the NTS of unanesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (April 1, 1997): R1135—R1142. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1135.
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In the present study, we analyzed in conscious rats the effects of microinjections of serotonin (5-HT; pmol range) into the nucleus of the solitary tract (NTS) on basal mean arterial pressure (MAP) and heart rate (HR) and also on the reflex bradycardia induced by the activation of the baro- and chemoreflex evaluated 1 min after 5-HT microinjection into the NTS. The data show that unilateral microinjection of 5-HT in the picomolar range into the NTS of unanesthetized rats produced a dose-dependent decrease in MAP and HR, which was blocked by previous microinjection of ketanserin (250 pmol/50 nl) into the NTS. The changes in MAP and HR induced by 5-HT were of very short duration, with a return to baseline values a few seconds later. The cardiovascular responses to baro- or chemoreflex activation 1 min after 5-HT microinjection into the NTS did not differ from the control, indicating that low doses of 5-HT produced no effect on the cardiovascular reflexes tested at that time. The present data show that, as also observed in anesthetized rats, the microinjection of picomolar doses of 5-HT into the NTS elicits the typical cardiovascular responses to baroreceptor activation. These effects, hypotension and bradycardia, seem to be mediated by 5-HT2 receptors because both were blocked by a selective 5-HT2 receptor antagonist. However, since microinjection of 5-HT (1 pmol) into the NTS produced no changes in the cardiovascular responses to the baro- and chemoreflex activated 1 min later, the role of 5-HT2 receptors in the processing of the cardiovascular afferent messages in the NTS remains to be elucidated.
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Imeri, L., S. Bianchi, P. Angeli, and M. Mancia. "Stimulation of cholinergic receptors in the medial preoptic area affects sleep and cortical temperature." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 2 (August 1, 1995): R294—R299. http://dx.doi.org/10.1152/ajpregu.1995.269.2.r294.
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The medial preoptic area (MPA), a cholinoceptive brain area devoid of cholinergic cells, plays an important role in the regulation of different physiological functions, particularly sleep control and thermoregulation. To investigate the effects of the stimulation of cholinergic receptors in this area on sleep and cortical temperature (Tcort), carbachol (a mixed cholinergic agonist) was directly microinjected into the MPA of freely moving rats. Carbachol (0.25 and 0.5 microgram, corresponding to 1.37 and 2.74 nmol) microinjection induced an increase in wakefulness and an inhibition of both slow wave and desynchronized sleep phases. The temperature of the cerebral cortex was reduced in comparison with control conditions (saline microinjection). Sterile needle insertion and saline microinjections induced a significant increase in Tcort, but no changes in the sleep-wake cycle compared with the handling of the animal. The results suggest that 1) carbachol microinjection into the MPA can activate an arousal-generating system and affect thermoregulatory mechanisms, and 2) sleep and temperature responses may be dissociated.
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Poliacek, Ivan, Cheng Wang, Lu Wen-Chi Corrie, Melanie J. Rose, and Donald C. Bolser. "Microinjection of codeine into the region of the caudal ventral respiratory column suppresses cough in anesthetized cats." Journal of Applied Physiology 108, no. 4 (April 2010): 858–65. http://dx.doi.org/10.1152/japplphysiol.00783.2009.
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We investigated the influence of microinjection of codeine into the caudal ventral respiratory column (cVRC) on the cough reflex. Experiments were performed on 36 anesthetized spontaneously breathing cats. Electromyograms (EMGs) were recorded bilaterally from inspiratory parasternal and expiratory transversus abdominis (ABD) muscles and unilaterally from laryngeal posterior cricoarytenoid and thyroarytenoid muscles. Repetitive coughing was elicited by mechanical stimulation of the intrathoracic airways. The unilateral microinjection of codeine (3.3 mM, 20–32 nl) in the cVRC reduced cough number by 29% ( P < 0.01) and expiratory cough amplitudes of esophageal pressure by 33% ( P < 0.05) as well as both ipsilateral and contralateral ABD EMGs by 35% and 48% ( P < 0.01 and P < 0.01, respectively). No cough depression was observed after microinjections of vehicle. There was no significant effect of microinjection of codeine in the cVRC (3.3 mM, 30–40 nl) on ABD activity induced by a microinjection of d,l-homocysteic acid (30 mM, 27–40 nl) in the same location. However, a cumulative dose of codeine (0.1 mg/kg, 330 nmol/kg) applied into the brain stem circulation through the vertebral artery reduced the ABD motor response to cVRC d,l-homocysteic acid microinjection (30 mM, 28–32 nl) by 47% ( P < 0.01). These results suggest that 1) codeine can act within the cVRC to suppress cough and 2) expiratory premotoneurons within the cVRC are relatively insensitive to this opioid.
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Chen, Shuang, and Sheng-Xing Ma. "Nitric Oxide in the Gracile Nucleus Mediates Depressor Response to Acupuncture (ST36)." Journal of Neurophysiology 90, no. 2 (August 2003): 780–85. http://dx.doi.org/10.1152/jn.00170.2003.
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The purpose of these studies was to determine the role of gracile nucleus and the effects of l-arginine-derived nitric oxide (NO) synthesis in the nucleus on the cardiovascular responses to electroacupuncture (EA) stimulation of “Zusanli” (ST36). Arterial blood pressure and heart rate were monitored during EA stimulation of ST36 following microinjections of agents into gracile nucleus. EA ST36 produced depressor and bradycardiac responses in anesthetized Sprague-Dawley rats. The cardiovascular responses to EA ST36 were blocked by bilateral microinjection of lidocaine into gracile nucleus. Microinjection of l-arginine into gracile nucleus facilitated the hypotensive and bradycardiac responses to EA ST36. The cardiovascular responses to EA ST36 were attenuated by bilateral microinjection of neuronal NO synthase (nNOS) antisense oligos into gracile nucleus. Microinjection of nNOS sense oligos into gracile nucleus did not alter the cardiovascular response to EA ST36. The results demonstrate that a blockade of neuronal conduction in the gracile nucleus inhibits the cardiovascular responses to EA ST36. The hypotensive and bradycardiac responses to EA ST36 are modified by influences of l-arginine-derived NO synthesis in the gracile nucleus. We conclude that NO plays an important role in mediating the cardiovascular responses to EA ST36 through gracile nucleus.
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Ardeleanu, Popescu, Udroiu, Diaconu, Mihai, Lungu, Alhalaili, and Vidu. "Novel PDMS-based Sensor System for MPWM Measurements of Picoliter Volumes in Microfluidic Devices." Sensors 19, no. 22 (November 8, 2019): 4886. http://dx.doi.org/10.3390/s19224886.
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In order for automatic microinjection to serve biomedical and genetic research, we have designed and manufactured a PDMS-based sensor with a circular section channel using the microwire molding technique. For the very precise control of microfluidic transport, we developed a microfluidic pulse width modulation system (MPWM) for automatic microinjections at a picoliter level. By adding a computer-aided detection and tracking of fluid-specific elements in the microfluidic circuit, the PDMS microchannel sensor became the basic element in the automatic control of the microinjection sensor. With the PDMS microinjection sensor, we precise measured microfluidic volumes under visual detection, assisted by very precise computer equipment (with precision below 1 μm) based on image processing. The calibration of the MPWM system was performed to increase the reproducibility of the results and to detect and measure microfluidic volumes. The novel PDMS-based sensor system for MPWM measurements of microfluidic volumes contributes to the advancement of intelligent control methods and techniques, which could lead to new developments in the design, control, and in applications of real-time intelligent sensor system control.
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Ling, L., D. R. Karius, R. R. Fiscus, and D. F. Speck. "Endogenous nitric oxide required for an integrative respiratory function in the cat brain." Journal of Neurophysiology 68, no. 5 (November 1, 1992): 1910–12. http://dx.doi.org/10.1152/jn.1992.68.5.1910.
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1. The involvement of nitric oxide (NO) in the respiratory function of the pons was examined by microinjecting NO synthase-related drugs into discrete regions of the pontine respiratory group (PRG) in decerebrate and decerebellate cats. 2. Microinjection of N omega-nitro-L-arginine (L-NNA, inhibitor of NO synthase), but not D-NNA (the inactive enantiomer), significantly prolonged the duration of inspiration in all 10 cats when lung inflation was withheld. 3. The prolongation of inspiration produced by L-NNA was partially reversed in three cats by microinjections of L-arginine (NO synthase substrate) at the same sites. 4. We conclude that endogenous production of NO from L-arginine in the PRG region is involved in the normal function of the pontine pneumotaxic mechanism. These findings provide the first conclusive evidence that endogenous NO formation is involved in the mechanisms associated with respiratory rhythm generation.
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Frederickson, Robert. "Plastid microinjection." Nature Biotechnology 17, no. 9 (September 1999): 840. http://dx.doi.org/10.1038/12816.
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Wall, Robert J. "Pronuclear Microinjection." Cloning and Stem Cells 3, no. 4 (December 2001): 209–20. http://dx.doi.org/10.1089/15362300152725936.
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Aguero, Tristan, Karen Newman, and Mary Lou King. "Microinjection ofXenopusOocytes." Cold Spring Harbor Protocols 2018, no. 2 (January 10, 2018): pdb.prot096974. http://dx.doi.org/10.1101/pdb.prot096974.
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Nagy, Andras, Marina Gertsenstein, Kristina Vintersten, and Richard Behringer. "Microinjection Setup." Cold Spring Harbor Protocols 2006, no. 1 (June 2006): pdb.prot4396. http://dx.doi.org/10.1101/pdb.prot4396.
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De Novellis, V., E. H. Stotz-Potter, S. M. Morin, F. Rossi, and J. A. DiMicco. "Hypothalamic sites mediating cardiovascular effects of microinjected bicuculline and EAAs in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 1 (July 1, 1995): R131—R140. http://dx.doi.org/10.1152/ajpregu.1995.269.1.r131.
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Microinjection of gamma-aminobutyric acidA receptor antagonist bicuculline methiodide (BMI) into either the dorsomedial hypothalamic nucleus (DMH) or the nearby paraventricular hypothalamic nucleus (PVN) has been reported to evoke marked tachycardia and modest pressor effects. We compared the effects of microinjecting BMI and excitatory amino acids (EAAs) into 1) the DMH, 2) the PVN, and 3) an intermediate area between the two nuclei. In conscious rats, microinjection of (in pmol) 10 BMI, 0.5 kainic acid, or 5 N-methyl-D-aspartate into the DMH markedly increased heart rate and slightly elevated arterial pressure, whereas injections into other regions provoked changes that progressively declined in magnitude with increasing distance from the nucleus. A similar pattern was evident in urethan-anesthetized rats, where the shortest latency to onset of BMI-induced increases in heart rate was seen after injection into the DMH. These findings demonstrate that the cardiovascular changes seen after microinjection of BMI or EAAs into the medial hypothalamus result from an action in the DMH and not from spread to the PVN.
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Dean, C. "Cannabinoid and GABA modulation of sympathetic nerve activity and blood pressure in the dorsal periaqueductal gray of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 6 (December 2011): R1765—R1772. http://dx.doi.org/10.1152/ajpregu.00398.2011.
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Sympathoexcitation and increased blood pressure evoked by central networks integrating defensive behavior are fundamental to the acute stress response. A balance between excitatory glutamatergic and inhibitory GABAergic neurotransmission in the dorsal periaqueductal gray (dPAG) results in a tonic level of activity in the alerting system. Neuromodulators such as endocannabinoids have been shown to influence the sympathoexcitatory and pressor components of acute stress in the dPAG, exemplified by the defense response as a model, but the mechanism of integration remains unknown. The present study examines the role of GABA and its interaction with endocannabinoids in modulating sympathetic nerve activity and blood pressure related to the defense response. Microinjection of the broad-spectrum excitatory amino acid dl-homocysteic acid (DLH) identified sites of the defense pathway in the dPAG from which an increase in renal sympathetic nerve activity and blood pressure could be evoked, and subsequent microinjections were made at the same site through a multibarrelled micropipette. Blockade of GABAA receptors or microinjection of the cannabinoid 1 receptor agonist anandamide elicited a renal sympathoexcitation and pressor response. Prior microinjection of the GABAA receptor antagonist gabazine attenuated the sympathoexcitation and pressor response associated with anandamide microinjection. In contrast, the sympathetic response to DLH was enhanced by GABAA receptor blockade. These data demonstrate that sympathoexcitatory neurons in the dPAG are under tonic inhibition by GABA and that endocannabinoids modulate this GABAergic neurotransmission to help regulate components of the defense response.
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Kenney, Michael J., Mark L. Weiss, Tammy Mendes, Yan Wang, and Richard J. Fels. "Role of paraventricular nucleus in regulation of sympathetic nerve frequency components." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 5 (May 1, 2003): H1710—H1720. http://dx.doi.org/10.1152/ajpheart.00673.2002.
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Autospectral and coherence analyses were used to determine the role of and interactions between paraventricular nucleus (PVN) nitric oxide, γ-aminobutyric acid (GABA), and the N-methyl-d-aspartic acid (NMDA)-glutamate receptor in regulation of sympathetic nerve discharge (SND) frequency components in anesthetized rats. Four observations were made. First, PVN microinjection of bicuculline (BIC) (GABAAreceptor antagonist), but not single PVN injections of NMDA (excitatory amino acid) or N G-monomethyl-l-arginine (l-NMMA; a nitric oxide synthase inhibitor), altered SND frequency components. Second, combined PVN microinjections ofl-NMMA and NMDA changed the SND bursting pattern; however, the observed pattern change was different from that produced by PVN BIC and not observed after sinoaortic denervation. Third, PVN microinjection of kynurenic acid prevented and reversed BIC-induced changes in the SND bursting pattern. Finally, vascular resistance (renal and splenic) was significantly increased after PVN BIC microinjection despite the lack of change in the level of renal and splenic SND. These data demonstrate that the PVN contains the neural substrate for altering SND frequency components and suggest complex interactions between specific PVN neurotransmitters and between PVN neurotransmitters and the arterial baroreceptor reflex in SND regulation.
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Ren, K., A. Randich, and G. F. Gebhart. "Electrical stimulation of cervical vagal afferents. I. Central relays for modulation of spinal nociceptive transmission." Journal of Neurophysiology 64, no. 4 (October 1, 1990): 1098–114. http://dx.doi.org/10.1152/jn.1990.64.4.1098.
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1. Supraspinal relays for vagal afferent modulation of responses of spinal dorsal horn neurons to 50 degrees C heating of the skin were examined by the use of nonselective, reversible local anesthesia or soma-selective, irreversible neurotoxic damage of neural tissue. Eighty-five neurons were isolated in the lumbar spinal dorsal horn of 80 pentobarbital-anesthetized, paralyzed rats. All neurons studied had receptive fields on the glabrous skin of the plantar surface of the ipsilateral hind paw and responded to mechanical stimuli of both low and high intensity as well as noxious thermal stimulation. 2. Intensity-dependent modulation by vagal afferent stimulation (VAS) of neuronal responses to heating of the skin was established. Responses of 40 units were facilitated by low and inhibited by greater intensities of VAS. Another 36 units were only inhibited by VAS, and four were only facilitated. 3. Local anesthesia of the dorsolateral pons by bilateral microinjections of lidocaine (4%, 0.5 microliter) were made to examine the contribution of this area to VAS-produced spinal modulation. The microinjection of lidocaine bilaterally into the ventral locus coeruleus/subcoeruleus (LC/SC) reversibly and significantly attenuated VAS-produced inhibition of unit responses to heat from 63 to 89% of control and abolished VAS-produced facilitation. The microinjection of lidocaine bilaterally into the dorsal LC had no significant effect on VAS-produced modulation of spinal dorsal horn neurons. 4. Ibotenic acid (10 micrograms, 0.5 microliter) was microinjected into the dorsolateral pons to determine the relative contributions of cell bodies in this area to VAS-produced spinal modulation. Unilateral microinjection of ibotenic acid into the LC/SC ipsilateral to the vagus nerve stimulated had no significant effect on VAS-produced inhibition but significantly attenuated VAS-produced facilitation of unit responses to heat. Bilateral microinjections of ibotenic acid significantly attenuated VAS-produced inhibition of unit responses to heat from 48 to 94% of control. 5. Local anesthesia of the medial rostroventral medulla (RVM), primarily the nucleus raphe magnus (NRM), significantly attenuated VAS-produced inhibition of unit responses to heat from 55 to 87% of control but had no significant effect on VAS-produced facilitation. Microinjection of ibotenic acid into the RVM also significantly reduced VAS-produced inhibition of unit responses to heat. No significant change in VAS-produced spinal modulation was found after lidocaine microinjection into areas dorsal to the NRM, the nucleus raphe pallidus, or the olivary nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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Datta, Subimal, and Donald F. Siwek. "Excitation of the Brain Stem Pedunculopontine Tegmentum Cholinergic Cells Induces Wakefulness and REM Sleep." Journal of Neurophysiology 77, no. 6 (June 1, 1997): 2975–88. http://dx.doi.org/10.1152/jn.1997.77.6.2975.
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Datta, Subimal and Donald F. Siwek. Excitation of the brain stem pedunculopontine tegmentum cholinergic cells induces wakefulness and REM sleep. J. Neurophysiol. 77: 2975–2988, 1997. Considerable evidence suggests that brain stem pedunculopontine tegmentum (PPT) cholinergic cells are critically involved in the normal regulation of wakefulness and rapid eye movement (REM) sleep. However, much of this evidence comes from indirect studies. Thus, although involvement of PPT cholinergic neurons has been suggested by numerous investigations, the excitation of PPT cholinergic neurons causal to the behavioral state of wakefulness and REM sleep has never been directly demonstrated. In the present study we examined the effects of three different levels of activation of PPT cholinergic cells in wakefulness and sleep behavior. The effects of glutamate on the activity of PPT cholinergic cells were studied by microinjection of one of the three different doses of l-glutamate (0.3, 1.0, and 3.0 μg) or saline (vehicle control) into the PPT cholinergic cell compartment while quantifying the effects on wakefulness and sleep in free moving chronically instrumented cats. All microinjections were made during wakefulness and were followed by 4 h of recording. Polygraphic records were scored for wakefulness, slow-wave sleep states 1 and 2, slow-wave sleep with pontogeniculooccipital waves, and REM sleep. Dependent variables quantified after each microinjection included the percentage of recording time spent in each state, the latency to onset of REM sleep, the number of episodes per hour for REM sleep, and the duration of each REM sleep episode. A total of 48 microinjections was made into 12 PPT sites in six cats. Microinjection of 0.3- and 1.0-μg doses of l-glutamate into the cholinergic cell compartment of the PPT increased the total amount of REM sleep in a dose-dependent manner. Both doses of l-glutamate increased REM sleep at the expense of slow-wave sleep but not wakefulness. Microinjection of 3.0 μg l-glutamate kept animals awake for 2–3 h by eliminating slow-wave and REM sleep. The results show that the microinjection of the excitatory amino acid l-glutamate into the PPT cholinergic cell compartments can increase wakefulness and/or REM sleep depending on the l-glutamate dosage. These findings unambiguously confirm the hypothesis that the excitation of the PPT cholinergic cells is causal to the generation of wakefulness and REM sleep.
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Potas, J. R., and R. A. L. Dampney. "Sympathoinhibitory pathway from caudal midline medulla to RVLM is independent of baroreceptor reflex pathway." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 4 (April 1, 2003): R1071—R1078. http://dx.doi.org/10.1152/ajpregu.00559.2002.
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Glutamate stimulation of the caudal midline medulla (CMM) causes profound sympathoinhibition due to GABAergic inhibition of presympathetic neurons in the rostral ventrolateral medulla (RVLM). We investigated whether the sympathoinhibitory pathway from CMM to RVLM, like the central baroreceptor reflex pathway, includes a glutamatergic synapse in the caudal ventrolateral medulla (CVLM). In pentobarbital sodium-anesthetized rats, the RVLM on one side was inhibited by a muscimol microinjection. Then the response evoked by glutamate microinjections into the CMM or by baroreceptor stimulation was determined before and after 1) microinjection of the GABA receptor antagonist bicuculline into the RVLM on the other side or 2) microinjections of the glutamate receptor antagonist kynurenate bilaterally into the CVLM. Bicuculline in the RVLM greatly reduced both CMM- and baroreceptor-evoked sympathoinhibition. Compared with the effect of vehicle solution, kynurenate in the CVLM greatly reduced baroreceptor-evoked sympathoinhibition, whereas its effect on CMM-evoked sympathoinhibition was not different from that of the vehicle solution. These findings indicate that the output pathway from CMM sympathoinhibitory neurons, unlike the baroreceptor and other reflex sympathoinhibitory pathways, does not include a glutamatergic synapse in the CVLM.
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Callera, João Carlos, Leni G. H. Bonagamba, Anne Nosjean, Raul Laguzzi, and Benedito H. Machado. "Activation of GABAA but not GABAB receptors in the NTSblocked bradycardia of chemoreflex in awake rats." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1902—H1910. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1902.
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In the present study we analyzed effects of bilateral microinjections of muscimol (a GABAA agonist) and baclofen (a GABAB agonist) into the nucleus tractus solitarius (NTS) on bradycardic and pressor responses to chemoreflex activation (potassium cyanide, 40 μg/rat iv) in awake rats. Bilateral microinjections of muscimol (25 and 50 pmol/50 nl) into the NTS increased baseline mean arterial pressure (MAP): 119 ± 8 vs. 107 ± 2 mmHg ( n = 6) and 121 ± 8 vs. 103 ± 3 mmHg ( n= 6), respectively. Muscimol at 25 pmol/50 nl reduced the bradycardic response to chemoreflex activation 5 min after microinjection; with 50 pmol/50 nl the bradycardic response to chemoreflex activation was reduced 5, 15, 30, and 60 min after microinjection. Neither muscimol dose produced an effect on the pressor response of the chemoreflex. Effects of muscimol (50 pmol/50 nl) on basal MAP and on the bradycardic response of the chemoreflex were prevented by prior microinjection of bicuculline (a GABAA antagonist, 40 pmol/50 nl) into the NTS. Bilateral microinjections of baclofen (12.5 and 25 pmol/50 nl) into the NTS produced an increase in baseline MAP [137 ± 9 vs. 108 ± 4 ( n= 7) and 145 ± 5 vs. 105 ± 2 mmHg ( n = 7), respectively], no changes in basal heart rate, and no effects on the bradycardic response; 25 pmol/50 nl only attenuated the pressor response to chemoreflex activation. The data show that activation of GABAA receptors in the NTS produces a significant reduction in the bradycardic response, whereas activation of GABAB receptors produces a significant reduction in the pressor response of the chemoreflex. We conclude that 1) GABAA but not GABAB plays an inhibitory role in neurons of the lateral commissural NTS involved in the parasympathetic component of the chemoreflex and 2) attenuation of the pressor response of the chemoreflex by activation of GABAB receptors may be due to inhibition of sympathoexcitatory neurons in the NTS or may be secondary to the large increase in baseline MAP produced by baclofen.
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Orer, Hakan S., Gerard L. Gebber, and Susan M. Barman. "Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 5 (May 2008): R1435—R1444. http://dx.doi.org/10.1152/ajpregu.00012.2008.
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We studied the changes in inferior cardiac sympathetic nerve discharge (SND) produced by unilateral microinjections of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Microinjection of the 5-HT2 receptor antagonist LY-53857 (10 mM) into either the rostral or caudal VLM significantly reduced ( P ≤ 0.05) the 10-Hz rhythmic component of basal SND without affecting its lower-frequency, aperiodic component. The selective depression of 10-Hz power was accompanied by a statistically significant decrease in mean arterial pressure (MAP). Microinjection of LY-53857 into the VLM also attenuated the increase in 10-Hz power that followed tetanic stimulation of depressor sites in the caudal medullary raphé nuclei. Microinjection of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI; 10 μM) into the VLM selectively enhanced 10-Hz SND, and intravenous DOI (1 mg/kg) partially reversed the reduction in 10-Hz SND produced by 5-HT2 receptor blockade in the VLM. Microinjection of the 5-HT1A receptor agonist, 8-hydroxy-2-(di- n-propylamino)tetralin (8-OHDPAT; 10 mM), into either the rostral or caudal VLM also selectively attenuated 10-Hz SND and significantly reduced MAP. The reduction in 10-Hz SND produced by 8-OHDPAT was partially reversed by intravenous WAY-100635 (1 mg/kg), which selectively blocks 5-HT1A receptors. These results support the view that serotonergic inputs to the VLM play an important role in expression of the 10-Hz rhythm in SND.
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Pelham, R. J., J. J. Lin, and Y. L. Wang. "A high molecular mass non-muscle tropomyosin isoform stimulates retrograde organelle transport." Journal of Cell Science 109, no. 5 (May 1, 1996): 981–89. http://dx.doi.org/10.1242/jcs.109.5.981.
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Although non-muscle tropomyosins (TM) have been implicated in various cellular functions, such as stabilization of actin filaments and possibly regulation of organelle transport, their physiological role is still poorly understood. We have probed the role of a high molecular mass isoform of human fibroblast TM, hTM3, in regulating organelle transport by microinjecting an excess amount of bacterially-expressed protein into normal rat kidney (NRK) epithelial cells. The microinjection induced the dramatic retrograde translocation of organelles into the perinuclear area. Microinjection of hTM5, a low molecular mass isoform had no effect on organelle distribution. Fluorescent staining indicated that hTM3 injection stimulated the retrograde movement of both mitochondria and lysosomes. Moreover, both myosin I and cytoplasmic dynein were found to redistribute with the translocated organelles to the perinuclear area, indicating that these organelles were able to move along both microtubules and actin filaments. The involvement of microtubules was further suggested by the partial inhibition of hTM3-induced organelle movement by the microtubule-depolymerizing drug nocodazole. Our results, along with previous genetic and antibody microinjection studies, suggest that hTM3 may be involved in the regulation of organelle transport.
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Couto, Aurea S., Ovidiu Baltatu, Robson A. S. Santos, Detlev Ganten, Michael Bader, and Maria J. Campagnole-Santos. "Differential Effects of Angiotensin II and Angiotensin-(1-7) at the Nucleus Tractus Solitarii of Transgenic Rats with Low Brain Angiotensinogen." Hypertension 36, suppl_1 (October 2000): 700. http://dx.doi.org/10.1161/hyp.36.suppl_1.700-c.
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P42 The potential importance of permanent alteration of the brain renin-angiotensin system on angiotensin (Ang) II and Ang-(1-7) effects at the level of the nucleus tractus solitarii (NTS) was investigated in transgenic rats with a deficit in brain angiotensinogen production TGR(ASrAOGEN) (TGR). Ang II (10 pmol), Ang-(1-7) (10 pmol) or NaCl (0.9%/ 50 nl) were microinjected into the NTS of urethane-anesthetized TGR (n=28) and Sprague-Dawley (SD, n=22) rats. Mean arterial pressure (MAP) and heart rate (HR) were measured via a femoral artery catheter and the baroreflex control of heart rate was evaluated after increases in MAP induced by phenylephrine (baroreflex bradycardia). Ang II microinjections into the NTS of the TGR induced a higher decrease in MAP and HR (-37 ± 5 mmHg and -69 ± 12.5 beats/min, respectively) in comparison with SD rats (-18 ± 1 mmHg and -51 ± 11 beats/min, respectively). In contrast, changes after Ang-(1-7) microinjections into the NTS of TGR (-6 ± 1 mmHg and -13 ± 5 beats/min) were significantly smaller than that induced in SD (-11 ± 2 mmHg and -24 ± 8 beats/min.). The baroreflex sensitivity was accentuated in TGR in comparison to SD rats (0.69 ± 0.06 vs. 0.44 ± 0.03 ms/ mmHg). Ang II microinjection into the NTS produced similar attenuation in the baroreflex bradycardia in both SD (0.28 ± 0.07 vs. 0.5 ± 0.07 ms/ mmHg, before injection) and TGR (0.44 ± 0.1 vs. 0.82 ± 0.1ms/ mmHg, before injection). Ang-(1-7) microinjection elicited a facilitation of the baroreflex bradycardia in SD (0.62 ± 0.1 vs. 0.4 ± 0.03 ms/ mmHg, before injection). However in TGR, baroreflex bradycardia after Ang-(1-7) was not different from saline microinjection. These results indicate that a permanent inhibition of angiotensinogen synthesis in the brain can lead to a functional up-regulation of Ang II receptors. However, the putative Ang-(1-7) receptors seem to be desensitized in the NTS of these transgenic rats. The alterated baroreflex sensitivity, both before and after Ang microinjection, indicates the functionally relevant decrease in brain Ang in TGR and supports differential regulatory mechanisms for the effects of the two Ang peptides.
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Alzamora, Andréia C., Robson A. S. Santos, and Maria J. Campagnole-Santos. "Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 4 (April 2006): R1027—R1034. http://dx.doi.org/10.1152/ajpregu.00852.2004.
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We determined the effect of microinjection of ANG-(1–7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1–7) and ANG II (25 pmol) after RVLM microinjection (11 ± 0.8 and 10 ± 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1–7) and ANG II produced hypotension (−11 ± 1.5 and −11 ± 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1–7) attenuated the baroreflex bradycardia (0.26 ± 0.06 ms/mmHg vs. 0.42 ± 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 ± 0.19 ms/mmHg vs. 0.42 ± 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 ± 0.06 ms/mmHg vs. 0.31 ± 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 ± 0.16 ms/mmHg vs. 0.41 ± 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1–7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1–7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.
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Falconi-Sobrinho, Luiz Luciano, Tayllon dos Anjos-Garcia, and Norberto Cysne Coimbra. "Nitric oxide-mediated defensive and antinociceptive responses organised at the anterior hypothalamus of mice are modulated by glutamatergic inputs from area 24b of the cingulate cortex." Journal of Psychopharmacology 35, no. 1 (December 10, 2020): 78–90. http://dx.doi.org/10.1177/0269881120967881.
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Background: Previous studies suggested that Cg1 area of the cingulate cortex of rats controls glutamate-mediated fear-induced defensive behaviour and antinociception organised at the posterior hypothalamus. In turn, microinjection of the nitric oxide donor SIN-1 into the anterior hypothalamus of mice produced defensive behaviours and fear-induced antinociception. However, it remains unknown whether Cg1 also modulates the latter mechanisms in mice. Aims: The present study examined the influence of Cg1 on SIN1-evoked fear-induced defensive behaviour and antinociception organised at the anterior hypothalamus of mice. Methods: The fear-like behavioural and antinociceptive responses to the microinjection of SIN-1 (300 nmol) into the anterior hypothalamus were evaluated after the microinjection of either N-methyl-D-aspartic acid receptor agonist (0.1, 1 and 10 nmol) or physiological saline into the cingulate cortex of C57BL/6 male mice. In addition, neurotracing and immunohistochemistry were used to characterise Cg1-anterior hypothalamus glutamatergic pathways. Results: The data showed that activation of Cg1 N-methyl-D-aspartic acid receptors increased escape while reducing freezing and antinociceptive responses to SIN-1 microinjections into the anterior hypothalamus. Anterograde neural tract tracer co-localised with VGLUT2-labelled fibres suggests these responses are mediated by glutamatergic synapses at the anterior hypothalamus. Conclusions: In contrast with previous studies showing that Cg1 facilitates both escape and antinociception to chemical stimulation of the posterior hypothalamus in rats, the present data suggest that Cg1 facilitates escape while inhibiting defensive antinociception produced by the microinjection of SIN-1 in the anterior hypothalamus of mice. Accordingly, Cg1 may have opposite effects on antinociceptive responses organised in the anterior and posterior hypothalamus of mice and rats, respectively.
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Mattos, L. S., E. Grant, R. Thresher, and K. Kluckman. "Blastocyst Microinjection Automation." IEEE Transactions on Information Technology in Biomedicine 13, no. 5 (September 2009): 822–31. http://dx.doi.org/10.1109/titb.2009.2023664.
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Morello, D. "Microinjection and transgenesis." Biochimie 80, no. 7 (July 1998): 632. http://dx.doi.org/10.1016/s0300-9084(98)80030-8.
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McGourty, Christine. "Microinjection patent granted." Nature 341, no. 6244 (October 1989): 681. http://dx.doi.org/10.1038/341681c0.
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Le Lannou, D., J. F. Griveau, M. C. Laurent, and B. Lobel. "Azoospermie et microinjection." Andrologie 11, no. 3 (September 2001): 142–48. http://dx.doi.org/10.1007/bf03036638.
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Block, F. "Electrophysiology and microinjection." Neurochemistry International 20, no. 2 (February 1992): 271. http://dx.doi.org/10.1016/0197-0186(92)90177-s.
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Randich, A., C. L. Thurston, P. S. Ludwig, J. D. Robertson, and C. Rasmussen. "Intravenous morphine-induced activation of vagal afferents: peripheral, spinal, and CNS substrates mediating inhibition of spinal nociception and cardiovascular responses." Journal of Neurophysiology 68, no. 4 (October 1, 1992): 1027–45. http://dx.doi.org/10.1152/jn.1992.68.4.1027.
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1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)
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Ling, L., D. R. Karius, and D. F. Speck. "Role of N-methyl-D-aspartate receptors in the pontine pneumotaxic mechanism in the cat." Journal of Applied Physiology 76, no. 3 (March 1, 1994): 1138–43. http://dx.doi.org/10.1152/jappl.1994.76.3.1138.
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Systemic injection of MK-801, an N-methyl-D-aspartate (NMDA) receptor-associated channel blocker, induces an apneusis in vagotomized cats similar to that produced by pontine respiratory group (PRG) lesions, suggesting the possible involvement of NMDA receptors in the pontine pneumotaxic mechanism. Previous results from our laboratory indicate that the efferent limb of the pontine pneumotaxic mechanism is unlikely to require NMDA receptor-mediated neurotransmission. Therefore, the present study examined the potential involvement of PRG NMDA receptors in the pontine pneumotaxic mechanism. Experiments were conducted in decerebrate, paralyzed, and ventilated adult cats. The effects on inspiratory time (TI) of MK-801 microinjection into PRG were tested in 12 cats. Pressure microinjection of MK-801 (15 mM, 80–3,000 nl) significantly prolonged TI in all animals when lung inflation was withheld. TI progressively increased in most animals for > or = 30 min. After this period, partial recovery of the effect occurred in eight cats as TI shortened toward predrug levels. In three animals, microinjection of MK-801 induced a complete apneusis in the absence of lung inflation from which there was no detectable recovery. Microinjections into regions approximately 2 mm distant from PRG produced little or no effect. These results provide evidence that NMDA receptors located in the region of PRG play an important functional role in the control of the breathing cycle.
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Poliacek, Ivan, Lu Wen-Chi Corrie, Cheng Wang, Melanie J. Rose, and Donald C. Bolser. "Microinjection of DLH into the region of the caudal ventral respiratory column in the cat: evidence for an endogenous cough-suppressant mechanism." Journal of Applied Physiology 102, no. 3 (March 2007): 1014–21. http://dx.doi.org/10.1152/japplphysiol.00616.2006.
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The caudal ventral respiratory column (cVRC) contains premotor expiratory neurons that play an important role in cough-related expiratory activity of chest wall and abdominal muscles. Microinjection of d,l-homocysteic acid (DLH) was used to test the hypothesis that local activation of cVRC neurons can suppress the cough reflex. DLH (20–50 mM, 10–30 nl) was injected into the region of cVRC in nine anesthetized spontaneously breathing cats. Repetitive coughing was elicited by mechanical stimulation of the intrathoracic airways. Electromyograms (EMG) were recorded bilaterally from inspiratory parasternal and expiratory transversus abdominis (ABD) and unilaterally from laryngeal posterior cricoarytenoid and thyroarytenoid muscles. Unilateral microinjection of DLH (1–1.5 nmol) elicited bilateral increases in tonic and phasic respiratory ABD EMG activity, and it altered the respiratory pattern and laryngeal motor activities. However, DLH also decreased cough frequency by 51 ± 7% compared with control ( P < 0.001) and the amplitude of the contralateral (−35 ± 3%; P < 0.001) and ipsilateral (−34 ± 5%; P < 0.001) ABD EMGs during postinjection coughs compared with control. The cough alterations were much less pronounced after microinjection of a lower dose of DLH (0.34–0.8 nmol). No cough depression was observed after microinjections of vehicle. These results suggest that an endogenous cough suppressant neuronal network in the region of the cVRC may exist, and this network may be involved in the control of cough reflex excitability.
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Cruz, Maureen T., Erin C. Murphy, Niaz Sahibzada, Joseph G. Verbalis, and Richard A. Gillis. "A reevaluation of the effects of stimulation of the dorsal motor nucleus of the vagus on gastric motility in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 1 (January 2007): R291—R307. http://dx.doi.org/10.1152/ajpregu.00863.2005.
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Our primary purpose was to characterize vagal pathways controlling gastric motility by microinjecting l-glutamate into the dorsal motor nucleus of the vagus (DMV) in the rat. An intragastric balloon was used to monitor motility. In 39 out of 43 experiments, microinjection of l-glutamate into different areas of the DMV rostral to calamus scriptorius (CS) resulted in vagally mediated excitatory effects on motility. We observed little evidence for inhibitory effects, even with intravenous atropine or with activation of gastric muscle muscarinic receptors by intravenous bethanechol. Inhibition of nitric oxide synthase with Nω-nitro-l-arginine methyl ester (l-NAME) HCl did not augment DMV-evoked excitatory effects on gastric motility. Microinjection of l-glutamate into the DMV caudal to CS produced vagally mediated gastric inhibition that was resistant to l-NAME. l-Glutamate microinjected into the medial subnucleus of the tractus solitarius (mNTS) also produced vagally mediated inhibition of gastric motility. Motility responses evoked from the DMV were always blocked by ipsilateral vagotomy, while responses evoked from the mNTS required bilateral vagotomy to be blocked. Microinjection of oxytocin into the DMV inhibited gastric motility, but the effect was never blocked by ipsilateral vagotomy, suggesting that the effect may have been due to diffusion of oxytocin to the mNTS. Microinjection of substance P and N-methyl-d-aspartate into the DMV also produced inhibitory effects attributable to excitation of nearby mNTS neurons. Our results do not support previous studies indicating parallel vagal excitatory and inhibitory pathways originating in the DMV rostral to CS. Our results do support previous findings of vagal inhibitory pathways originating in the DMV caudal to CS.
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Gultom, V. D. N. "Past, present and future prospect on microinjection gene transfer in aquaculture." IOP Conference Series: Earth and Environmental Science 1137, no. 1 (January 1, 2023): 012040. http://dx.doi.org/10.1088/1755-1315/1137/1/012040.
Full textAbstract:
Abstract Microinjection is arguably the most direct and reliable gene transfer method to date. Since the development of the first transgenic fish in 1984, microinjection continues to be the most commonly used gene transfer method in aquaculture. Microinjection is used to inject cells, nucleic acid, gene constructs, recombinant DNA, and morpholino oligonucleotides into fish cells, embryos, and larvae. Despite the development of various gene transfer methods, microinjection is preferable. Continuous improvement in micromanipulation tools and micro capillary further develop microinjection method. This review describes the past and present use of microinjection gene transfer methods for genetic manipulation and genetic improvement in fisheries and aquaculture, especially in fish transgenesis. Furthermore, we discuss the future prospects of microinjection method in tandem with recombinant DNA technology and CRISPR-Cas9 and its application in the aquaculture industry.
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Zhang, Pan Pan, Jian Wang, Peng Cheng Xie, Li Lei Miao, and Wei Min Yang. "Design of a Multi Microinjection Molding Module for Thermoplastic Polymer." Key Engineering Materials 501 (January 2012): 162–67. http://dx.doi.org/10.4028/www.scientific.net/kem.501.162.
Full textAbstract:
A new concept of microinjection molding module was designed and presented. The module was designed as a multi microinjection module, which is matched with a vertical injection molding machine (IMM) and can be applied to usual IMMs. A planetary gear pump was integrated in this module to complete the multi microinjection molding(MμIMM)。The module is fixed between the stationary platen and the mold of IMM. The plasticizing unit of the IMM provides the melt and initial pressure for the multi microinjection molding module. With this module, a usual IMM could be upgraded to a precise microinjection machine and has the capability of precise metering for the microinjection molding.
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de Paula, Patrícia M., Vagner R. Antunes, Leni G. H. Bonagamba, and Benedito H. Machado. "Cardiovascular responses to microinjection of ATP into the nucleus tractus solitarii of awake rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 5 (November 2004): R1164—R1171. http://dx.doi.org/10.1152/ajpregu.00722.2003.
Full textAbstract:
Microinjection of increasing doses of ATP (0.31, 0.62, 1.25, and 2.5 nmol/50 nl) into the nucleus tractus solitarii (NTS) produced a dose-dependent pressor response. Prazosin abolished the pressor response and produced no change in the bradycardic response to ATP. Microinjection of pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (0.25 nmol/50 nl), a nonselective P2 receptor antagonist into the NTS, reduced the bradycardic response but had no effect on the pressor response to microinjection of ATP (1.25 nmol/50 nl) into the NTS. Microinjection of suramin (2 nmol/50 nl), another nonselective P2 receptor antagonist, had no effect on the pressor and bradycardic responses to microinjection of ATP (1.25 nmol/50 nl) into the NTS. Antagonism of A1 receptors of adenosine with 1,3-dipropyl-8-cyclopentylxanthine also produced no changes in the cardiovascular responses to microinjection of ATP into the NTS. The involvement of excitatory amino acid (EAA) receptors in the pressor and bradycardic responses to microinjection of ATP into the NTS was also evaluated. Microinjection of kynurenic acid, a nonselective EAA receptor antagonist (10 nmol/50 nl), into the NTS reduced the bradycardic response and had no effect on the pressor response to microinjection of ATP into the NTS. The data show that 1) microinjection of ATP into the NTS of awake rats produced pressor and bradycardic responses by independent mechanisms, 2) the activation of parasympathetic component may involve an interaction of P2 and EAA receptors in the NTS, and 3) the sympathoexcitatory response to microinjection of ATP into the NTS was not affected by the blockade of P2, A1, or EAA receptors.
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Zhao, Yuliang, Hui Sun, Xiaopeng Sha, Lijia Gu, Zhikun Zhan, and Wen Li. "A Review of Automated Microinjection of Zebrafish Embryos." Micromachines 10, no. 1 (December 24, 2018): 7. http://dx.doi.org/10.3390/mi10010007.
Full textAbstract:
Cell microinjection is a technique of precise delivery of substances into cells and is widely used for studying cell transfection, signaling pathways, and organelle functions. Microinjection of the embryos of zebrafish, the third most important animal model, has become a very useful technique in bioscience. However, factors such as the small cell size, high cell deformation tendency, and transparent zebrafish embryo membrane make the microinjection process difficult. Furthermore, this process has strict, specific requirements, such as chorion softening, avoiding contacting the first polar body, and high-precision detection. Therefore, highly accurate control and detection platforms are critical for achieving the automated microinjection of zebrafish embryos. This article reviews the latest technologies and methods used in the automated microinjection of zebrafish embryos and provides a detailed description of the current developments and applications of robotic microinjection systems. The review covers key areas related to automated embryo injection, including cell searching and location, cell position and posture adjustment, microscopic visual servoing control, sensors, actuators, puncturing mechanisms, and microinjection.
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Wang, Zhenya, Shuyan Li, Huanzhu Lai, Liping Zhou, Guannan Meng, Menglong Wang, Yanqiu Lai, et al. "Interaction between Endothelin-1 and Left Stellate Ganglion Activation: A Potential Mechanism of Malignant Ventricular Arrhythmia during Myocardial Ischemia." Oxidative Medicine and Cellular Longevity 2019 (May 12, 2019): 1–11. http://dx.doi.org/10.1155/2019/6508328.
Full textAbstract:
Endothelin-1 (ET-1) is synthesized primarily by endothelial cells. ET-1 administration in vivo enhances the cardiac sympathetic afferent reflex and sympathetic activity. Previous studies have shown that sympathetic hyperactivity promotes malignant ventricular arrhythmia (VA). The aim of this study was to investigate whether ET-1 could activate the left stellate ganglion (LSG) and promote malignant VA. Twelve male beagle dogs who received local microinjections of saline (control, n=6) and ET-1 into the LSG (n=6) were included. The ventricular effective refractory period (ERP), LSG function, and LSG activity were measured at different time points. VA was continuously recorded for 1 h after left anterior descending occlusion (LADO), and LSG tissues were then collected for molecular detection. Compared to that of the control group, local ET-1 microinjection significantly decreased the ERP and increased the occurrence of VA. In addition, local microinjection of ET-1 increased the function and activity of the LSG in the normal and ischemic hearts. The expression levels of proinflammatory cytokines and the protein expression of c-fos and nerve growth factor (NGF) in the LSG were also increased. More importantly, endothelin A receptor (ETA-R) expression was found in the LSG, and its signaling was significantly activated in the ET-1 group. LSG activation induced by local ET-1 microinjection aggravates LADO-induced VA. Activated ETA-R signaling and the upregulation of proinflammatory cytokines in the LSG may be responsible for these effects.
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Yang, G., and C. Iadecola. "Glutamate microinjections in cerebellar cortex reproduce cerebrovascular effects of parallel fiber stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 6 (December 1, 1996): R1568—R1575. http://dx.doi.org/10.1152/ajpregu.1996.271.6.r1568.
Full textAbstract:
Electrical stimulation of cerebellar parallel fibers releases glutamate and increases local blood flow (BFcrb), an effect in part mediated by glutamate-induced nitric oxide (NO) production. We studied whether local microinjection of glutamate into the cerebellar cortex would produce increases in BFcrb comparable to those elicited by parallel fiber stimulation. In halothane-anesthetized rats equipped with a cranial window, glutamate was microinjected into the cerebellar molecular layer, and BFcrb was monitored by laser-Doppler flowmetry. Glutamate microinjections increased BFcrb dose dependently (2-200 pmol in 200 nl) (n = 9) and by 55 +/- 6% at 200 pmol (mean +/- SE). The magnitude and temporal profile of the increases in BFcrb compared favorably with the increase in flow produced by parallel fiber stimulation. The glutamate-induced BFcrb increase was attenuated by superfusion with the Na2+ channel blocker tetrodotoxin (10 microM; -50 +/- 10%; n = 5; P < 0.05; t-test) or by blocking synaptic activity by treatment of the cerebellar cortex with Ringer containing 20 mM Mg2+ and 0 mM Ca2+ (-80 +/- 4%; n = 6; P < 0.05). The glutamate-receptor antagonist kynurenate (10 mM) attenuated the increase in BFcrb by 59 +/- 6% (P < 0.05; n = 5). The relatively selective inhibitor of neuronal NO synthase 7-nitroindazole (100 mg/kg ip) reduced the flow response evoked by microinjection of glutamate (-46 +/- 7%; n = 5; P < 0.05) but not acetylcholine (10 microM; P > 0.05; n = 6). We conclude that glutamate microinjections increase local BFcrb via activation of glutamate receptors. The glutamate-induced vasodilation is mediated, in part, by neurally derived NO. The striking similarities between the vascular responses evoked by parallel fiber stimulation and that produced by microinjection of glutamate support the hypothesis that the increase in BFcrb produced by parallel fiber stimulation is mediated by glutamate release and activation of glutamate receptors. The data also strengthen the hypothesis that glutamate and NO are important mediators in the mechanisms linking synaptic activity to BFcrb in cerebellar cortex.