Journal articles: 'Intermediolateral cell column of spinal cord'

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Kirby, Michael A., Mary M. Groves, and Steven M. Yellon. "Retrograde tracing of spinal cord connections to the cervix with pregnancy in mice." REPRODUCTION 139, no. 3 (March 2010): 645–53. http://dx.doi.org/10.1530/rep-09-0361.

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In contrast to the uterus, the cervix is well innervated during pregnancy and the density of nerve fibers increases before birth. To assess neural connections between the cervix and the spinal cord, the cervix of pregnant mice was injected with the trans-synaptic retrograde neural tract tracer pseudorabies virus (PRV). After 5 days, the virus was present in nerve cells and fibers in specific areas of the sensory, autonomic, and motor subdivisions of the thoracolumbar spinal cord. In nonpregnant controls, the virus was predominantly distributed in laminae I–III in the dorsal gray sensory areas with the heaviest label in the substantia gelatinosa compared with the autonomic or motor areas. Labeled cells and processes were sparse in other regions, except for a prominent cluster in the intermediolateral column (lamina VII). Photomicrographs of spinal cord sections were digitized, and the total area with the virus was estimated. Compared with nonpregnant controls, the area with PRV was significantly decreased in all the spinal cord subdivisions in pregnant mice except in the intermediolateral column. However, areas with the virus were equivalent in mice injected with PRV at 4 days or 1 day before birth. These findings suggest that the predominant innervation of the murine cervix is from the sensory regions of the thoracolumbar spinal cord, and that these connections diminish with pregnancy. The results raise the possibility that the remaining connections from sensory and autonomic subdivisions, particularly the intermediolateral column, of the thoracolumbar spinal cord may be important for increased density of nerve fibers in the cervix as pregnancy nears term.

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Xu, Zemin, Ping Li, Chuanyao Tong, Jorge Figueroa, Joseph R. Tobin, and James C. Eisenach. "Location and Characteristics of Nitric Oxide Synthase in Sheep Spinal Cord and Its Interaction with α2-Adrenergic and Cholinergic Antinociception." Anesthesiology 84, no. 4 (April 1, 1996): 890–99. http://dx.doi.org/10.1097/00000542-199604000-00017.

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Background Nitric oxide synthase is located in the spinal cord dorsal horn and intermediolateral cell column, where it may modulate sensory and sympathetic neuronal activity. However, the biochemical characteristics of this enzyme have not been examined in these different areas in the spinal cord. Although alpha(2)-adrenergic agonists, muscarinic agonists, and nitric oxide may interact in the spinal cord to produce antinociception, these interactions have not been characterized. Methods Sheep spinal cord tissue was homogenized ad centrifuged at high sped to separate soluble and membrane-bound fractions. Nitric oxide synthase activity was determined by conversion of [(14)C]-L-arginine to [(14)C]-L-citrulline and its kinetic characteristics, dependency on cofactors, and sensitivity to inhibitors determined. Sheep spinal cord was stained for nicotinamide adenine dinucleotide phosphate diaphorase as a marker for nitric oxide synthase. Antinociception to a mechanical stimulus from intrathecal clonidine alone and with neostigmine was determined and the effects of L-arginine and n-methyl-L-arginine were determined. Results More than 85% of nitric oxide synthase activity was present in the soluble form and its kinetic, cofactor, and antagonist properties were similar to those of the neuronal isoform of nitric oxide synthase. Biochemical and histochemical studies localized nitric oxide synthase to the superficial dorsal horn and the intermediolateral cell column. Clonidine antinociception was enhanced by L-arginine and neostigmine, but not by D-arginine. Neostigmine's enhancement of clonidine antinociception was blocked by n-methyl-L-arginine. Conclusions These results confirm those of previous studies demonstrating localization of nitric oxide synthase to superficial dorsal horn and intermediolateral cell column of mammalian spinal cord, and suggesting its identity as the neuronal isoform. Spinal alpha(2)-adrenergic agonist antinociception may be partly dependent on cholinergic and nitric oxide mechanisms.

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McCartney, Annemarie M., Vanessa L. Abejuela, and Lori G. Isaacson. "Characterization of trkB immunoreactive cells in the intermediolateral cell column of the rat spinal cord." Neuroscience Letters 440, no. 2 (August 2008): 103–8. http://dx.doi.org/10.1016/j.neulet.2008.05.057.

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Llewellyn-Smith, I. J., J. B. Minson, D. A. Morilak, J. R. Oliver, and J. P. Chalmers. "Neuropeptide Y-immunoreactive synapses in the intermediolateral cell column of rat and rabbit thoracic spinal cord." Neuroscience Letters 108, no. 3 (January 1990): 243–48. http://dx.doi.org/10.1016/0304-3940(90)90648-s.

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Iigaya, Kamon, Hiroo Kumagai, Hiroshi Onimaru, Akira Kawai, Naoki Oshima, Toshiko Onami, Chie Takimoto, et al. "Novel axonal projection from the caudal end of the ventrolateral medulla to the intermediolateral cell column." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (February 2007): R927—R936. http://dx.doi.org/10.1152/ajpregu.00254.2006.

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We used an optical imaging technique to investigate whether axons of neurons in the caudal end of the ventrolateral medulla (CeVLM), as well as axons of neurons in the rostral ventrolateral medulla (RVLM), project to neurons in the intermediolateral cell column (IML) of the spinal cord. Brain stem-spinal cord preparations from neonatal normotensive Wistar-Kyoto and spontaneously hypertensive rats were stained with a voltage-sensitive dye, and responses to electrical stimulation of the IML at the Th2 level were detected as changes in fluorescence intensity with an optical imaging apparatus (MiCAM-01). The results were as follows: 1) depolarizing responses to IML stimulation during low-Ca high-Mg superfusion were detected on the ventral surface of the medulla at the level of the CeVLM, as well as at the level of the RVLM, 2) depolarizing responses were also detected on cross sections at the level of the CeVLM, and they had a latency of 24.0 ± 5.5 (SD) ms, 3) antidromic action potentials in response to IML stimulation were demonstrated in the CeVLM neurons where optical images were detected, and 4) glutamate application to the CeVLM increased the frequency of excitatory postsynaptic potentials (EPSPs) and induced depolarization of the IML neurons. The optical imaging findings suggested a novel axonal and functional projection from neurons in the CeVLM to the IML. The increase in EPSPs of the IML neurons in response to glutamate application suggests that the CeVLM participates in the regulation of sympathetic nerve activity and blood pressure and may correspond to the caudal pressor area.

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Jansen, A. S. P., and A. D. Loewy. "Neurons lying in the white matter of the upper cervical spinal cord project to the intermediolateral cell column." Neuroscience 77, no. 3 (February 1997): 889–98. http://dx.doi.org/10.1016/s0306-4522(96)00506-4.

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Ding, XiaoHui, Jeffrey L. Ardell, Fang Hua, Ryan J. McAuley, Kristopher Sutherly, Jala J. Daniel, and Carole A. Williams. "Modulation of cardiac ischemia-sensitive afferent neuron signaling by preemptive C2 spinal cord stimulation: effect on substance P release from rat spinal cord." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 1 (January 2008): R93—R101. http://dx.doi.org/10.1152/ajpregu.00544.2007.

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The upper cervical spinal region functions as an intraspinal controller of thoracic spinal reflexes and contributes to neuronal regulation of the ischemic myocardium. Our objective was to determine whether stimulation of the C2 cervical spinal cord (SCS) of rats modified the input signal at the thoracic spinal cord when cardiac ischemia-sensitive (sympathetic) afferents were activated by transient occlusion of the left anterior descending coronary artery (CoAO). Changes in c-Fos expression were used as an index of neuronal activation within the spinal cord and brain stem. The pattern of substance P (SP) release, a putative nociceptive transmitter, was measured using antibody-coated microprobes. Two SCS protocols were used: reactive SCS, applied concurrently with intermittent CoAO and preemptive, sustained SCS starting 15 min before and continuing during the repeated intermittent CoAO. CoAO increased SP release from laminae I and II in the T4 spinal cord above resting levels. Intermittent SCS with CoAO resulted in greater levels of SP release from deeper laminae IV–VII in T4 than CoAO alone. In contrast, SP release from laminae I and II was inhibited when CoAO was applied during preemptive, sustained SCS. Preemptive SCS likewise reduced c-Fos expression in the T4 spinal cord (laminae I–V) and nucleus tractus solitarius but increased expression in the intermediolateral cell column of T4 compared with CoAO alone. These results suggest that preemptive SCS from the high cervical region modulates sensory afferent signaling from the ischemic myocardium.

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Llewellyn-Smith, Ida J., Jane B. Minson, Paul M. Pilowsky, and John P. Chalmers. "THERE ARE FEW CATECHOLAMINE- OR NEUROPEPTIDE Y-CONTAINING SYNAPSES IN THE INTERMEDIOLATERAL CELL COLUMN OF RAT THORACIC SPINAL CORD." Clinical and Experimental Pharmacology and Physiology 18, no. 2 (February 1991): 111–15. http://dx.doi.org/10.1111/j.1440-1681.1991.tb01418.x.

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Sundaram, Kalyana, Jaya Murugaian, and Hreday Sapru. "Cardiac responses to the microinjections of excitatory amino acids into the intermediolateral cell column of the rat spinal cord." Brain Research 482, no. 1 (March 1989): 12–22. http://dx.doi.org/10.1016/0006-8993(89)90537-4.

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Rosas-Arellano, M. Patricia, L. Pastor Solano-Flores, and John Ciriello. "c-Fos induction in spinal cord neurons after renal arterial or venous occlusion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (January 1, 1999): R120—R127. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r120.

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Experiments were done in the anesthetized rat to identify the dorsal root ganglia (DRG) and the spinal cord segments that contain neurons activated by either renal venous occlusion (RVO) or by renal arterial occlusion (RAO). Fos induction, detected immunohistochemically in DRG and the spinal cord neurons, was used as a marker for neuronal activation. RVO induced Fos immunoreactivity in neurons in the DRG of spinal segments T8-L2on the side ipsilateral to that of occlusion. The largest number of Fos-labeled neurons was found in the T11 DRG. In the spinal cord the largest number of Fos-labeled neurons was found in the ipsilateral dorsal horn of spinal segments T11-T12, predominantly in a cluster near the dorsomedial edge of laminae I-II. A few additional Fos-labeled neurons were observed in laminae IV and V. After RAO Fos-labeled neurons were found in the ipsilateral DRG of spinal segments similar to those observed to contain neurons after RVO. However, most of the Fos-labeled neurons were observed within the T12-L1DRG. In the spinal cord Fos-labeled neurons were scattered throughout lamina I-II of the ipsilateral dorsal horn of spinal segments T8-L2, although the largest number was observed at the T13 level. Additionally, a distinct cluster of Fos-labeled neurons was observed predominantly in the region of the ipsilateral intermediolateral cell column, although a few neurons were found scattered throughout the nucleus intercalatus, central autonomic areas, and laminae IV and V of the cord bilaterally. No Fos labeling was observed in the complementary contralateral DRG or dorsal horns after either RVO or RAO. In addition, renal nerve transection prevented Fos labeling in the ipsilateral DRG and dorsal horns after RVO or RAO. Taken together, these data suggest that functionally different renal afferent fibers activate DRG neurons that may have distinct projections in the spinal cord.

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Deuchars, S. A., R. E. Brooke, B. Frater, and J. Deuchars. "Properties of interneurones in the intermediolateral cell column of the rat spinal cord: role of the potassium channel subunit Kv3.1." Neuroscience 106, no. 2 (September 2001): 433–46. http://dx.doi.org/10.1016/s0306-4522(01)00277-9.

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Poulat, P., L. Marlier, N. Rajaofetra, and A. Privat. "5-Hydroxytryptamine, substance P and thyrotropin-releasing hormone synapses in the intermediolateral cell column of the rat thoracic spinal cord." Neuroscience Letters 136, no. 1 (February 1992): 19–22. http://dx.doi.org/10.1016/0304-3940(92)90637-m.

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Patlevič, Peter, Janka Vašková, Ladislav Vaško, and Darina Kluchová. "Postnatal Development of Spinal Cord and Liver Antioxidant Status in the Young of Retinol-Overdosed Female Rats." Zeitschrift für Naturforschung C 68, no. 3-4 (April 1, 2013): 155–63. http://dx.doi.org/10.1515/znc-2013-3-412.

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The metabolic form of vitamin A, retinol, has a pivotal role in the nervous system development and neuronal differentiation, both during embryogenesis through maternal-fetal support and in the early postnatal life. Retinoic acid was administered orally at a dose of 10 mg/kg body weight to pregnant female rats through days 8 - 10 of gestation. Spinal cord sections were processed for histochemical visualization one day after birth and on day 21, when weaning is expected. NADPH-diaphorase (NADPH-d)-positive neurons were found in the dorsal horn, around the central canal, and at the intermediolateral cell column on postnatal days 1 and 21 in both control and experimental groups. There were no NADPHd- positive structures in the ventral horn. The results suggest that prenatal administration of high doses of retinoic acid is not associated with postnatal morphological changes in NADPH-d-positive neurons in the rat spinal cord. Levels of antioxidants and related enzymes in retinoid storage organs were measured to estimate possible side effects. The activities of enzymes detoxifying superoxide radicals and peroxides were supressed after birth. A decrease in the level of reduced glutathione was observed on postnatal day 21, indicating an unbalanced redox environment.

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Krukoff, Teresa L. "Peptidergic inputs to sympathetic preganglionic neurons." Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1619–23. http://dx.doi.org/10.1139/y87-254.

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This paper presents data showing that the sympathetic autonomic areas of the cat thoracolumbar spinal cord contain nerve terminals and fibres with immunoreactivity for at least seven neuropeptides. The distribution in the intermediolateral cell column of the terminals and fibres which contain enkephalin-, neuropeptide Y-, neurotensin-, substance P-, and neurophysin II-like immunoreactivity (ENK, NPY, NT, SP, and NP2, respectively) suggests that these peptides are involved in more generalized functions of the autonomic nervous system. On the other hand, peaks in density of immunoreactivity at certain levels suggest that different levels of influence of sympathetic preganglionic neurons by the various peptides may occur along the length of the thoracolumbar cord. The distribution of terminals and fibres containing somatostatin- and oxytocin-like immunoreactivity (SS and OXY) suggests that these peptides may be part of specific pathways to particular sympathetic preganglionic neurons. The possible sources of the terminals and fibres containing ENK, NPY, NT, SS, and SP include the spinal cord and supraspinal areas, whereas the source of these structrues with OXY and NP2 is most likely supraspinal. The data suggest that coexistence of peptides and interactions between structures containing different neuropeptides occur in the spinal autonomic areas. It is speculated that neuropeptides have an important role to play in the regulation of the cardiovascular division of the autonomic nervous system.

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Iwasa, Masamitsu, Kazumi Kawabe, and Hreday N. Sapru. "Activation of melanocortin receptors in the intermediolateral cell column of the upper thoracic cord elicits tachycardia in the rat." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 6 (September 15, 2013): H885—H893. http://dx.doi.org/10.1152/ajpheart.00443.2013.

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Melanocortin receptors (MCRs) are present in the intermediolateral cell column of the spinal cord (IML). We tested the hypothesis that activation of MCRs in the IML elicits cardioacceleratory responses and the source of melanocortins in the IML may be the melanocortin-containing neurons in the hypothalamic arcuate nucleus (ARCN). Experiments were done in urethane-anesthetized, artificially ventilated adult male Wistar rats. Microinjections (50 nl) of α-melanocyte stimulating hormone (α-MSH) (0.4–2 mM) and adrenocorticotropic hormone (ACTH) (0.5–2 mM) into the right IML elicited increases in heart rate (HR). These tachycardic responses were blocked by microinjections of melanocortin receptor 4 (MC4R) antagonists [SHU9119 (0.25 mM) or agouti-related protein (AGRP, 0.1 mM)] into the right IML. Stimulation of right ARCN by microinjections (30 nl) of N-methyl-d-aspartic acid (NMDA, 10 mM) elicited increases in HR. Blockade of MC4Rs in the ipsilateral IML at T1–T3 using SHU9119 (0.25 mM) attenuated the tachycardic responses elicited by subsequent microinjections of NMDA into the ipsilateral ARCN. ARCN neurons retrogradely labeled by microinjections of Fluoro-Gold into the right IML showed immunoreactivity for proopiomelanocortin (POMC), α-MSH, and ACTH. Fibers immunoreactive for POMC, α-MSH, and ACTH were present in the IML at T1-T3. These results indicated that activation of MC4Rs in the right IML elicited tachycardia and one of the sources of melanocortins in the IML is the ARCN. Melanocortin levels are elevated in stress and ARCN neurons are activated during stress. Our results allude to the possibility that cardiac effects of stress may be mediated via melanocortin containing ARCN neurons that project to the IML.

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Cormier, Christen M., Karim Mukhida, Greg Walker, and Daniel R. Marsh. "Development of Autonomic Dysreflexia after Spinal Cord Injury Is Associated with a Lack of Serotonergic Axons in the Intermediolateral Cell Column." Journal of Neurotrauma 27, no. 10 (October 2010): 1805–18. http://dx.doi.org/10.1089/neu.2010.1441.

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Sundaram, Kalayana, Jaya Murugaian, Abbott Krieger, and Hreday Sapru. "Microinjections of cholinergic agonists into the intermediolateral cell column of the spinal cord at T1-T3 increase heart rate and contractility." Brain Research 503, no. 1 (November 1989): 22–31. http://dx.doi.org/10.1016/0006-8993(89)91698-3.

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Appel, NM, and RP Elde. "The intermediolateral cell column of the thoracic spinal cord is comprised of target-specific subnuclei: evidence from retrograde transport studies and immunohistochemistry." Journal of Neuroscience 8, no. 5 (May 1, 1988): 1767–75. http://dx.doi.org/10.1523/jneurosci.08-05-01767.1988.

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Krukoff, T. L., M. C. Fernandez, and D. H. Vincent. "Effects of neonatal sympathectomy with 6-hydroxydopamine or guanethidine on survival of neurons in the intermediolateral cell column of rat spinal cord." Journal of the Autonomic Nervous System 31, no. 2 (November 1990): 119–26. http://dx.doi.org/10.1016/0165-1838(90)90068-t.

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Chao, Jie, Juan Gao, Karma-Jaya K. Parbhu, and Lie Gao. "Angiotensin type 2 receptors in the intermediolateral cell column of the spinal cord: Negative regulation of sympathetic nerve activity and blood pressure." International Journal of Cardiology 168, no. 4 (October 2013): 4046–55. http://dx.doi.org/10.1016/j.ijcard.2013.06.051.

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Hu, Lian, Da-Nian Zhu, Zhang Yu, John Q. Wang, Zhong-Jie Sun, and Tai Yao. "Expression of angiotensin II type 1 (AT1) receptor in the rostral ventrolateral medulla in rats." Journal of Applied Physiology 92, no. 5 (May 1, 2002): 2153–61. http://dx.doi.org/10.1152/japplphysiol.00261.2001.

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In the present study, the changes of amino acids release in the spinal cord after the application of angiotensin II (ANG II) in the rostral ventrolateral medulla (RVLM) and the distribution of ANG receptors on neurons of the RVLM were investigated. A microdialysis experiment showed that microinjection of angiotensin II into the RVLM significantly ( P < 0.01) increased the release of aspartate and glutamate in the intermediolateral column of the spinal cord. Immunofluorescence technique combined with confocal microscopy demonstrated that most of the glutamatergic and GABAergic neurons in the RVLM of both Wistar and spontaneously hypertensive rats (SHR) were double labeled with ANG type 1 (AT1) receptor. Immunocytochemical studies demonstrated that the mean optic density of AT1 receptor of the cell surface as well as the whole cell was higher ( P < 0.05) in SHR than that in Wistar rats, indicating that the higher expression of AT1 receptors in the RVLM may contribute to the higher responsiveness of SHR to ANG II stimulation. Immunogold staining and electronmicroscopic study demonstrated that AT1 receptor in the RVLM was distributed on the rough endoplasmic reticulum, cell membrane, and nerve processes. The results suggest that effects evoked by ANG II in the RVLM are closely related to glutamatergic and GABAergic pathways. These results indirectly support the hypothesis that ANG II in the RVLM may activate vasomotor sympathetic glutamatergic neurons, leading to an increase in sympathetic nerve activity and arterial blood pressure.

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Lai, Chih-Chia, Su Ying Wu, Chiung-Tong Chen, and Nae J. Dun. "Nociceptin inhibits rat sympathetic preganglionic neurons in situ and in vitro." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 3 (March 1, 2000): R592—R597. http://dx.doi.org/10.1152/ajpregu.2000.278.3.r592.

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In vitro and in situ experiments were conducted to evaluate the hypothesis that the nonclassical opioid peptide nociceptin acting on sympathetic preganglionic neurons (SPNs) inhibits spinal sympathetic outflow. First, whole cell patch recordings were made from antidromically identified SPNs from immature (12–16 day old) rat spinal cord slices. Nociceptin (0.1, 0.3, and 1 μM) concentration dependently suppressed the excitatory postsynaptic potentials (EPSPs) evoked by focal stimulation and hyperpolarized a population of SPNs; these effects were naloxone insensitive.l-Glutamate-induced depolarizations were not significantly changed by nociceptin. Results from this series of experiments indicate that nociceptin inhibits the activity of SPNs by either a presynaptic or postsynaptic site of action, whereby the peptide reduces, respectively, the amplitude of EPSPs or the excitability of SPNs. Second, intrathecal injection of nociceptin (3, 10, and 30 nmol) to urethan-anesthetized rats dose dependently reduced the mean arterial pressure and heart rate; these effects were not prevented by prior intravenous administration of naloxone (1 mg/kg). Physiological saline given intrathecally was without appreciable effects. These results, together with earlier observations of the detection of nociceptin-immunoreactive nerve fibers and nociceptin receptor immunoreactivity in the rat intermediolateral cell column, raise the possibility that the opioid peptide, which may be released endogenously, reduces spinal sympathetic outflow by depressing the activity of SPNs.

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Schober, Andreas, Nicole Wolf, Nitza Kahane, Chaya Kalcheim, Kerstin Krieglstein, and K. Unsicker. "Expression of neurotrophin receptors trkB and trkC and their ligands in rat adrenal gland and the intermediolateral column of the spinal cord." Cell and Tissue Research 296, no. 2 (April 21, 1999): 271–79. http://dx.doi.org/10.1007/s004410051288.

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Huangfu, D. H., N. Koshiya, and P. G. Guyenet. "A5 noradrenergic unit activity and sympathetic nerve discharge in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (August 1, 1991): R393—R402. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r393.

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Unit recording experiments were designed to determine whether A5 noradrenergic neurons contribute to the generation of the splanchnic sympathetic nerve discharge (SSND) of halothane-anesthetized rats. Neurons (presumed A5 cells) were selected on the following bases: location in the ventrolateral tegmentum rostrolateral to facial nucleus (FN), antidromic (AD) activation from thoracic spinal cord, and complete inhibition by clonidine (10-15 micrograms/kg iv). These cells (n = 59) had low rates of spontaneous firing (1.4 +/- 0.2 spikes/s) and slow conduction velocities (2.6 +/- 0.2 m/s). The AD activation of seven of eight neurons was abolished within 1 h after intraspinal microinjection of 6-hydroxydopamine (4 micrograms), but the drug failed to affect the AD responses of eight sympathoexcitatory cells located caudal to the FN (control cells). The terminal fields of 16 A5 area neurons were found in the intermediolateral cell column of the spinal cord. Most neurons (63%, 37/59) were inhibited by raising arterial pressure and by train stimulation of the aortic depressor nerve (ADN, 47%, 9/20). A few cells responded to ADN stimulation but not to arterial pressure elevation or vice versa. The discharge of the cells was correlated to the SSND and preceded a peak of SSND by 69 +/- 6 ms (12/29 in intact and 3/9 in debuffered rats). We conclude that 40% of A5 cells may have a visceral vasomotor sympathoexcitatory function.

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Bains, J. S., and A. V. Ferguson. "Paraventricular nucleus neurons projecting to the spinal cord receive excitatory input from the subfornical organ." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (March 1, 1995): R625—R633. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r625.

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The present study utilized electrophysiological techniques to determine the effects of subfornical organ (SFO) stimulation on the activity of neurons in the paraventricular nucleus (PVN) projecting to the spinal cord. Single-unit recordings were obtained from 79 PVN neurons antidromically identified as projecting to the intermediolateral cell column (IML). Antidromically evoked action potentials showed a mean latency of 94.6 +/- 5.3 ms and a mean threshold for activation of 1.58 +/- 0.11 mA. Electrical stimulation of SFO (100 microA-1.5 mA, 0.1 ms) resulted in excitatory responses in 18 of the 27 neurons tested (67%). Peristimulus histogram analysis of such effects demonstrated a duration of < 50 ms in 14 of the 18 cells so influenced (78%), whereas the remaining 4 cells (22%) showed excitatory responses with a longer duration. Systemic administration of the nonpeptidergic angiotensin II (ANG) type 1 (AT1) receptor antagonist losartan (3 mg/kg) blocked the long-duration excitatory responses in 100% (3 of 3) of the cells tested but was without effect on the short-duration excitations (0 of 5). Twenty-two identified PVN neurons were also tested for their responses to systemic ANG (20-500 ng), which had no observable effect on the activity of any of these cells. These data demonstrate that neurons in SFO provide excitatory input to PVN cells that project to the IML. One of the neurotransmitters responsible for communication in this pathway is ANG.

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Dale, Erica A., Jasmine Kipke, Yukiko Kubo, Michael D. Sunshine, Peter A. Castro, Jeffrey L. Ardell, and Aman Mahajan. "Spinal cord neural network interactions: implications for sympathetic control of the porcine heart." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 4 (April 1, 2020): H830—H839. http://dx.doi.org/10.1152/ajpheart.00635.2019.

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Inherent and acquired factors determine the integrated autonomic response to cardiovascular stressors. Excessive sympathoexcitation to ischemic stress is a major contributor to the potential for sudden cardiac death. To define fundamental aspects of cardiac-related autonomic neural network interactions within the thoracic cord, specifically as related to modulating sympathetic preganglionic (SPN) neural activity. Adult, anesthetized Yorkshire pigs ( n = 10) were implanted with penetrating high-density microarrays (64 electrodes) at the T2 level of the thoracic spinal cord to record extracellular potentials concurrently from left-sided dorsal horn (DH) and SPN neurons. Electrical stimulation of the T2 paravertebral chain allowed for antidromic identification of SPNs located in the intermediolateral cell column (57 of total 1,760 recorded neurons). Cardiac stressors included epicardial touch, occlusion of great vessels to transiently alter preload/afterload, and transient occlusion of the left anterior descending coronary artery (LAD). Spatial/temporal assessment of network interactions was characterized by cross-correlation analysis. While some DH neurons responded solely to changes in preload/afterload (8.5 ± 1.9%) or ischemic stress (10.5 ± 3.9%), the majority of cardiovascular-related DH neurons were multimodal (30.2 ± 4.7%) with ischemia sensitivity being one of the modalities (26.1 ± 4.7%). The sympathoexcitation associated with transient LAD occlusion was associated with increased correlations from baseline within DH neurons (2.43 ± 0.61 to 7.30 ± 1.84%, P = 0.04) and between SPN to DH neurons (1.32 ± 0.78 to 7.24 ± 1.84%, P = 0.02). DH to SPN network correlations were reduced during great vessel occlusion. In conclusion, increased intrasegmental network coherence within the thoracic spinal cord contributes to myocardial ischemia-induced sympathoexcitation. NEW & NOTEWORTHY In an in vivo pig model, we demonstrate using novel high-resolution neural electrode arrays that increased intrasegmental network coherence within the thoracic spinal cord contributes to myocardial ischemia-induced sympathoexcitation.

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Sundaram, K., J. Murugaian, and H. Sapru. "Microinjections of norepinephrine into the intermediolateral cell column of the spinal cord exert excitatory as well as inhibitory effects on the cardiac function." Brain Research 544, no. 2 (March 1991): 227–34. http://dx.doi.org/10.1016/0006-8993(91)90058-4.

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Antunes, Vagner R., G. Cristina Brailoiu, Ernest H. Kwok, Phouangmala Scruggs, and Nae J. Dun. "Orexins/hypocretins excite rat sympathetic preganglionic neurons in vivo and in vitro." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 6 (December 1, 2001): R1801—R1807. http://dx.doi.org/10.1152/ajpregu.2001.281.6.r1801.

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The two recently isolated hypothalamic peptides orexin A and orexin B, also known as hypocretin 1 and 2, are reported to be important signaling molecules in feeding and sleep/wakefulness. Orexin-containing neurons in the lateral hypothalamus project to numerous areas of the rat brain and spinal cord including the intermediolateral cell column (IML) of the thoracolumbar spinal cord. An in vivo and in vitro study was undertaken to evaluate the hypothesis that orexins, acting on sympathetic preganglionic neurons (SPNs) in the rat spinal cord, increase sympathetic outflow. First, orexin A (0.3, 1, and 10 nmol) by intrathecal injection increased mean arterial pressure (MAP) and heart rate (HR) by an average of 5, 18, and 30 mmHg and 10, 42, and 85 beats/min in urethane-anesthetized rats. Intrathecal injection of saline had no significant effects. Orexin B (3 nmol) by intrathecal administration increased MAP and HR by an average of 11 mmHg and 40 beats/min. The pressor effects of orexin A were attenuated by prior intrathecal injection of orexin A antibodies (1:500 dilution) but not by normal serum albumin. Intravenous administration of the α1-adrenergic receptor antagonist prazosin (0.5 mg/kg) or the β-adrenergic receptor antagonist propranolol (0.5 mg/kg) markedly diminished, respectively, the orexin A-induced increase of MAP and HR. Second, whole cell patch recordings were made from antidromically identified SPNs of spinal cord slices from 12- to 16-day-old rats. Superfusion of orexin A or orexin B (100 or 300 nM) excited 12 of 17 SPNs, as evidenced by a membrane depolarization and/or increase of neuronal discharges. Orexin A- or B-induced depolarizations persisted in TTX (0.5 μM)-containing Krebs solution, indicating that the peptide acted directly on SPNs. Results from our in vivo and in vitro studies together with the previous observation of the presence of orexin A-immunoreactive fibers in the IML suggest that orexins, when released within the IML, augment sympathetic outflow by acting directly on SPNs.

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Minoura, Yoshino, Hiroshi Onimaru, Kamon Iigaya, Ikuo Homma, and Youichi Kobayashi. "Electrophysiological responses of sympathetic preganglionic neurons to ANG II and aldosterone." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 3 (September 2009): R699—R706. http://dx.doi.org/10.1152/ajpregu.00041.2009.

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The intermediolateral cell column (IML) of the spinal cord is an important area where sympathetic impulses propagate to peripheral sympathetic organs. ANG II and aldosterone are important components of the renin-angiotensin-aldosterone system (RAAS), which activate the sympathetic nervous system. Each is partly synthesized in the brain and plays a paracrine role in the regulation of blood pressure independently of RAAS in the periphery. Our purpose in the present study was to clarify the contributions of sympathetic preganglionic neurons in the IML (IML neurons) and the effects of ANG II and aldosterone on the sympathetic nervous system. To examine responses to ANG II and aldosterone, we intracellularly recorded 104 IML neurons using a whole cell patch-clamp technique in spinal cord slice preparations. IML neurons were classified into two types: silent and firing. Both neuron types were significantly depolarized by ANG II, and candesartan inhibited this depolarization. After pretreatment with TTX, firing neurons (but not silent neurons) were significantly depolarized by ANG II. Aldosterone significantly increased the number of excitatory postsynaptic potentials (EPSPs) in both neuron types, but this response disappeared after pretreatment with TTX. ANG II and aldosterone had no synergistic effects on the IML neurons. The silent neurons had large cell soma, and many more dendrites than the firing neurons. These results suggest that ANG II acts presynaptically and postsynaptically in IML neurons, while aldosterone acts mainly presynaptically. Thus, the physiological effects of these substances are likely to be transmitted via specific membrane receptors of IML and/or presynaptic neurons.

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Madden, Christopher J., and Shaun F. Morrison. "Endogenous activation of spinal 5-hydroxytryptamine (5-HT) receptors contributes to the thermoregulatory activation of brown adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 3 (March 2010): R776—R783. http://dx.doi.org/10.1152/ajpregu.00614.2009.

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Neurons in the rostral raphe pallidus (RPa) play an essential role in the regulation of sympathetically mediated metabolism and thermogenesis in brown adipose tissue (BAT). The presence of serotonergic neurons in the RPa that are retrogradely labeled following pseudorabies virus injections into BAT suggests that these neurons play a role in the regulation of BAT. In urethane/chloralose-anesthetized rats, whole body cooling decreased skin (−5.7 ± 2.3°C) and core (−1.3 ± 0.2°C) temperatures and resulted in an increase in BAT sympathetic nerve activity (SNA; +1,026 ± 344% of baseline activity). Serial microinjections of the 5-hydroxytryptamine (5-HT) receptor antagonist, methysergide (1.2 nmol/site), but not saline vehicle, into the intermediolateral cell column (IML) in spinal segments T2–T5 markedly attenuated the cooling-evoked increase in BAT SNA (remaining area under the curve, AUC: 36 ± 9% of naive cooling response). Microinjections of the 5-HT1A receptor antagonist, WAY-100635 (1.2 nmol/site), or the 5-HT7 receptor antagonist, SB-269970 (1.2 nmol/site), into the T2–T5 IML also attenuated the cold-evoked increase in BAT SNA (remaining activity at peak inhibition: 47 ± 8% and 39 ± 12% of the initial cold-evoked response, respectively). The increases in BAT SNA evoked by microinjection of N-methyl-d-aspartate (NMDA) (12 pmol) or bicuculline (30 pmol) into the RPa were attenuated following microinjections of methysergide, but not saline vehicle, into the T2–T5 IML (NMDA remaining AUC, 64 ± 13% of naive response; bicuculline remaining AUC, 52 ± 5% of naive response). These results are consistent with our earlier demonstration of a potentiating effect of 5-HT within the IML on BAT SNA and indicate that activation of 5-HT1A and 5-HT7 receptors in the spinal cord contributes to increases in BAT SNA and thermogenesis.

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Hierlihy, L. E., J. L. Wallace, and A. V. Ferguson. "Autonomic pathways in development of neural stimulation-induced gastric mucosal damage." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 2 (February 1, 1994): G179—G185. http://dx.doi.org/10.1152/ajpgi.1994.266.2.g179.

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Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P < 0.05). In contrast animals that underwent cervical cord transection exhibited gastric damage after both vagal and PVN stimulation that was not significantly different compared with animals with an intact cord undergoing similar stimulation (P > 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.

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Cui, Dapeng, Kimberly J. Dougherty, David W. Machacek, Michael Sawchuk, Shawn Hochman, and Deborah J. Baro. "Divergence between motoneurons: gene expression profiling provides a molecular characterization of functionally discrete somatic and autonomic motoneurons." Physiological Genomics 24, no. 3 (March 2006): 276–89. http://dx.doi.org/10.1152/physiolgenomics.00109.2005.

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Studies in the developing spinal cord suggest that different motoneuron (MN) cell types express very different genetic programs, but the degree to which adult programs differ is unknown. To compare genetic programs between adult MN columnar cell types, we used laser capture microdissection (LCM) and Affymetrix microarrays to create expression profiles for three columnar cell types: lateral and medial MNs from lumbar segments and sympathetic preganglionic motoneurons located in the thoracic intermediolateral nucleus. A comparison of the three expression profiles indicated that ∼7% (813/11,552) of the genes showed significant differences in their expression levels. The largest differences were observed between sympathetic preganglionic MNs and the lateral motor column, with 6% (706/11,552) of the genes being differentially expressed. Significant differences in expression were observed for 1.8% (207/11,552) of the genes when comparing sympathetic preganglionic MNs with the medial motor column. Lateral and medial MNs showed the least divergence, with 1.3% (150/11,552) of the genes being differentially expressed. These data indicate that the amount of divergence in expression profiles between identified columnar MNs does not strictly correlate with divergence of function as defined by innervation patterns (somatic/muscle vs. autonomic/viscera). Classification of the differentially expressed genes with regard to function showed that they underpin all fundamental cell systems and processes, although most differentially expressed genes encode proteins involved in signal transduction. Mining the expression profiles to examine transcription factors essential for MN development suggested that many of the same transcription factors participate in combinatorial codes in embryonic and adult neurons, but patterns of expression change significantly.

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Zimmerman, Amanda, and Shawn Hochman. "Heterogeneity of Membrane Properties in Sympathetic Preganglionic Neurons of Neonatal Mice: Evidence of Four Subpopulations in the Intermediolateral Nucleus." Journal of Neurophysiology 103, no. 1 (January 2010): 490–98. http://dx.doi.org/10.1152/jn.00622.2009.

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Spinal cord sympathetic preganglionic neurons (SPNs) integrate activity from descending and sensory systems to determine the final central output of the sympathetic nervous system. The intermediolateral column (IML) has the highest number and density of SPNs and, within this region, SPN somas are found in distinct clusters within thoracic and upper lumbar spinal segments. Whereas SPNs exhibit a rostrocaudal gradient of end-target projections, individual clusters contain SPNs with diverse functional roles. Here we explored diversity in the electrophysiological properties observed in Hb9-eGFP–identified SPNs in the IML of neonatal mice. Overall, mouse SPN intrinsic membrane properties were comparable with those seen in other species. A wide range of values was obtained for all measured properties (up to a 10-fold difference), suggesting that IML neurons are highly differentiated. Using linear regression we found strong correlations between many cellular properties, including input resistance, rheobase, time constant, action potential shape, and degree of spike accommodation. The best predictor of cell function was rheobase, which correlated well with firing frequency–injected current ( f– I) slopes as well as other passive and active membrane properties. The range in rheobase suggests that IML neurons have a recruitment order with stronger synaptic drives required for maximal recruitment. Using cluster analysis, we identified at least four subpopulations of SPNs, including one with a long time constant, low rheobase, and high f– I gain. We thus propose that the IML contains populations of neurons that are differentiable by their membrane properties and hypothesize they represent diverse functional classes.

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Swiatkowski, Kenneth, Lynn M. Dellamano, John Vissing, Kenneth J. Rybicki, Gerald P. Kozlowski, and Gary A. Iwamoto. "Differential effects from parapyramidal region and rostral ventrolateral medulla mediated by substance P." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 4 (October 1, 1999): R1120—R1129. http://dx.doi.org/10.1152/ajpregu.1999.277.4.r1120.

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Rostral ventrolateral medulla (rVLM) and parapyramidal region (PPr) serve as important medullary control sites for sympathoexcitation. rVLM and PPr have direct projections to the intermediolateral cell column (IML) that are thought to be important in maintaining mean arterial blood pressure (MAP). Substance P (SP) is found in PPr neurons and in and near the subretrofacial area of the rVLM. At least some of these cells project to the IML. We investigated the involvement of SP at the IML in mediating rVLM- and PPr-evoked pressor responses in the chloralose-anesthetized cat. Pressor responses to electrical and chemical PPr and rVLM stimulation were altered after intrathecal injection, at the level of the T1-T3 spinal cord, of either SP antagonist [d-Pro2,d-Phe7,d-Trp9]-SP, SP antagonist CP 96,345, or SP antiserum. Although MAP and heart rate responses to PPr stimulation were attenuated by intrathecal SP antagonists or antiserum, MAP responses to rVLM stimulation were augmented. Previous studies have revealed differences in transmitters associated with these two areas, even though the general response of both areas is sympathoexcitatory. The present study implies that the identical substance may increase or decrease the MAP response depending on the pathway activated.

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Wu, S. Y., and N. J. Dun. "Potentiation of NMDA Currents by Pituitary Adenylate Cyclase Activating Polypeptide in Neonatal Rat Sympathetic Preganglionic Neurons." Journal of Neurophysiology 78, no. 2 (August 1, 1997): 1175–79. http://dx.doi.org/10.1152/jn.1997.78.2.1175.

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Wu, S. Y. and N. J. Dun. Potentiation of NMDA currents by pituitary adenylate cyclase activating polypeptide in neonatal rat sympathetic preganglionic neurons. J. Neurophysiol. 78: 1175–1179, 1997. Whole cell patch-clamp recordings were made from sympathetic preganglionic neurons (SPNs) in the intermediolateral cell column of thoracolumbar spinal cord slices of 12- to 16-day-old rats, and the effects of pituitary adenylate cyclase activating polypeptide (PACAP)-38 on N-methyl-d-aspartate (NMDA)- and kainate (KA)-induced inward currents were examined. PACAP, in concentrations (10–30 nM) that caused no significant change of holding currents, reversibly increased NMDA-induced currents but not KA-induced currents. At higher concentrations (>30 nM), the peptide produced a sustained inward current. The potentiating effect of PACAP was nullified by prior incubation of the slices with the adenylate cyclase inhibitor MDL-12,330A (25 μM). Further, superfusing the slices with the membrane-permeable cyclic AMP analogue N6,2′-0-dibutyryladenosine 3′:5′-cyclic monophosphate (100–300 μM) in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (700 μM) increased the NMDA currents. This result suggests that PACAP selectively increases NMDA-receptor-mediated responses in the rat SPNs, probably via a cyclic-AMP-dependent mechanism, providing evidence that the peptide may be involved in synaptic plasticity.

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Uno, Tadashi, and Masaaki Shibata. "Role of inferior olive and thoracic IML neurons in nonshivering thermogenesis in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (February 1, 2001): R536—R546. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r536.

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Removal of the midbrain tonic inhibitory mechanism on nonshivering thermogenesis (NST) results in increased temperatures of the interscapular brown adipose tissue (IBAT) and rectum (TIBAT and Trec, respectively) via an enhanced central sympathetic output. Because it is unlikely that neurons (primary) of the midbrain inhibitory mechanism tonically inhibit the IBAT monosynaptically, there must be secondary or tertiary neurons posterior to the midbrain. Such neurons, therefore, may increase their activity during enhanced NST after removal of the midbrain tonic inhibition. The aim of the present experiments was to localize these secondary or tertiary neurons and establish descending neuronal pathway(s) that may project to the major NST effector IBAT. TIBAT and Trec increases induced by removal of the tonic inhibition by midbrain procaine microinjections were accompanied with appearance of c-Fos-positive neurons in the inferior olive (IO) and the intermediolateral (IML) cell column of the thoracic spinal cord. Electrical stimulation of and l-glutamate microinjections into the IO increased TIBAT and Trec. Midbrain procaine-induced TIBAT and Trec increases were blocked by electrolytic IO lesions. These results suggest that central thermal signals produced from the lower midbrain are transmitted to IBAT through the IO and IML and that the IO has a role in the central sympathetic functions.

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Cham, Joo Lee, Rudi Klein, Neil C. Owens, Michael Mathai, Michael McKinley, and Emilio Badoer. "Activation of spinally projecting and nitrergic neurons in the PVN following heat exposure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 1 (July 2006): R91—R101. http://dx.doi.org/10.1152/ajpregu.00675.2005.

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The present study investigated the effect of acute thermal stimulation in conscious rats on the production of Fos, a marker of increased neuronal activity, in spinally projecting and nitrergic neurons in the hypothalamic paraventricular nucleus (PVN). The PVN contains a high concentration of nitrergic neurons, as well as neurons that project to the intermediolateral cell column (IML) of the spinal cord that can directly influence sympathetic nerve activity (SNA). During thermal stimulation, the PVN is activated, but it is unknown whether spinally projecting PVN neurons and the nitrergic neurons are involved. Compared with controls, rats exposed to an environmental temperature of 39°C for 1 h had a 10-fold increase in the number of cells producing Fos in the PVN (133 ± 23 vs. 1,336 ± 43, respectively, P < 0.0001). Of the spinally projecting neurons in the PVN of heated rats (98 ± 10), over 20% expressed Fos. Additionally, of the nitrergic neurons (NADPH-diaphorase positive) located in the parvocellular PVN (723 ± 17), ∼40% also expressed Fos ( P < 0.0001 compared with controls). Finally, there was a significant increase in the number of spinally projecting neurons in the PVN that were nitrergic and expressed Fos after heat exposure (12%) compared with controls (0.1%) ( P < 0.0001). These results suggest that spinally projecting and nitrergic neurons in the PVN may contribute to the central pathways activated by thermal stimulation.

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Lan, C. T., W. C. Wu, E. A. Ling, and C. Y. Chai. "Evidence of a direct projection from the cardiovascular-reactive dorsal medulla to the intermediolateral cell column of the spinal cord in cats as revealed by light and electron microscopy." Neuroscience 77, no. 2 (February 1997): 521–33. http://dx.doi.org/10.1016/s0306-4522(96)00502-7.

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Bajayo, Alon, Arik Bar, Adam Denes, Marilyn Bachar, Vardit Kram, Malka Attar-Namdar, Alberta Zallone, Krisztina J. Kovács, Raz Yirmiya, and Itai Bab. "Skeletal parasympathetic innervation communicates central IL-1 signals regulating bone mass accrual." Proceedings of the National Academy of Sciences 109, no. 38 (September 4, 2012): 15455–60. http://dx.doi.org/10.1073/pnas.1206061109.

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Bone mass accrual is a major determinant of skeletal mass, governed by bone remodeling, which consists of bone resorption by osteoclasts and bone formation by osteoblasts. Bone mass accrual is inhibited by sympathetic signaling centrally regulated through activation of receptors for serotonin, leptin, and ACh. However, skeletal activity of the parasympathetic nervous system (PSNS) has not been reported at the bone level. Here we report skeletal immune-positive fibers for the PSNS marker vesicular ACh transporter (VAChT). Pseudorabies virus inoculated into the distal femoral metaphysis is identifiable in the sacral intermediolateral cell column and central autonomic nucleus, demonstrating PSNS femoral innervation originating in the spinal cord. The PSNS neurotransmitter ACh targets nicotinic (nAChRs), but not muscarinic receptors in bone cells, affecting mainly osteoclasts. nAChR agonists up-regulate osteoclast apoptosis and restrain bone resorption. Mice deficient of the α2nAChR subunit have increased bone resorption and low bone mass. Silencing of the IL-1 receptor signaling in the central nervous system by brain-specific overexpression of the human IL-1 receptor antagonist (hIL1raAst+/+ mice) leads to very low skeletal VAChT expression and ACh levels. These mice also exhibit increased bone resorption and low bone mass. In WT but not in hIL1raAst+/+ mice, the cholinergic ACh esterase inhibitor pyridostigmine increases ACh levels and bone mass apparently by inhibiting bone resorption. Taken together, these results identify a previously unexplored key central IL-1–parasympathetic–bone axis that antagonizes the skeletal sympathetic tone, thus potently favoring bone mass accrual.

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Chen, Qing-Hui, and Glenn M. Toney. "In Vivo Discharge Properties of Hypothalamic Paraventricular Nucleus Neurons With Axonal Projections to the Rostral Ventrolateral Medulla." Journal of Neurophysiology 103, no. 1 (January 2010): 4–15. http://dx.doi.org/10.1152/jn.00094.2009.

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The hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) are key components of a neural network that generates and regulates sympathetic nerve activity (SNA). Although each region has been extensively studied, little is presently known about the in vivo discharge properties of individual PVN neurons that directly innervate the RVLM. Here extracellular recording was performed in anesthetized rats, and antidromic stimulation was used to identify single PVN neurons with axonal projections to the RVLM ( n = 94). Neurons were divided into two groups that had either unbranched axons terminating in the RVLM (i.e., PVN-RVLM neurons, n = 65) or collateralized axons targeting both the RVLM and spinal cord [i.e., PVN-RVLM/intermediolateral cell column (IML) neurons, n = 29]. Many PVN-RVLM (32/65, 49%) and PVN-RVLM/IML (17/29, 59%) neurons were spontaneously active. The average firing frequency was not different across groups. Spike-triggered averaging revealed that spontaneous discharge of most neurons was temporally correlated with renal SNA (PVN-RVLM: 12/21, 57%; PVN-RVLM/IML: 6/9, 67%). Time histograms triggered by the electrocardiogram (ECG) R-wave indicated that discharge of most cells was also cardiac rhythmic (PVN-RVLM: 25/32, 78%; PVN-RVLM/IML: 10/17, 59%). Raising and lowering arterial blood pressure to increase and decrease arterial baroreceptor input caused a corresponding decrease and increase in firing frequency among cells of both groups (PVN-RVLM: 9/13, 69%; PVN-RVLM/IML: 4/4, 100%). These results indicate that PVN-RVLM and PVN-RVLM/IML neurons are both capable of contributing to basal sympathetic activity and its baroreflex modulation.

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Deuchars, Susan A., K. Michael Spyer, and Michael P. Gilbey. "Stimulation Within the Rostral Ventrolateral Medulla Can Evoke Monosynaptic GABAergic IPSPs in Sympathetic Preganglionic Neurons In Vitro." Journal of Neurophysiology 77, no. 1 (January 1, 1997): 229–35. http://dx.doi.org/10.1152/jn.1997.77.1.229.

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Deuchars, Susan A., K. Michael Spyer, and Michael P. Gilbey. Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro. J. Neurophysiol. 77: 229–235, 1997. The inhibitory responses of identified sympathetic preganglionic neurons (SPNs) to stimulation within the rostral ventrolateral medulla (RVLM) were studied to determine their nature and pharmacology. Whole cell patch-clamp recordings were made from 36 SPNs in the upper thoracic segments of the spinal cord in a neonatal rat brain stem-spinal cord preparation. Neurons were identified as SPNs on the basis of their antidromic activation after stimulation of the ipsilateral segmental ventral root and their morphology and location in the intermediolateral cell column and intercalated nucleus. In all SPNs, electrical stimulation of the RVLM evoked fast excitatory postsynaptic potentials (EPSPs) that were mediated by non- N-methyl-d-aspartate (NMDA) and NMDA receptors. These excitatory responses were the most prominent response in control artificial cerebrospinal fluid and have been studied previously. In 22 of the SPNs, RVLM stimulation also elicited fast inhibitory postsynaptic potentials (IPSPs), which increased in amplitude as the membrane was depolarized. Five of these neurons were not studied further as they responded occasionally with IPSPs that had highly variable onset latencies indicating the involvement of a polysynaptic pathway. In the remaining SPNs ( n = 17), the evoked IPSPs persisted in the presence of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3,-dione and d,l-2-amino-5-phosphonopentanoic acid. In eight of these SPNs, it was necessary to block the EPSPs to reveal the IPSPs. In the 7 SPNs tested, the onset latencies of the IPSPs were not significantly different from the onset latencies of the fast EPSPs. The low sweep-to-sweep fluctuations in onset latency of individual IPSPs (absolute average deviation: 0.4 ms) indicated that the IPSPs were elicited by activation of a monosynaptic pathway. The amplitudes of the IPSPs decreased in amplitude as the membrane was hyperpolarized and reversed in polarity at −70.3 ± 1.7 mV (mean ± SD), which was close to the equilibrium potential for chloride ions. In addition, in seven SPNs, bath applications of 5 μM bicuculline, a γ-aminobuturic acid-A (GABAA) antagonist, abolished or reduced the evoked IPSPs. Five SPNs also were studied that displayed ongoing IPSPs. The amplitudes of these IPSPs increased with membrane depolarization and were blocked by bath applications of 5 μM bicuculline, suggesting that they also were mediated by activation of GABAA receptors. These results demonstrate the existence of a bulbospinal GABAergic pathway impinging directly onto SPNs. This pathway may be tonically active in the neonatal rat brain stem-spinal cord preparation.

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Fields, H. L., A. Malick, and R. Burstein. "Dorsal horn projection targets of ON and OFF cells in the rostral ventromedial medulla." Journal of Neurophysiology 74, no. 4 (October 1, 1995): 1742–59. http://dx.doi.org/10.1152/jn.1995.74.4.1742.

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1. The rostral ventromedial medulla (RVM) participates in the modulation of nociceptive transmission by spinal cord neurons. Previous anatomic studies have demonstrated that RVM neurons project to laminae I, II, and V of the dorsal horn; laminae VII and VIII of the intermediate and ventral horns; the intermediolateral column; and lamina X. The RVM contains at least three physiologically defined classes of neurons, two of which, the ON and the OFF cells, have been implicated in nociceptive modulation. Because these cells classes are intermingled in the RVM, it has not been possible to determine the spinal laminar projection targets of ON and OFF cells by anatomic methods. Therefore in the current study we employed antidromic microstimulation methods to determine the laminar projections of two of the three classes of RVM neurons, the ON and the OFF cells. 2. In lightly anesthetized (with methohexital sodium) rats, single-unit extracellular recordings were made from 48 RVM neurons that were physiologically characterized as ON (30) or OFF (18) cells. The recording locations of 45 of these neurons were recovered. Thirty-seven were found in the nucleus raphe magnus and eight were located near its dorsal and lateral borders. 3. Thirty-two physiologically identified RVM neurons (18 ON and 14 OFF cells) were antidromically activated from the cervical spinal cord using a monopolar stimulating electrode. The stimulating electrode was moved systematically in the white matter until antidromic activation could be produced with currents of < or = 20 microA (6.1 +/- 0.7 microA, mean +/- SE). The points from which minimum currents were required to antidromically activate the neurons were located mainly in the ipsilateral dorsolateral funiculus (DLF) (27 of 32). In a few cases, lowest antidromic threshold currents were found near the border between the DLF and ventrolateral funiculus (VLF) or, rarely, in the VLF itself. In these cases, the cell recordings were found to be near the dorsal boundary of the RVM. 4. While one electrode was used to stimulate the parent axon in the lateral funiculus, a second was used to explore the gray matter for the presence of collateral branches. The identification of a branch was initially determined by an increase in antidromic latency. At the same rostrocaudal plane of the spinal cord, stimulation of the DLF induced an antidromic spike that invaded the neuron earlier than the antidromic spike elicited by stimulation in the gray matter. Collateral branches were confirmed by establishing that the location of the minimum threshold point for antidromic activation of the neurons from the second electrode was in the gray matter, that the minimum current required to antidromically activate the neuron from that point was too low to activate the parent axon in the DLF, and that a collision occurred between the spikes induced by the two stimulating electrodes. 5. In 17 cases, physiologically identified RVM neurons (10 ON and 7 OFF cells) were antidromically activated from the gray matter of the cervical spinal cord using a current of 8.4 +/- 2.1 (SE) microA. Minimum threshold points for antidromic activation were found in laminae I-II (3 ON and 4 OFF cells), lamina V (5 ON and 6 OFF cells), and regions ventral to the lateral reticulated area (3 ON and 2 OFF cells) of the gray matter. As indicated by these numbers, some neurons were antidromically activated from more than one gray matter region. In general, all OFF cells and 9 of 10 ON cells were antidromically activated from low threshold points in either laminae I-II or lamina V. 6. In six cases, neurons were activated from separate points located in two or three different laminae of the gray matter. Three OFF cells were activated from laminae I-II and V, one OFF cell and one ON cell were activated from lamina V and from more ventral points, and one ON cell was activated from laminae I-II and from points ventral to lamina V.

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Poon, Y. Y., Alice Y. W. Chang, and Samuel H. H. Chan. "DIFFERENTIAL CONTRIBUTION OF N-METHYL-d-ASPARTATE AND NON-N-METHYL-d-ASPARTATE RECEPTORS IN THE INTERMEDIOLATERAL CELL COLUMN OF THE THORACIC SPINAL CORD TO SYMPATHETIC VASOMOTOR TONE DURING EXPERIMENTAL ENDOTOXEMIA IN THE RAT." Shock 26, no. 4 (October 2006): 372–78. http://dx.doi.org/10.1097/01.shk.0000226340.25163.75.

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Klos, K. J., J. E. Ahlskog, K. A. Josephs, H. Apaydin, J. E. Parisi, B. F. Boeve, M. W. DeLucia, and D. W. Dickson. "α-Synuclein pathology in the spinal cords of neurologically asymptomatic aged individuals." Neurology 66, no. 7 (April 10, 2006): 1100–1102. http://dx.doi.org/10.1212/01.wnl.0000204179.88955.fa.

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The authors assessed the frequency of spinal cord α-synuclein pathology in neurologically asymptomatic individuals older than 60 years of age (N = 106). Using α-synuclein immunohistochemistry, nine cases (8%) had incidental Lewy neurites in the intermediolateral column and at least some α-synuclein pathology in the dorsal motor nucleus of the vagus, locus ceruleus, and central raphe nucleus. Sparse α-synuclein pathology was also detected in the substantia nigra, basal forebrain, amygdala, or cortex in all but two cases.

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FERINGA, EARL R., GILBERT W. LEE, and H. LEE VAHLSING. "Cell Death in Clarkeʼs Column after Spinal Cord Transection." Journal of Neuropathology and Experimental Neurology 44, no. 2 (March 1985): 156–64. http://dx.doi.org/10.1097/00005072-198503000-00004.

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46

Spanswick, D., and S. D. Logan. "Spontaneous rhythmic activity in the intermediolateral cell nucleus of the neonate rat thoracolumbar spinal cord in vitro." Neuroscience 39, no. 2 (January 1990): 395–403. http://dx.doi.org/10.1016/0306-4522(90)90276-a.

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Zhou, Wei, Aman Mahajan, and John C. Longhurst. "Spinal nociceptin mediates electroacupuncture-related modulation of visceral sympathoexcitatory reflex responses in rats." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (August 2009): H859—H865. http://dx.doi.org/10.1152/ajpheart.00149.2009.

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The role of nociceptin and its spinal cord neural pathways in electroacupuncture (EA)-related inhibition of visceral excitatory reflexes is not clear. Nociceptin/orphanin FQ (N/OFQ) is an endogenous ligand for a G protein-coupled receptor, called the N/OFQ peptide (NOP) receptor, which has been found to be distributed in the spinal cord. The present study investigated the importance of this system in visceral-cardiovascular reflex modulation during EA. Cardiovascular pressor reflex responses were induced by gastric distension in Sprague-Dawley rats anesthetized by ketamine and xylazine. An intrathecal injection of nociceptin (10 nM) at T1–2 attenuated the pressor responses by 35%, similar to the influence of EA at P 5–6 (42% decrease). An intrathecal injection of the NOP antagonist, [ N-Phe1]nociceptin1-13 NH2, partially reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not alter the EA-like inhibitory effect of nociceptin on the pressor reflex, whereas a combination of nociceptin receptor antagonist with naloxone completely abolished the EA response. An intrathecal injection of nociceptin attenuated the pressor responses to the electrical stimulation of the rostral ventrolateral medulla by 46%, suggesting that nociceptin can regulate sympathetic outflow. Furthermore, a bilateral microinjection of NOP antagonist into either the dorsal horn or the intermediolateral column at T1 partially reversed the EA inhibitory effect. These results suggest that nociceptin in the spinal cord mediates part of the EA-related modulation of visceral reflex responses.

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Sundaram, K., and H. Sapru. "NMDA receptors in the intermediolateral column of the spinal cord mediate sympathoexcitatory cardiac responses elicited from the ventrolateral medullary pressor area." Brain Research 544, no. 1 (March 1991): 33–41. http://dx.doi.org/10.1016/0006-8993(91)90882-v.

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Lee, Chang Hyun, Han Sol Jung, Tae Young Lee, Sang Ryoung Lee, Sang Won Yuk, Kwang Gyu Lee, and Bong Hee Lee. "Studies of the Central Neural Pathways to the Stomach and Zusanli (ST36)." American Journal of Chinese Medicine 29, no. 02 (January 2001): 211–20. http://dx.doi.org/10.1142/s0192415x01000241.

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The purpose of this morphological study was to investigate the relation between the meridian, meridian points and viscera using neuroanatomical tracers. The common locations of the spinal cord and brain projecting to the stomach and Zusanli were observed following injection of CTB (cholera toxin B subunit) and pseudorabies viruses (PRV-Ba, Bartha strain and PRV-Ba-Gal, galactosidase insertion) into the stomach and Zusanli (ST36). After 4–5 days of survival following injection into twelve rats, they were perfused, and their spinal cords and brains were frozen sectioned (30 μm). These sections were stained by X-gal histochemical, CTB and PRV-Bia immunohistochemical staining methods, and examined with the light microscope. The results were as follows: Commonly labeled medulla oblongata regions were dorsal motor nucleus of vagus nerve (DMV), nucleus tractus solitarius (NTS) and area postrema (AP) following injection of CTB and PRV-Ba-Gal into stomach and Zusanli, respectively. In the spinal cord, commonly labeled neurons were found in thoracic, lumbar and sacral spinal segments. Densely labeled areas were found in lamina IV, V, VII (intermediolateral nucleus) and X of the spinal cord. In the brain, commonly labeled neurons were found in the A1 noradrenalin cells/C1 adrenalin cells/caudoventrolateral reticular nucleus, dorsal motor nucleus of vagus nerve, nucleus tractus solitarius, area postrema, raphe obscurus nucleus, raphe pallidus nucleus, raphe magnus nucleus, gigantocellular nucleus, locus coeruleus, parabrachial nucleus, Kolliker-Fuse nucleus, A5 cell group, central gray matter, paraventricular hypothalamic nucleus, lateral hypothalamic nucleus, retrochiasmatic hypothalamic nucleus, bed nucleus of stria terminals and amygdaloid nucleus. Thus central autonomic center project both to the stomach and Zusanli. These morphological results suggest that there is a commonality of CNS cell groups in brain controlling stomach (viscera) and Zusanli (limb).

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Szilasi, Anna, Lilla Dénes, Csaba Jakab, Ildikó Erdélyi, Talita Resende, Fabio Vannucci, Judit Csomor, Míra Mándoki, and Gyula Balka. "In situ hybridization of feline leukemia virus in a primary neural B-cell lymphoma." Journal of Veterinary Diagnostic Investigation 32, no. 3 (April 10, 2020): 454–57. http://dx.doi.org/10.1177/1040638720915449.

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An 8-y-old castrated male, outdoor European shorthair cat was presented with a history of hindlimb weakness and paralysis. Disease progression was continuous from the onset; deep algesia disappeared at the final stage. Radiography of the vertebral column was unremarkable; along with patient history and physical examination results, magnetic resonance imaging suggested inflammatory lesions in the spinal cord, although neoplasia could not be ruled out. Feline leukemia virus (FeLV) positivity was confirmed by a serum ELISA prior to euthanasia. Upon postmortem examination, hemorrhages were present in the spinal cord at the level of vertebrae T7-8. Histologic and immunohistochemical analysis revealed primary diffuse large B-cell lymphoma of the spinal cord with multifocal myelomalacia and hemorrhages. To determine the presence of a pathogen within the lesion, we developed a novel in situ hybridization protocol for FeLV (RNAscope). The reaction revealed large amounts of FeLV viral RNA in the tumor cells.

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Journal articles on the topic 'Intermediolateral cell column of spinal cord'

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