Biology:Neural top–down control of physiology

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Short description: Systemic Brain Function of Human Physiology

Neural top–down control of physiology concerns the direct regulation by the brain of physiological functions (in addition to smooth muscle and glandular ones). Cellular functions include the immune system’s production of T-lymphocytes and antibodies, and nonimmune related homeostatic functions such as liver gluconeogenesis, sodium reabsorption, osmoregulation, and brown adipose tissue nonshivering thermogenesis. This regulation occurs through the sympathetic and parasympathetic system (the autonomic nervous system), and their direct innervation of body organs and tissues that starts in the brainstem. There is also a noninnervation hormonal control through the hypothalamus and pituitary (HPA). These lower brain areas are under control of cerebral cortex ones. Such cortical regulation differs between its left and right sides. Pavlovian conditioning shows that brain control over basic cell level physiological function can be learned.

Higher brain

Cerebral cortex

Sympathetic and parasympathetic nervous systems and the hypothalamus are regulated by the higher brain.[1][2][3][4] Through them, the higher cerebral cortex areas can control the immune system, and the body’s homeostatic and stress physiology. Areas doing this include the insular cortex,[5][6][7] the orbital, and the medial prefrontal cortices.[8][9] These cerebral areas also control smooth muscle and glandular physiological processes through the sympathetic and parasympathetic nervous system including blood circulation, urogenital, gastrointestinal[10] functions, pancreatic gut secretions,[11] respiration, coughing, vomiting, piloerection, pupil dilation, lacrimation and salivation.[12]

Lateralization

The sympathetic nervous system is predominantly controlled by the right side of the brain (focused upon the insular cortex), while the left side predominantly controls the parasympathetic nervous system.[4] The cerebral cortex in rodents shows lateral specialization in its regulation of immunity with immunosuppression being controlled by the right hemisphere, and immunopotention by the left one.[9][13] Humans show similar lateral specialized control of the immune system from the evidence of strokes,[14] surgery to control epilepsy,[15] and the application of TMS.[16]

Brainstem

The higher brain top down control of physiology is mediated by the sympathetic and parasympathetic nervous systems in the brainstem,[1][2][3][4] and the hypothalamus.[1][17][18] The sympathetic nervous system arises in brainstem nuclei that project down into intermediolateral columns of thoracolumbar spinal cord neurons in spinal segments T1–L2. The parasympathetic nervous system in the motor nuclei of cranial nerves III, VII, IX, (control over the pupil and salivary glands) and X (vagus –many functions including immunity) and sacral spinal segments (gastrointestinal and urogenital systems).[12] Another control occurs through top down control by the medial areas of the prefrontal cortex.[1][17][18] upon the hypothalamus which has a nonnerve control of the body through hormonal secretions of the pituitary.

Immunity

The brain controls immunity both indirectly through HPA glucocorticoid secretions from the pituitary, and by various direct innervations.[19]

  • Antibodies. There is sympathetic innervation of the thymus gland.[20] Sympathetic control exists over antibody production,[21] and the modulation of cytokine concentrations.[22]
  • Cellular immunity. An intact sympathetic nervous system is required to maintain full cellular immunoregulation as denervated mice do not produce and activate, for example, splenic suppressor T cells, or thymic NKT cells.[23]
  • Organ inflammation. Sympathetic innervation of various organs[19] contacts macrophages and dendritic cells and can increase local inflammation including the kidney[24] gut,[25] the skin,[26] and the synovial joints[27]
  • Antiinflammation. The vagus nerve carries a parasympathetic cholinergic antiinflammatory pathway that reduces proinflammatory cytokines such as TNF by spleen macrophages in the red pulp and the marginal zone and so the activation of inflammation.[28][29] This control is in part controlled by direct innervation of body organs such as the spleen.[30] However, the existence of the parasympathetic antiinflammatory nerve pathway is controversial with one reviewer stating: “there is no evidence for an anti-inflammatory role of the efferent vagus nerve that is independent of the sympathetic nervous system.”[31]

Metabolism

The liver receives both sympathetic and parasympathetic nervous system innervation.[32]

  • Plasma glucose levels. A vagus brain-liver axis exists that detects lipids produced by the gut and acts to regulate glucose homeostasis.[10][33]
  • Glycogenesis. Vagal activation also controls glycogen synthesis in the liver.[34]
  • lipogenesis. Vagal activation also controls the generation of lipids in brown adipose tissue.[34]
  • Insulin. Vagal innervation of the pancreas controls the release of insulin release from its beta cells (and this is inhibited by norepinephrine released under sympathetic control from the splanchnic nerve).[35]
  • Thyroid hormones can control glucose production via the hypothalamus and its sympathetic and parasympathetic innervation of the liver.[36]

Other

Conditioning

The brains of animals can anticipatorily learn to control cell level physiology such as immunity through Pavlovian conditioning. In this conditioning, a neutral stimulus saccharin is paired in a drink with an agent, cyclophosphamide, that produces an unconditioned response (immunosuppression). After learning this pairing, the taste of saccharin by itself through neural top down control created immunosuppression, as a new conditioned response.[42] This work was originally done on rats, however, the same conditioning can also occur in humans.[43] The conditioned response happens in the brain with the ventromedial nucleus of the hypothalamus providing the output pathway to the immune system, the amygdala, the input of visceral information, and the insular cortex acquires and creates the conditioned response.[5] The production of different components of the immune system can be controlled as conditioned responses:

  • Antibodies[43][44][45]
  • IL-2[46][47]
  • B, CD8+ T cells and CD4+ naive and memory T cells, and granulocytes.[48] Such conditioning in rats can last a year.[49]

Nonimmune functions can also be conditioned:

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 Cerqueira, J. O. J.; Almeida, O. F. X.; Sousa, N. (2008). "The stressed prefrontal cortex. Left? Right!". Brain, Behavior, and Immunity 22 (5): 630–638. doi:10.1016/j.bbi.2008.01.005. PMID 18281193. 
  2. ↑ 2.0 2.1 Critchley, H. D. (2005). "Neural mechanisms of autonomic, affective, and cognitive integration". The Journal of Comparative Neurology 493 (1): 154–166. doi:10.1002/cne.20749. PMID 16254997. 
  3. ↑ 3.0 3.1 Van Eden, C. G.; Buijs, R. M. (2000). "Functional neuroanatomy of the prefrontal cortex: autonomic interactions". Cognition, emotion and autonomic responses: The integrative role of the prefrontal cortex and limbic structures. Progress in Brain Research. 126. pp. 49–62. doi:10.1016/S0079-6123(00)26006-8. ISBN 9780444503329. 
  4. ↑ 4.0 4.1 4.2 Craig, A. D. (B. (2005). "Forebrain emotional asymmetry: A neuroanatomical basis?". Trends in Cognitive Sciences 9 (12): 566–571. doi:10.1016/j.tics.2005.10.005. PMID 16275155. 
  5. ↑ 5.0 5.1 Pacheco-Lopez, G.; Niemi, M. B.; Kou, W.; Härting, M.; Fandrey, J.; Schedlowski, M. (2005). "Neural Substrates for Behaviorally Conditioned Immunosuppression in the Rat". Journal of Neuroscience 25 (9): 2330–2337. doi:10.1523/JNEUROSCI.4230-04.2005. PMID 15745959. 
  6. ↑ Ramírez-Amaya, V.; Alvarez-Borda, B.; Ormsby, C. E.; Martínez, R. D.; Pérez-Montfort, R.; Bermúdez-Rattoni, F. (1996). "Insular cortex lesions impair the acquisition of conditioned immunosuppression". Brain, Behavior, and Immunity 10 (2): 103–114. doi:10.1006/brbi.1996.0011. PMID 8811934. 
  7. ↑ Ramı́Rez-Amaya, V.; Bermudez-Rattoni, F. (1999). "Conditioned Enhancement of Antibody Production is Disrupted by Insular Cortex and Amygdala but Not Hippocampal Lesions". Brain, Behavior, and Immunity 13 (1): 46–60. doi:10.1006/brbi.1998.0547. PMID 10371677. 
  8. ↑ Ohira, H.; Isowa, T.; Nomura, M.; Ichikawa, N.; Kimura, K.; Miyakoshi, M.; Iidaka, T.; Fukuyama, S. et al. (2008). "Imaging brain and immune association accompanying cognitive appraisal of an acute stressor". NeuroImage 39 (1): 500–514. doi:10.1016/j.neuroimage.2007.08.017. PMID 17913515. 
  9. ↑ 9.0 9.1 Vlajković, S.; Nikolić, V.; Nikolić, A.; Milanović, S.; Janković, B. D. (1994). "Asymmetrical modulation of immune reactivity in left- and right-biased rats after ipsilateral ablation of the prefrontal, parietal and occipital brain neocortex". The International Journal of Neuroscience 78 (1–2): 123–134. doi:10.3109/00207459408986051. PMID 7829286. 
  10. ↑ 10.0 10.1 Pocai, A.; Obici, S.; Schwartz, G. J.; Rossetti, L. (2005). "A brain-liver circuit regulates glucose homeostasis". Cell Metabolism 1 (1): 53–61. doi:10.1016/j.cmet.2004.11.001. PMID 16054044. 
  11. ↑ Love, J. A.; Yi, E.; Smith, T. G. (2007). "Autonomic pathways regulating pancreatic exocrine secretion". Autonomic Neuroscience 133 (1): 19–34. doi:10.1016/j.autneu.2006.10.001. PMID 17113358. 
  12. ↑ 12.0 12.1 Brading, A. (1999). The autonomic nervous system and its effectors. Oxford: Blackwell Science. ISBN 978-0-632-02624-1. 
  13. ↑ Barnéoud, P.; Neveu, P. J.; Vitiello, S.; Mormède, P.; Le Moal, M. (1988). "Brain neocortex immunomodulation in rats". Brain Research 474 (2): 394–398. doi:10.1016/0006-8993(88)90458-1. PMID 3145098. 
  14. ↑ Koch, H. J.; Uyanik, G.; Bogdahn, U.; Ickenstein, G. W. (2006). "Relation between Laterality and Immune Response after Acute Cerebral Ischemia". Neuroimmunomodulation 13 (1): 8–12. doi:10.1159/000092108. PMID 16612132. 
  15. ↑ Meador, K. J.; Loring, D. W.; Ray, P. G.; Helman, S. W.; Vazquez, B. R.; Neveu, P. J. (2004). "Role of cerebral lateralization in control of immune processes in humans". Annals of Neurology 55 (6): 840–844. doi:10.1002/ana.20105. PMID 15174018. 
  16. ↑ Clow, A.; Lambert, S.; Evans, P.; Hucklebridge, F.; Higuchi, K. (2003). "An investigation into asymmetrical cortical regulation of salivary S-IgA in conscious man using transcranial magnetic stimulation". International Journal of Psychophysiology 47 (1): 57–64. doi:10.1016/S0167-8760(02)00093-4. PMID 12543446. 
  17. ↑ 17.0 17.1 Radley, J. J.; Arias, C. M.; Sawchenko, P. E. (2006). "Regional Differentiation of the Medial Prefrontal Cortex in Regulating Adaptive Responses to Acute Emotional Stress". Journal of Neuroscience 26 (50): 12967–12976. doi:10.1523/JNEUROSCI.4297-06.2006. PMID 17167086. 
  18. ↑ 18.0 18.1 Kern, S.; Oakes, T. R.; Stone, C. K.; McAuliff, E. M.; Kirschbaum, C. (2008). "Glucose metabolic changes in the prefrontal cortex are associated with HPA axis response to a psychosocial stressor". Psychoneuroendocrinology 33 (4): 517–529. doi:10.1016/j.psyneuen.2008.01.010. PMID 18337016. 
  19. ↑ 19.0 19.1 Sternberg, E. M. (2006). "Neural regulation of innate immunity: A coordinated nonspecific host response to pathogens". Nature Reviews Immunology 6 (4): 318–328. doi:10.1038/nri1810. PMID 16557263. 
  20. ↑ Trotter, R. N.; Stornetta, R. L.; Guyenet, P. G.; Roberts, M. R. (2007). "Transneuronal mapping of the CNS network controlling sympathetic outflow to the rat thymus". Autonomic Neuroscience 131 (1–2): 9–20. doi:10.1016/j.autneu.2006.06.001. PMID 16843070. 
  21. ↑ Besedovsky, H. O.; Del Rey, A.; Sorkin, E.; Da Prada, M.; Keller, H. H. (1979). "Immunoregulation mediated by the sympathetic nervous system". Cellular Immunology 48 (2): 346–355. doi:10.1016/0008-8749(79)90129-1. PMID 389444. 
  22. ↑ Kin, N. W.; Sanders, V. M. (2006). "It takes nerve to tell T and B cells what to do". Journal of Leukocyte Biology 79 (6): 1093–1104. doi:10.1189/jlb.1105625. PMID 16531560. 
  23. ↑ Li, X.; Taylor, S.; Zegarelli, B.; Shen, S.; O'Rourke, J.; Cone, R. E. (2004). "The induction of splenic suppressor T cells through an immune-privileged site requires an intact sympathetic nervous system". Journal of Neuroimmunology 153 (1–2): 40–49. doi:10.1016/j.jneuroim.2004.04.008. PMID 15265662. 
  24. ↑ Veelken, R.; Vogel, E. -M.; Hilgers, K.; Amann, K.; Hartner, A.; Sass, G.; Neuhuber, W.; Tiegs, G. (2008). "Autonomic Renal Denervation Ameliorates Experimental Glomerulonephritis". Journal of the American Society of Nephrology 19 (7): 1371–1378. doi:10.1681/ASN.2007050552. PMID 18400940. 
  25. ↑ Straub, R. H.; Grum, F.; Strauch, U.; Capellino, S.; Bataille, F.; Bleich, A.; Falk, W.; Schölmerich, J. et al. (2008). "Anti-inflammatory role of sympathetic nerves in chronic intestinal inflammation". Gut 57 (7): 911–921. doi:10.1136/gut.2007.125401. PMID 18308830. 
  26. ↑ Pavlovic, S.; Daniltchenko, M.; Tobin, D. J.; Hagen, E.; Hunt, S. P.; Klapp, B. F.; Arck, P. C.; Peters, E. M. J. (2007). "Further Exploring the Brain–Skin Connection: Stress Worsens Dermatitis via Substance P-dependent Neurogenic Inflammation in Mice". Journal of Investigative Dermatology 128 (2): 434–446. doi:10.1038/sj.jid.5701079. PMID 17914449. 
  27. ↑ Miller, L. E.; Jüsten, H. P.; Schölmerich, J.; Straub, R. H. (2000). "The loss of sympathetic nerve fibers in the synovial tissue of patients with rheumatoid arthritis is accompanied by increased norepinephrine release from synovial macrophages". The FASEB Journal 14 (13): 2097–2107. doi:10.1096/fj.99-1082com. PMID 11023994. 
  28. ↑ Huston, J. M.; Ochani, M.; Rosas-Ballina, M.; Liao, H.; Ochani, K.; Pavlov, V. A.; Gallowitsch-Puerta, M.; Ashok, M. et al. (2006). "Splenectomy inactivates the cholinergic antiinflammatory pathway during lethal endotoxemia and polymicrobial sepsis". Journal of Experimental Medicine 203 (7): 1623–1628. doi:10.1084/jem.20052362. PMID 16785311. 
  29. ↑ Rosas-Ballina, M.; Ochani, M.; Parrish, W. R.; Ochani, K.; Harris, Y. T.; Huston, J. M.; Chavan, S.; Tracey, K. J. (2008). "Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia". Proceedings of the National Academy of Sciences 105 (31): 11008–11013. doi:10.1073/pnas.0803237105. PMID 18669662. Bibcode: 2008PNAS..10511008R. 
  30. ↑ Exton, M. S.; Schult, M.; Donath, S.; Strubel, T.; Bode, U.; Del Rey, A.; Westermann, J.; Schedlowski, M. (1999). "Conditioned immunosuppression makes subtherapeutic cyclosporin effective via splenic innervation". The American Journal of Physiology 276 (6 Pt 2): R1710–R1717. doi:10.1152/ajpregu.1999.276.6.R1710. PMID 10362751. 
  31. ↑ Nance, D. M.; Sanders, V. M. (2007). "Autonomic innervation and regulation of the immune system (1987–2007)". Brain, Behavior, and Immunity 21 (6): 736–745. doi:10.1016/j.bbi.2007.03.008. PMID 17467231.  p. 741
  32. ↑ Uyama, N.; Geerts, A.; Reynaert, H. (2004). "Neural connections between the hypothalamus and the liver". The Anatomical Record 280A (1): 808–820. doi:10.1002/ar.a.20086. PMID 15382020. 
  33. ↑ Wang, P. Y. T.; Caspi, L.; Lam, C. K. L.; Chari, M.; Li, X.; Light, P. E.; Gutierrez-Juarez, R.; Ang, M. et al. (2008). "Upper intestinal lipids trigger a gut–brain–liver axis to regulate glucose production". Nature 452 (7190): 1012–1016. doi:10.1038/nature06852. PMID 18401341. Bibcode: 2008Natur.452.1012W. 
  34. ↑ 34.0 34.1 Shimazu, T. (1981). "Central nervous system regulation of liver and adipose tissue metabolism". Diabetologia 20 Suppl (3): 343–356. doi:10.1007/BF00254502. PMID 7014330. 
  35. ↑ Brunicardi, F. C.; Shavelle, D. M.; Andersen, D. K. (1995). "Neural regulation of the endocrine pancreas". International Journal of Pancreatology 18 (3): 177–195. doi:10.1007/BF02784941. PMID 8708389. https://link.springer.com/article/10.1007/BF02784941. 
  36. ↑ Klieverik, L. P.; Janssen, S. F.; Riel, A. V.; Foppen, E.; Bisschop, P. H.; Serlie, M. J.; Boelen, A.; Ackermans, M. T. et al. (2009). "Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver". Proceedings of the National Academy of Sciences 106 (14): 5966–5971. doi:10.1073/pnas.0805355106. PMID 19321430. Bibcode: 2009PNAS..106.5966K. 
  37. ↑ Nakamura, K.; Morrison, S. F. (2006). "Central efferent pathways mediating skin cooling-evoked sympathetic thermogenesis in brown adipose tissue". AJP: Regulatory, Integrative and Comparative Physiology 292 (1): R127–R136. doi:10.1152/ajpregu.00427.2006. PMID 16931649. 
  38. ↑ Edwards, A. V.; Jones, C. T. (1993). "Autonomic control of adrenal function". Journal of Anatomy 183 (Pt 2): 291–307. PMID 8300417. 
  39. ↑ Engeland, W. (2007). "Functional Innervation of the Adrenal Cortex by the Splanchnic Nerve". Hormone and Metabolic Research 30 (6/07): 311–314. doi:10.1055/s-2007-978890. PMID 9694555. 
  40. ↑ Dibona, G. F. (2000). "Neural control of the kidney: Functionally specific renal sympathetic nerve fibers". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 279 (5): R1517–R1524. doi:10.1152/ajpregu.2000.279.5.r1517. PMID 11049831. 
  41. ↑ Denton, K. M.; Luff, S. E.; Shweta, A.; Anderson, W. P. (2004). "Differential Neural Control of Glomerular Ultrafiltration". Clinical and Experimental Pharmacology and Physiology 31 (5–6): 380–386. doi:10.1111/j.1440-1681.2004.04002.x. PMID 15191417. 
  42. ↑ Ader, R.; Cohen, N. (1975). "Behaviorally conditioned immunosuppression". Psychosomatic Medicine 37 (4): 333–340. doi:10.1097/00006842-197507000-00007. PMID 1162023. 
  43. ↑ 43.0 43.1 Goebel, M. U.; Trebst, A. E.; Steiner, J.; Xie, Y. F.; Exton, M. S.; Frede, S.; Canbay, A. E.; Michel, M. C. et al. (2002). "Behavioral conditioning of immunosuppression is possible in humans". The FASEB Journal 16 (14): 1869–1873. doi:10.1096/fj.02-0389com. PMID 12468450. 
  44. ↑ Alvarez-Borda, B.; Ramírez-Amaya, V.; Pérez-Montfort, R.; Bermúdez-Rattoni, F. (1995). "Enhancement of antibody production by a learning paradigm". Neurobiology of Learning and Memory 64 (2): 103–105. doi:10.1006/nlme.1995.1048. PMID 7582817. 
  45. ↑ Oberbeck, R.; Kromm, A.; Exton, M. S.; Schade, U.; Schedlowski, M. (2003). "Pavlovian conditioning of endotoxin-tolerance in rats". Brain, Behavior, and Immunity 17 (1): 20–27. doi:10.1016/S0889-1591(02)00031-4. PMID 12615046. 
  46. ↑ Pacheco-López, G.; Niemi, M. -B.; Kou, W.; Härting, M.; Del Rey, A.; Besedovsky, H. O.; Schedlowski, M. (2004). "Behavioural endocrine immune-conditioned response is induced by taste and superantigen pairing". Neuroscience 129 (3): 555–562. doi:10.1016/j.neuroscience.2004.08.033. PMID 15541877. 
  47. ↑ Exton, M. S.; Von Hörsten, S.; Schult, M.; Vöge, J.; Strubel, T.; Donath, S.; Steinmüller, C.; Seeliger, H. et al. (1998). "Behaviorally conditioned immunosuppression using cyclosporine A: Central nervous system reduces IL-2 production via splenic innervation". Journal of Neuroimmunology 88 (1–2): 182–191. doi:10.1016/S0165-5728(98)00122-2. PMID 9688340. 
  48. ↑ Von Hörsten, S.; Exton, M. S.; Schult, M.; Nagel, E.; Stalp, M.; Schweitzer, G.; Vöge, J.; Del Rey, A. et al. (1998). "Behaviorally conditioned effects of Cyclosporine a on the immune system of rats: Specific alterations of blood leukocyte numbers and decrease of granulocyte function". Journal of Neuroimmunology 85 (2): 193–201. doi:10.1016/S0165-5728(98)00011-3. PMID 9630168. 
  49. ↑ Exton, M. S.; Von Hörsten, S.; Strubel, T.; Donath, S.; Schedlowski, M.; Westermann, J. (2000). "Conditioned alterations of specific blood leukocyte subsets are reconditionable". Neuroimmunomodulation 7 (2): 106–114. doi:10.1159/000026428. PMID 10686521. 
  50. ↑ Exton, M. S.; Bull, D. F.; King, M. G.; Husband, A. J. (1995). "Behavioral conditioning of endotoxin-induced plasma iron alterations". Pharmacology Biochemistry and Behavior 50 (4): 675–679. doi:10.1016/0091-3057(94)00353-X. PMID 7617718. 
  51. ↑ Irie, M.; Asami, S.; Nagata, S.; Miyata, M.; Kasai, H. (2000). "Classical conditioning of oxidative DNA damage in rats". Neuroscience Letters 288 (1): 13–16. doi:10.1016/S0304-3940(00)01194-0. PMID 10869804. 
  52. ↑ Stockhorst, U.; Steingrüber, H. J.; Scherbaum, W. A. (2000). "Classically conditioned responses following repeated insulin and glucose administration in humans". Behavioural Brain Research 110 (1–2): 143–159. doi:10.1016/S0166-4328(99)00192-8. PMID 10802311. 
  53. ↑ 53.0 53.1 Stockhorst, U.; Mahl, N.; Krueger, M.; Huenig, A.; Schottenfeldnaor, Y.; Huebinger, A.; Berresheim, H.; Steingrueber, H. et al. (2004). "Classical conditioning and conditionability of insulin and glucose effects in healthy humans". Physiology & Behavior 81 (3): 375–388. doi:10.1016/j.physbeh.2003.12.019. PMID 15135009. 
  54. ↑ Fehm-Wolfsdorf, G.; Gnadler, M.; Kern, W.; Klosterhalfen, W.; Kerner, W. (1993). "Classically conditioned changes of blood glucose level in humans". Physiology & Behavior 54 (1): 155–160. doi:10.1016/0031-9384(93)90058-N. PMID 8327595. 



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