Is there a link between depression, neurochemical asymmetry and cardiovascular function?

AB Segarra; I Prieto; M Martínez-Cañamero; Manuel Ramírez-Sánchez; AB Segarra; I Prieto; M Martínez-Cañamero; Manuel Ramírez-Sánchez

doi:10.3934/Neuroscience.2020022

AIMS Neuroscience

2020, Volume 7, Issue 4: 360-372. doi: 10.3934/Neuroscience.2020022

Previous Article Next Article

Review Topical Sections

Is there a link between depression, neurochemical asymmetry and cardiovascular function?

Department of Health Sciences, University of Jaén, Jaén, Spain

Received: 21 July 2020 Accepted: 23 September 2020 Published: 28 September 2020

Although at present depression is one of the most disabling disorders in our social environment, the understanding of its pathogenesis and the resources for its treatment are still unsatisfactory. The importance of brain asymmetry in the pathogenesis of disorders in brain function, including mood disorders such as depression, is a highly unexplored, sometimes underrated, and even ignored topic. It is important to note that the basal and pathological functional lateralization must have an underlying neurochemical substrate. It is also necessary to indicate that the brain asymmetry extends to a neurovisceral integration whose behavior may also be lateralized. One of the most studied axis from the functional point of view is the brain-heart connection, in whose operation there are observations that suggest an asymmetric behavior in basal conditions that is modified by central and peripheral changes, as well as by pharmacological treatments. There are evidences that connect cardiovascular function, neurochemical asymmetries, and depression. A deep understanding of the bilateral behavior of the brain following pathophysiological changes in blood pressure as well as pharmacologically induced, can provide us with therapeutic suggestions for the treatment of depression. In this article, we analyze remarkable results of some representative selected contributions, with which we discuss our proposal on the relationship between hypertension, depression and neurochemical asymmetry.
- brain asymmetry,
- brain-heart connection,
- brain-gut connection,
- hypertension,
- neurovisceral integration,
- neuropeptidases
Citation: AB Segarra, I Prieto, M Martínez-Cañamero, Manuel Ramírez-Sánchez. Is there a link between depression, neurochemical asymmetry and cardiovascular function?[J]. AIMS Neuroscience, 2020, 7(4): 360-372. doi: 10.3934/Neuroscience.2020022

Related Papers:

Abstract

Although at present depression is one of the most disabling disorders in our social environment, the understanding of its pathogenesis and the resources for its treatment are still unsatisfactory. The importance of brain asymmetry in the pathogenesis of disorders in brain function, including mood disorders such as depression, is a highly unexplored, sometimes underrated, and even ignored topic. It is important to note that the basal and pathological functional lateralization must have an underlying neurochemical substrate. It is also necessary to indicate that the brain asymmetry extends to a neurovisceral integration whose behavior may also be lateralized. One of the most studied axis from the functional point of view is the brain-heart connection, in whose operation there are observations that suggest an asymmetric behavior in basal conditions that is modified by central and peripheral changes, as well as by pharmacological treatments. There are evidences that connect cardiovascular function, neurochemical asymmetries, and depression. A deep understanding of the bilateral behavior of the brain following pathophysiological changes in blood pressure as well as pharmacologically induced, can provide us with therapeutic suggestions for the treatment of depression. In this article, we analyze remarkable results of some representative selected contributions, with which we discuss our proposal on the relationship between hypertension, depression and neurochemical asymmetry.

Conflict of interest

The authors declare no conflicts of interest.

References

[1]	Kaltenboeck A, Harmer C (2018) The neuroscience of depressive disorders: A brief review of the past and some considerations about the future. Brain Neurosci Adv 2: 239821281879926. doi: 10.1177/2398212818799269
[2]	Prieto I, Segarra AB, Martinez-Canamero M, et al. (2017) Bidirectional asymmetry in the neurovisceral communication for the cardiovascular control: New insights. Endocr Regul 51: 157-167. doi: 10.1515/enr-2017-0017
[3]	Segarra AB, Prieto-Gomez I, Banegas I, et al. (2019) Functional and neurometabolic asymmetry in SHR and WKY rats following vasoactive treatments. Sci Rep 9: 16098. doi: 10.1038/s41598-019-52658-9
[4]	Madison A, Kiecolt-Glaser JK (2019) Stress, depression, diet, and the gut microbiota: human-bacteria interactions at the core of psychoneuroimmunology and nutrition. Curr Opin Behav Sci 28: 105-110. doi: 10.1016/j.cobeha.2019.01.011
[5]	Harmer CJ, Duman RS, Cowen PJ (2017) How do antidepressants work? New perspectives for refining future treatment approaches. Lancet Psychiatry 4: 409-418. doi: 10.1016/S2215-0366(17)30015-9
[6]	Prieto I, Segarra AB, De Gasparo M, et al. (2016) Neuropeptidases, Stress and Memory—A Promising Perspective. AIMS Neurosci 3: 487-501. doi: 10.3934/Neuroscience.2016.4.487
[7]	Bogdan R, Pizzagalli DA (2006) Acute stress reduces reward responsiveness: implications for depression. Biol Psychiatry 60: 1147-1154. doi: 10.1016/j.biopsych.2006.03.037
[8]	Barber BA, Kohl KL, Kassam-Adams N, et al. (2014) Acute stress, depression, and anxiety symptoms among English and Spanish speaking children with recent trauma exposure. J Clin Psychol Med Settings 21: 66-71. doi: 10.1007/s10880-013-9382-z
[9]	Broca MP (1861) Remarques sur le siége de la faculté du language articulé, suivies d'une observation d'aphémie (perte de la parole). Bull Soc Anat (París) VI: 330-357.
[10]	Corballis MC (2014) Left brain, right brain: facts and fantasies. PLoS Biol 12: e1001767. doi: 10.1371/journal.pbio.1001767
[11]	Hellige JB (1993) Hemispheric asymmetry: what's right and what's left London: Harvard University Press.
[12]	Rogers LJ, Vallortigara G, Andrew RJ (2013) Divided Brains. The biology and behaviour of brain asymmetries Cambridge: Cambridge University Press. doi: 10.1017/CBO9780511793899
[13]	Gazzaniga MS (2015) Tales from both sides of the brain. A life in neuroscience New York: Harper Collins.
[14]	Zimmerberg B, Glick SD, Jerussi TP (1974) Neurochemical correlate of a spatial preference in rats. Science 185: 623-625. doi: 10.1126/science.185.4151.623
[15]	Oke A, Keller R, Mefford I, et al. (1978) Lateralization of norepinephrine in human thalamus. Science 200: 1411-1413. doi: 10.1126/science.663623
[16]	Bernard C (1878) Etude sur la physiologie du coeur. La Sci Exp 316-366.
[17]	Domínguez-Vías G, Aretxaga G, Prieto I, et al. (2020) Asymmetrical influence of a standard light/dark cycle and constant light conditions on the alanyl-aminopeptidase activity of the left and right retinas in adult male rats. Exp Eye Res 198: 108149. doi: 10.1016/j.exer.2020.108149
[18]	Segarra AB, Prieto I, Banegas I, et al. (2012) Asymmetrical effect of captopril on the angiotensinase activity in frontal cortex and plasma of the spontaneously hypertensive rats: expanding the model of neuroendocrine integration. Behav Brain Res 230: 423-427. doi: 10.1016/j.bbr.2012.02.039
[19]	Segarra AB, Prieto I, Banegas I, et al. (2013) The brain-heart connection: frontal cortex and left ventricle angiotensinase activities in control and captopril-treated hypertensive rats—a bilateral study. Int J Hypertens 2013: 156179. doi: 10.1155/2013/156179
[20]	Prieto I, Segarra AB, Villarejo AB, et al. (2019) Neuropeptidase activity in the frontal cortex of Wistar-Kyoto and spontaneously hypertensive rats treated with vasoactive drugs: a bilateral study. J Hypertens 37: 612-628. doi: 10.1097/HJH.0000000000001884
[21]	Henriques JB, Davidson RJ (1991) Left frontal hypoactivation in depression. J Abnorm Psychol 100: 535-545. doi: 10.1037/0021-843X.100.4.535
[22]	Ramírez M, Prieto I, Vives F, et al. (2004) Neuropeptides, neuropeptidases and brain asymmetry. Curr Protein Pept Sci 5: 497-506. doi: 10.2174/1389203043379350
[23]	Cohen BE, Edmondson D, Kronish IM (2015) State of the Art Review: Depression, Stress, Anxiety, and Cardiovascular Disease. Am J Hypertens 28: 1295-1302. doi: 10.1093/ajh/hpv047
[24]	Liguori I, Russo G, Curcio F, et al. (2018) Depression and chronic heart failure in the elderly: an intriguing relationship. J Geriatr Cardiol 15: 451-459.
[25]	Testa G, Cacciatore F, Galizia G, et al. (2011) Depressive symptoms predict mortality in elderly subjects with chronic heart failure. Eur J Clin Invest 41: 1310-1317. doi: 10.1111/j.1365-2362.2011.02544.x
[26]	Agustini B, Mohebbi M, Woods RL, et al. (2020) The association of antihypertensive use and depressive symptoms in a large older population with hypertension living in Australia and the United States: a cross-sectional study. J Hum Hypertens 30.
[27]	Eze-Nliam CM, Thombs BD, Lima BB, et al. (2010) The association of depression with adherence to antihypertensive medications: a systematic review. J Hypertens 28: 1785-1795. doi: 10.1097/HJH.0b013e32833b4a6f
[28]	Bautista LE, Vera-Cala LM, Colombo C, et al. (2012) Symptoms of depression and anxiety and adherence to antihypertensive medication. Am J Hypertens 25: 505-511. doi: 10.1038/ajh.2011.256
[29]	Braszko JJ, Karwowska-Polecka W, Halicka D, et al. (2003) Captopril and enalapril improve cognition and depressed mood in hypertensive patients. J Basic Clin Physiol Pharmacol 14: 323-343. doi: 10.1515/JBCPP.2003.14.4.323
[30]	Cacciatore F, Amarelli C, Maiello C, et al. (2020) Effect of Sacubitril-Valsartan in reducing depression in patients with advanced heart failure. J Affect Disord 272: 132-137. doi: 10.1016/j.jad.2020.03.158
[31]	Rotenberg VS (2008) Functional brain asymmetry as a determinative factor in the treatment of depression: theoretical implications. Prog Neuropsychopharmacol Biol Psychiatry 32: 1772-1777. doi: 10.1016/j.pnpbp.2008.08.011
[32]	Banegas I, Prieto I, Segarra AB, et al. (2011) Blood pressure increased dramatically in hypertensive rats after left hemisphere lesions with 6-hydroxydopamine. Neurosci Lett 500: 148-150. doi: 10.1016/j.neulet.2011.06.025
[33]	Segarra AB, Banegas I, Prieto I, et al. (2016) Brain asymmetry and dopamine: beyond motor implications in Parkinson's disease and experimental hemiparkinsonism. Rev Neurol 63: 415-421.
[34]	Banegas I, Prieto I, Segarra AB, et al. (2019) Angiotensin II, dopamine and nitric oxide. An asymmetrical neurovisceral interaction between brain and plasma to regulate blood pressure. AIMS Neurosci 6: 116-127. doi: 10.3934/Neuroscience.2019.3.116
[35]	Banegas I, Segarra AB, Prieto I, et al. (2019) Asymmetrical response of aminopeptidase A in the medial prefrontal cortex and striatum of 6-OHDA-unilaterally-lesioned Wistar Kyoto and spontaneously hypertensive rats. Pharmacol Biochem Behav 182: 12-21. doi: 10.1016/j.pbb.2019.05.007
[36]	Guo SX, Kendrick KM, Zhang J, et al. (2013) Brain-wide functional inter-hemispheric disconnection is a potential biomarker for schizophrenia and distinguishes it from depression. Neuroimage Clin 2: 818-826. doi: 10.1016/j.nicl.2013.06.008
[37]	Xu K, Jiang WY, Ren L, et al. (2013) Impaired interhemispheric connectivity in medication-naive patients with major depressive disorder. J Psychiatry Neurosci 38: 43-48. doi: 10.1503/jpn.110132
[38]	Ben-Shimol E, Gass N, Vollmayr B, et al. (2015) Reduced connectivity and inter-hemispheric symmetry of the sensory system in a rat model of vulnerability to developing depression. Neuroscience 310: 742-750. doi: 10.1016/j.neuroscience.2015.09.057
[39]	Bohlender J, Imboden H (2012) Angiotensinergic neurotransmission in the peripheral autonomic nervous system. Front Biosci (Landmark Ed) 17: 2419-2432. doi: 10.2741/4062
[40]	Foster PS, Harrison DW (2006) Magnitude of cerebral asymmetry at rest: covariation with baseline cardiovascular activity. Brain Cogn 61: 286-297. doi: 10.1016/j.bandc.2006.02.004
[41]	Swislocki AL, LaPier TL, Khuu DT, et al. (1999) Metabolic, hemodynamic, and cardiac effects of captopril in young, spontaneously hypertensive rats. Am J Hypertens 12: 581-589. doi: 10.1016/S0895-7061(99)00012-6
[42]	Thayer JF, Lane RD (2009) Claude Bernard and the heart-brain connection: further elaboration of a model of neurovisceral integration. Neurosci Biobehav Rev 33: 81-88. doi: 10.1016/j.neubiorev.2008.08.004
[43]	Holzer P, Farzi A (2014) Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol 817: 195-219. doi: 10.1007/978-1-4939-0897-4_9
[44]	Prieto I, Hidalgo M, Segarra AB, et al. (2018) Influence of a diet enriched with virgin olive oil or butter on mouse gut microbiota and its correlation to physiological and biochemical parameters related to metabolic syndrome. PLoS One 13: e0190368. doi: 10.1371/journal.pone.0190368
[45]	Hidalgo M, Prieto I, Abriouel H, et al. (2018) Changes in Gut Microbiota Linked to a Reduction in Systolic Blood Pressure in Spontaneously Hypertensive Rats Fed an Extra Virgin Olive Oil-Enriched Diet. Plant Foods Hum Nutr 73: 1-6. doi: 10.1007/s11130-017-0650-1
[46]	Fujiwara Y, Kubo M, Kohata Y, et al. (2011) Association between left-handedness and gastrointestinal symptoms. Digestion 84: 114-118. doi: 10.1159/000324680
[47]	Morris DL, Montgomery SM, Galloway ML, et al. (2001) Inflammatory bowel disease and laterality: is left handedness a risk? Gut 49: 199-202. doi: 10.1136/gut.49.2.199
[48]	Denny K (2009) Handedness and depression: evidence from a large population survey. Laterality 14: 246-255. doi: 10.1080/13576500802362869
[49]	Işcen S, Özenç S, Tavlasoglu U (2014) Association between left-handedness and cardiac autonomic function in healthy young men. Pacing Clin Electrophysiol 37: 884-888. doi: 10.1111/pace.12365
[50]	Vagena E, Ryu JK, Baeza-Raja B, et al. (2019) A high-fat diet promotes depression-like behavior in mice by suppressing hypothalamic PKA signaling. Transl Psychiatry 9: 141. doi: 10.1038/s41398-019-0470-1
[51]	Sarris J, Murphy J, Mischoulon D, et al. (2016) Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses. Am J Psychiatry 173: 575-587. doi: 10.1176/appi.ajp.2016.15091228
[52]	Segarra AB, Ramirez M, Banegas I, et al. (2008) Dietary fat influences testosterone, cholesterol, aminopeptidase A, and blood pressure in male rats. Horm Metab Res 40: 289-291. doi: 10.1055/s-2008-1046800
[53]	Vancassel S, Aïd S, Pifferi F, et al. (2005) Cerebral asymmetry and behavioral lateralization in rats chronically lacking n-3 polyunsaturated fatty acids. Biol Psychiatry 58: 805-811. doi: 10.1016/j.biopsych.2005.04.045
[54]	Tryon MS, Stanhope KL, Epel ES, et al. (2015) Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body. J Clin Endocrinol Metab 100: 2239-2247. doi: 10.1210/jc.2014-4353
[55]	Redondo-Useros N, Nova E, González-Zancada N, et al. (2020) Microbiota and Lifestyle: A Special Focus on Diet. Nutrients 12: E1776. doi: 10.3390/nu12061776

Reader Comments

Your name:*

Email:*
© 2020 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)