Грелиновые механизмы пищевого вознаграждения. Часть 2. Взаимодействие грелина с гормонами, нейропептидами и другими эндогенными лигандами

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Аннотация

Гормон голода, грелин, вырабатывается не только в ответ на недостаток пищи, но и выделяется при различных видах стресса. В последние годы подъем уровня грелина стал рассматриваться как неотъемлемый компонент стресс-реакции. Обзор посвящен грелин-зависимым механизмам, обеспечивающим реципрокное взаимодействие между осью гипоталамус – гипофиз – кора надпочечников и дофаминергической системой вознаграждения. Рассматриваются прямые и обратные связи между стресс-реализующей системой паравентрикулярного ядра, нейросетями латерального гипоталамуса и дугообразного ядра (образующие центры голода/насыщения), и мезолимбической системой награды. Обсуждается роль периферических гормонов сытости и глюкокортикоидов в регуляции мотивации и подкрепления, а также участие эндогенных опиоидных и эндоканнабиноидных рецепторов в «обучении» дофаминергических нейронов вентральной области покрышки и гиппокампа.

Об авторах

Борис Андреевич Рейхардт

Институт экспериментальной медицины

Автор, ответственный за переписку.
Email: reihardt@mail.ru
ORCID iD: 0000-0003-3371-9161
SPIN-код: 8980-1073

канд. мед. наук, старший научный сотрудник

Россия, 197376, Санкт-Петербург, ул. Академика Павлова, д. 12

Петр Дмитриевич Шабанов

Институт экспериментальной медицины

Email: pdshabanov@mail.ru
ORCID iD: 0000-0003-1464-1127
SPIN-код: 8974-7477

д-р мед. наук, профессор, заведующий отделом

Россия, 197376, Санкт-Петербург, ул. Академика Павлова, д. 12

Список литературы

  1. Perelló M, Zigman JM. The role of ghrelin in reward-based eating. Biol Psychiatry. 2012;72(5):347–353. doi: 10.1016/j.biopsych.2012.02.016
  2. Asakawa A, Inui A, Kaga T, et al. A role of ghrelin in neuroendocrine and behavioral responses to stress in mice. Neuroendocrinology. 2001;74(3):143–147. doi: 10.1159/000054680
  3. Kristenssson E, Sundqvist M, Astin M, et al. Acute psychological stress raises plasma ghrelin in the rat. Regul Pept. 2006; 134(2–3):114–117. doi: 10.1016/j.regpep.2006.02.003
  4. Lutter M, Sakata I, Osborne-Lawrence S, et al. The orexigenic hormone ghrelin defends against depressive symptoms of chronic stress. Nat Neurosci. 2008;11(7):752–753. doi: 10.1038/nn.2139
  5. Chuang JC, Perello M, Sakata I, et al. Ghrelin mediates stress-induced food-reward behavior in mice. J Clin Invest. 2011;121(7): 2684–2692. doi: 10.1172/JCI57660
  6. Ochi M, Tominaga K, Tanaka F, et al. Effect of chronic stress on gastric emptying and plasma ghrelin levels in rats. Life Sci. 2008;82(15–16):862–868. doi: 10.1016/j.lfs.2008.01.020
  7. Stengel A, Wang L, Taché Y. Stress-related alterations of acyl and desacyl ghrelin circulating levels: mechanisms and functional implications. Peptides. 2011;32(11):2208–2217. doi: 10.1016/j.peptides.2011.07.002
  8. Nestler EJ, Hyman SE. Animal models of neuropsychiatric disorders. Nat Neurosci. 2010;13(10):1161–1169. doi: 10.1038/nn.2647
  9. Patterson ZR, Ducharme R, Anisman H, Abizaid A. Altered metabolic and neurochemical responses to chronic unpredictable stressors in ghrelin receptor-deficient mice. Eur J Neurosci. 2010;32(4):632–639. doi: 10.1111/j.1460-9568.2010.07310.x
  10. Rouach V, Bloch M, Rosenberg N, et al. The acute ghrelin response to a psychological stress challenge does not predict the post-stress urge to eat. Psychoneuroendocrinology. 2007;32(6):693–702. doi: 10.1016/j.psyneuen.2007.04.010
  11. Raspopow K, Abizaid A, Matheson K, Anisman H. Psychosocial stressor effects on cortisol and ghrelin in emotional and non-emotional eaters: influence of anger and shame. Horm Behav. 2010;58(4):677–684. doi: 10.1016/j.yhbeh.2010.06.003
  12. Zhao TJ, Sakata I, Li RL, et al. Ghrelin secretion stimulated by {beta}1-adrenergic receptors in cultured ghrelinoma cells and in fasted mice. Proc Natl Acad Sci USA. 2010;107(36):15868–15873. doi: 10.1073/pnas.1011116107
  13. Mundinger TO, Cummings DE, Taborsky GJ Jr. Direct stimulation of ghrelin secretion by sympathetic nerves. Endocrinology. 2006;147(6):2893–2901. doi: 10.1210/en.2005-1182
  14. Sgoifo A, Koolhaas J, De Boer S, et al. Social stress, autonomic neural activation, and cardiac activity in rats. Neurosci Biobehav Rev. 1999;23(7):915–923. doi: 10.1016/s0149-7634(99)00025-1
  15. Cabral A, Fernandez G, Perello M. Analysis of brain nuclei accessible to ghrelin present in the cerebrospinal fluid. Neuroscience. 2013;253:406–415. doi: 10.1016/j.neuroscience.2013.09.008
  16. Wren AM, Small CJ, Fribbens CV, et al. The hypothalamic mechanisms of the hypophysiotropic action of ghrelin. Neuroendocrinology. 2002;76(5):316–324. doi: 10.1159/000066629
  17. Mozid AM, Tringali G, Forsling ML, et al. Ghrelin is released from rat hypothalamic explants and stimulates corticotrophin-releasing hormone and arginine-vasopressin. Horm Metab Res. 2003;35(8):455–459. doi: 10.1055/s-2003-41801
  18. Bali A, Jaggi AS. An Integrative review on role and mechanisms of ghrelin in stress, anxiety and depression. Curr Drug Targets. 2016;17(5):495–507. doi: 10.2174/1389450116666150518095650
  19. Kageyama K, Kumata Y, Akimoto K, et al. Ghrelin stimulates corticotropin-releasing factor and vasopressin gene expression in rat hypothalamic 4B cells. Stress. 2011;14(5):520–529. doi: 10.3109/10253890.2011.558605
  20. Kageyama K, Akimoto K, Yamagata S, et al. Dexamethasone stimulates the expression of ghrelin and its receptor in rat hypothalamic 4B cells. Regul Pept. 2012;174(1–3):12–17. doi: 10.1016/j.regpep.2011.11.003
  21. Aguilera G, Liu Y. The molecular physiology of CRH neurons. Front Neuroendocrinol. 2012;33(1):67–84. doi: 10.1016/j.yfrne.2011.08.002
  22. Deussing JM, Chen A. The Corticotropin-releasing factor family: physiology of the stress response. Physiol Rev. 2018;98(4): 2225–2286. doi: 10.1152/physrev.00042.2017
  23. Sawchenko PE, Swanson LW. Localization, colocalization, and plasticity of corticotropin-releasing factor immunoreactivity in rat brain. Fed Proc. 1985;44(1 Pt 2):221–227.
  24. Foster MT, Warne JP, Ginsberg AB, et al. Palatable foods, stress, and energy stores sculpt corticotropin-releasing factor, adrenocorticotropin, and corticosterone concentrations after restraint. Endocrinology. 2009;150(5):2325–2333. doi: 10.1210/en.2008-1426
  25. Suemaru S, Hashimoto K, Hattori T, et al. Starvation-induced changes in rat brain corticotropin-releasing factor (CRF) and pituitary-adrenocortical response. Life Sci. 1986;39(13):1161–1166. doi: 10.1016/0024-3205(86)90347-4
  26. Cavagnini F, Croci M, Putignano P, et al. Glucocorticoids and neuroendocrine function. Int J Obes Relat Metab Disord. 2000;24.Suppl 2: S77–S79. doi: 10.1038/sj.ijo.0801284
  27. Carlini VP, Monzón ME, Varas MM, et al. Ghrelin increases anxiety-like behavior and memory retention in rats. Biochem Biophys Res Commun. 2002;299(5):739–743. doi: 10.1016/s0006-291x(02)02740-7
  28. Cabral A, Suescun O, Zigman JM, Perello M. Ghrelin indirectly activates hypophysiotropic CRF neurons in rodents. PLoS One. 2012;7(2): e31462. doi: 10.1371/journal.pone.0031462
  29. Willesen MG, Kristensen P, Rømer J. Co-localization of growth hormone secretagogue receptor and NPY mRNA in the arcuate nucleus of the rat. Neuroendocrinology. 1999;70(5):306–316. doi: 10.1159/000054491
  30. Li C, Chen P, Smith MS. Corticotropin releasing hormone neurons in the paraventricular nucleus are direct targets for neuropeptide Y neurons in the arcuate nucleus: an anterograde tracing study. Brain Res. 2000;854(1–2):122–129. doi: 10.1016/s0006-8993(99)02324-0
  31. Campbell RE, Grove KL, Smith MS. Distribution of corticotropin releasing hormone receptor immunoreactivity in the rat hypothalamus: coexpression in neuropeptide Y and dopamine neurons in the arcuate nucleus. Brain Res. 2003;973(2):223–232. doi: 10.1016/s0006-8993(03)02487-9
  32. Yakabi K, Noguchi M, Ohno S, et al. Urocortin 1 reduces food intake and ghrelin secretion via CRF(2) receptors. Am J Physiol Endocrinol Metab. 2011;301(1): E72–E82. doi: 10.1152/ajpendo.00695.2010
  33. Luque RM, Park S, Kineman RD. Severity of the catabolic condition differentially modulates hypothalamic expression of growth hormone-releasing hormone in the fasted mouse: potential role of neuropeptide Y and corticotropin-releasing hormone. Endocrinology. 2007;148(1):300–309. doi: 10.1210/en.2006-0592
  34. Bchini-Hooft van Huijsduijnen OB, Rohner-Jeanrenaud F, Jeanrenaud B. Hypothalamic neuropeptide Y messenger ribonucleic acid levels in pre-obese and genetically obese (fa/fa) rats; potential regulation thereof by corticotropin-releasing factor. J Neuroendocrinol. 1993;5(4):381–386. doi: 10.1111/j.1365-2826.1993.tb00498.x
  35. Palmiter RD, Erickson JC, Hollopeter G, et al. Life without neuropeptide Y. Recent Prog Horm Res. 1998;53:163–199.
  36. Nakayama S, Nishiyama M, Iwasaki Y, et al. Corticotropin-releasing hormone (CRH) transgenic mice display hyperphagia with increased Agouti-related protein mRNA in the hypothalamic arcuate nucleus. Endocr J. 2011;58(4):279–286. doi: 10.1507/endocrj.k10e-370
  37. Suda T, Tozawa F, Iwai I, et al. Neuropeptide Y increases the corticotropin-releasing factor messenger ribonucleic acid level in the rat hypothalamus. Brain Res Mol Brain Res. 1993;18(4):311–315. doi: 10.1016/0169-328x(93)90094-6
  38. Dimitrov EL, DeJoseph MR, Brownfield MS, Urban JH. Involvement of neuropeptide Y Y1 receptors in the regulation of neuroendocrine corticotropin-releasing hormone neuronal activity. Endocrinology. 2007;148(8):3666–3673. doi: 10.1210/en.2006-1730
  39. Pleil KE, Rinker JA, Lowery-Gionta EG, et al. NPY signaling inhibits extended amygdala CRF neurons to suppress binge alcohol drinking. Nat Neurosci. 2015;18(4):545–552. doi: 10.1038/nn.3972
  40. Kask A, Nguyen HP, Pabst R, Von Hörsten S. Neuropeptide Y Y1 receptor-mediated anxiolysis in the dorsocaudal lateral septum: functional antagonism of corticotropin-releasing hormone-induced anxiety. Neuroscience. 2001;104(3):799–806. doi: 10.1016/s0306-4522(01)00116-6
  41. Maniam J, Morris MJ. The link between stress and feeding behaviour. Neuropharmacology. 2012;63(1):97–110. doi: 10.1016/j.neuropharm.2012.04.017
  42. Ciccocioppo R, Gehlert DR, Ryabinin A, et al. Stress-related neuropeptides and alcoholism: CRH, NPY, and beyond. Alcohol. 2009;43(7):491–498. doi: 10.1016/j.alcohol.2009.08.003
  43. Winsky-Sommerer R, Yamanaka A, Diano S, et al. Interaction between the corticotropin-releasing factor system and hypocretins (orexins): a novel circuit mediating stress response. J Neurosci. 2004;24(50):11439–11448. doi: 10.1523/JNEUROSCI.3459-04.2004
  44. Trivedi P, Yu H, MacNeil DJ, et al. Distribution of orexin receptor mRNA in the rat brain. FEBS Lett. 1998;438(1–2):71–75. doi: 10.1016/s0014-5793(98)01266-6
  45. Hervieu GJ, Cluderay JE, Harrison DC, et al. Gene expression and protein distribution of the orexin-1 receptor in the rat brain and spinal cord. Neuroscience. 2001;103(3):777–797. doi: 10.1016/s0306-4522(01)00033-11
  46. Cluderay JE, Harrison DC, Hervieu GJ. Protein distribution of the orexin-2 receptor in the rat central nervous system. Regul Pept. 2002;104(1–3):131–144. doi: 10.1016/s0167-0115(01)00357-3
  47. Bäckberg M, Hervieu G, Wilson S, Meister B. Orexin receptor-1 (OX-R1) immunoreactivity in chemically identified neurons of the hypothalamus: focus on orexin targets involved in control of food and water intake. Eur J Neurosci. 2002;15(2):315–328. doi: 10.1046/j.0953-816x.2001.01859.x
  48. Russell SH, Small CJ, Dakin CL, et al. The central effects of orexin-A in the hypothalamic-pituitary-adrenal axis in vivo and in vitro in male rats. J Neuroendocrinol. 2001;13(6):561–566. doi: 10.1046/j.1365-2826.2001.00672.x
  49. Samson WK, Taylor MM, Follwell M, Ferguson AV. Orexin actions in hypothalamic paraventricular nucleus: physiological consequences and cellular correlates. Regul Pept. 2002;104(1–3): 97–103. doi: 10.1016/s0167-0115(01)00353-6
  50. Bonnavion P, Jackson AC, Carter ME, de Lecea L. Antagonistic interplay between hypocretin and leptin in the lateral hypothalamus regulates stress responses. Nat Commun. 2015;6:6266. doi: 10.1038/ncomms7266
  51. Blais A, Drouin G, Chaumontet C, et al. Impact of orexin-A treatment on food intake, energy metabolism and body weight in mice. PLoS One. 2017;12(1): e0169908. doi: 10.1371/journal.pone.0169908
  52. Sutcliffe JG, de Lecea L. The hypocretins: excitatory neuromodulatory peptides for multiple homeostatic systems, including sleep and feeding. J Neurosci Res. 2000;62(2):161–168. doi: 10.1002/1097-4547(20001015)62:2<161::AID-JNR1>3.0.CO;2-1
  53. Slater PG, Noches V, Gysling K. Corticotropin-releasing factor type-2 receptor and corticotropin-releasing factor-binding protein coexist in rat ventral tegmental area nerve terminals originated in the lateral hypothalamic area. Eur J Neurosci. 2016;43(2):220–229. doi: 10.1111/ejn.13113
  54. Horvath TL, Peyron C, Diano S, et al. Hypocretin (orexin) activation and synaptic innervation of the locus coeruleus noradrenergic system. J Comp Neurol. 1999;415(2):145–159.
  55. Grafe LA, Bhatnagar S. Orexins and stress. Front Neuroendocrinol. 2018;51:132–145. doi: 10.1016/j.yfrne.2018.06.003
  56. Sargin D. The role of the orexin system in stress response. Neuropharmacology. 2019;154:68–78. doi: 10.1016/j.neuropharm.2018.09.034
  57. James MH, Campbell EJ, Dayas CV. Role of the orexin/hypocretin system in stress-related psychiatric disorders. Curr Top Behav Neurosci. 2017;33:197–219. doi: 10.1007/7854_2016_56
  58. Orozco-Cabal L, Pollandt S, Liu J, et al. Regulation of synaptic transmission by CRF receptors. Rev Neurosci. 2006;17(3): 279–307. doi: 10.1515/revneuro.2006.17.3.279
  59. Ungless MA, Singh V, Crowder TL, et al. Corticotropin-releasing factor requires CRF binding protein to potentiate NMDA receptors via CRF receptor 2 in dopamine neurons. Neuron. 2003;39(3):401–407. doi: 10.1016/s0896-6273(03)00461-6
  60. Hillhouse EW, Grammatopoulos DK. The molecular mechanisms underlying the regulation of the biological activity of corticotropin-releasing hormone receptors: implications for physiology and pathophysiology. Endocr Rev. 2006;27(3):260–286. doi: 10.1210/er.2005-0034
  61. Van Pett K, Viau V, Bittencourt JC, et al. Distribution of mRNAs encoding CRF receptors in brain and pituitary of rat and mouse. J Comp Neurol. 2000;428(2):191–212. doi: 10.1002/1096-9861(20001211)428:2<191::aid-cne1>3.0.co;2-u
  62. Ungless MA, Argilli E, Bonci A. Effects of stress and aversion on dopamine neurons: implications for addiction. Neurosci Biobehav Rev. 2010;35(2):151–156. doi: 10.1016/j.neubiorev.2010.04.006
  63. Korotkova TM, Brown RE, et al. Effects of arousal- and feeding-related neuropeptides on dopaminergic and GABAergic neurons in the ventral tegmental area of the rat. Eur J Neurosci. 2006;23(10): 2677–2685. doi: 10.1111/j.1460-9568.2006.04792.x
  64. Wanat MJ, Hopf FW, Stuber GD, et al. Corticotropin-releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C-dependent enhancement of Ih. J Physiol. 2008;586(8):2157–2170. doi: 10.1113/jphysiol.2007.150078
  65. Holly EN, Boyson CO, Montagud-Romero S, et al. Episodic social stress-escalated cocaine self-administration: role of phasic and tonic corticotropin releasing factor in the anterior and posterior ventral tegmental area. J Neurosci. 2016;36(14):4093–4105. doi: 10.1523/JNEUROSCI.2232-15.2016
  66. Tagliaferro P, Morales M. Synapses between corticotropin-releasing factor-containing axon terminals and dopaminergic neurons in the ventral tegmental area are predominantly glutamatergic. J Comp Neurol. 2008;506(4):616–626. doi: 10.1002/cne.21576
  67. Wang B, Shaham Y, Zitzman D, et al. Cocaine experience establishes control of midbrain glutamate and dopamine by corticotropin-releasing factor: a role in stress-induced relapse to drug seeking. J Neurosci. 2005;25(22):5389–5396. doi: 10.1523/JNEUROSCI.0955-05.2005
  68. Fitzgerald LW, Ortiz J, Hamedani AG, Nestler EJ. Drugs of abuse and stress increase the expression of GluR1 and NMDAR1 glutamate receptor subunits in the rat ventral tegmental area: common adaptations among cross-sensitizing agents. J Neurosci. 1996;16(1): 274–282. doi: 10.1523/JNEUROSCI.16-01-00274.1996
  69. Whitaker LR, Degoulet M, Morikawa H. Social deprivation enhances VTA synaptic plasticity and drug-induced contextual learning. Neuron. 2013;77(2):335–345. doi: 10.1016/j.neuron.2012.11.022
  70. Stelly CE, Pomrenze MB, Cook JB, Morikawa H. Repeated social defeat stress enhances glutamatergic synaptic plasticity in the VTA and cocaine place conditioning. Elife. 2016;5:e15448. doi: 10.7554/eLife.15448
  71. Beckstead MJ, Gantz SC, Ford CP, et al. CRF enhancement of GIRK channel-mediated transmission in dopamine neurons. Neuropsychopharmacology. 2009;34(8):1926–1935. doi: 10.1038/npp.2009.25
  72. Lemos JC, Wanat MJ, Smith JS, et al. Severe stress switches CRF action in the nucleus accumbens from appetitive to aversive. Nature. 2012;490(7420):402–406. doi: 10.1038/nature11436
  73. Munck A, Guyre PM, Holbrook NJ. Physiological functions of glucocorticoids in stress and their relation to pharmacological actions. Endocr Rev. 1984;5(1):25–44. doi: 10.1210/edrv-5-1-25
  74. Lambert WM, Xu CF, Neubert TA, Chao MV, Garabedian MJ, Jeanneteau FD. Brain-derived neurotrophic factor signaling rewrites the glucocorticoid transcriptome via glucocorticoid receptor phosphorylation. Mol Cell Biol. 2013;33(18):3700–3714. doi: 10.1128/MCB.00150-13
  75. Weikum ER, Knuesel MT, Ortlund EA, Yamamoto KR. Glucocorticoid receptor control of transcription: precision and plasticity via allostery. Nat Rev Mol Cell Biol. 2017;18(3):159–174. doi: 10.1038/nrm.2016.152
  76. Makara GB, Haller J. Non-genomic effects of glucocorticoids in the neural system. Evidence, mechanisms and implications. Prog Neurobiol. 2001;65(4):367–390. doi: 10.1016/s0301-0082(01)00012-0
  77. Groeneweg FL, Karst H, de Kloet ER, Joëls M. Mineralocorticoid and glucocorticoid receptors at the neuronal membrane, regulators of nongenomic corticosteroid signalling. Mol Cell Endocrinol. 2012;350(2):299–309. doi: 10.1016/j.mce.2011.06.020
  78. Morimoto M, Morita N, Ozawa H, et al. Distribution of glucocorticoid receptor immunoreactivity and mRNA in the rat brain: an immunohistochemical and in situ hybridization study. Neurosci Res. 1996;26(3):235–269. doi: 10.1016/s0168-0102(96)01105-4
  79. Vyas S, Rodrigues AJ, Silva JM, et al. Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration. Neural Plast. 2016;2016:6391686. doi: 10.1155/2016/6391686
  80. Brain Reward Systems and Abuse. Engel J., Oreland L., et al. editors. Raven Press: New York; 1987. 198 p.
  81. Orchinik M, Licht P, Crews D. Plasma steroid concentrations change in response to sexual behavior in Bufo marinus. Horm Behav. 1988;22(3):338–350. doi: 10.1016/0018-506x(88)90006-2
  82. Piazza PV, Le Moal M. Glucocorticoids as a biological substrate of reward: physiological and pathophysiological implications. Brain Res Brain Res Rev. 1997;25(3):359–372. doi: 10.1016/s0165-0173(97)00025-8
  83. Honma KI, Honma S, Hiroshige T. Feeding-associated corticosterone peak in rats under various feeding cycles. Am J Physiol. 1984;246(5 Pt 2): R721–R726. doi: 10.1152/ajpregu.1984.246.5.R721
  84. Krieger DT. Food and water restriction shifts corticosterone, temperature, activity and brain amine periodicity. Endocrinology. 1974;95(5):1195–1201. doi: 10.1210/endo-95-5-1195
  85. Epel E, Lapidus R, McEwen B, Brownell K. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology. 2001;26(1): 37–49. doi: 10.1016/s0306-4530(00)00035-4
  86. Ulrich-Lai YM, Christiansen AM, Ostrander MM, et al. Pleasurable behaviors reduce stress via brain reward pathways. Proc Natl Acad Sci USA. 2010;107(47):20529–20534. doi: 10.1073/pnas.1007740107
  87. Bell ME, Bhatnagar S, Liang J, et al. Voluntary sucrose ingestion, like corticosterone replacement, prevents the metabolic deficits of adrenalectomy. J Neuroendocrinol. 2000;12(5):461–470. doi: 10.1046/j.1365-2826.2000.00488.x
  88. Bhatnagar S, Bell ME, Liang J, et al. Corticosterone facilitates saccharin intake in adrenalectomized rats: does corticosterone increase stimulus salience? J Neuroendocrinol. 2000;12(5):453–460. doi: 10.1046/j.1365-2826.2000.00487.x
  89. Dallman MF, Pecoraro NC, la Fleur SE. Chronic stress and comfort foods: self-medication and abdominal obesity. Brain Behav Immun. 2005;19(4):275–280. doi: 10.1016/j.bbi.2004.11.004
  90. Micco DJ Jr, McEwen BS, Shein W. Modulation of behavioral inhibition in appetitive extinction following manipulation of adrenal steroids in rats: implications for involvement of the hippocampus. J Comp Physiol Psychol. 1979;93(2):323–329. doi: 10.1037/h0077560
  91. Weiss JM, McEwen BS, Silva MT, Kalkut M. Pituitary-adrenal alterations and fear responding. Am J Physiol. 1970;218(3): 864–868. doi: 10.1152/ajplegacy.1970.218.3.864
  92. Piazza PV, Deroche V, Deminière JM, et al. Corticosterone in the range of stress-induced levels possesses reinforcing properties: implications for sensation-seeking behaviors. Proc Natl Acad Sci USA. 1993;90(24):11738–11742. doi: 10.1073/pnas.90.24.11738
  93. Deroche V, Piazza PV, Deminière JM, et al. Rats orally self-administer corticosterone. Brain Res. 1993;622(1–2):315–320. doi: 10.1016/0006-8993(93)90837-d
  94. Piazza PV, Barrot M, Rougé-Pont F, et al. Suppression of glucocorticoid secretion and antipsychotic drugs have similar effects on the mesolimbic dopaminergic transmission. Proc Natl Acad Sci USA. 1996;93(26):15445–15450. doi: 10.1073/pnas.93.26.15445
  95. Badiani A, Morano MI, Akil H, Robinson TE. Circulating adrenal hormones are not necessary for the development of sensitization to the psychomotor activating effects of amphetamine. Brain Res. 1995;673(1):13–24. doi: 10.1016/0006-8993(94)01365-o
  96. Piazza PV, Rougé-Pont F, Deroche V, et al. Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission. Proc Natl Acad Sci USA. 1996;93(16):8716–8720. doi: 10.1073/pnas.93.16.8716
  97. Lewis EJ, Harrington CA, Chikaraishi DM. Transcriptional regulation of the tyrosine hydroxylase gene by glucocorticoid and cyclic AMP. Proc Natl Acad Sci USA. 1987;84(11):3550–3554. doi: 10.1073/pnas.84.11.3550
  98. Ortiz J, DeCaprio JL, Kosten TA, Nestler EJ. Strain-selective effects of corticosterone on locomotor sensitization to cocaine and on levels of tyrosine hydroxylase and glucocorticoid receptor in the ventral tegmental area. Neuroscience. 1995;67(2):383–397. doi: 10.1016/0306-4522(95)00018-e
  99. Rani CS, Elango N, Wang SS, et al. Identification of an activator protein-1-like sequence as the glucocorticoid response element in the rat tyrosine hydroxylase gene. Mol Pharmacol. 2009;75(3): 589–598. doi: 10.1124/mol.108.051219
  100. Busceti CL, Ferese R, Bucci D, et al. Corticosterone upregulates gene and protein expression of catecholamine markers in organotypic brainstem cultures. Int J Mol Sci. 2019;20(12):2901. doi: 10.3390/ijms20122901
  101. Niwa M, Jaaro-Peled H, Tankou S, et al. Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids. Science. 2013;339(6117):335–339. doi: 10.1126/science.1226931
  102. Núñez C, Földes A, Pérez-Flores D, et al. Elevated glucocorticoid levels are responsible for induction of tyrosine hydroxylase mRNA expression, phosphorylation, and enzyme activity in the nucleus of the solitary tract during morphine withdrawal. Endocrinology. 2009;150(7):3118–3127. doi: 10.1210/en.2008-1732
  103. Jalali Mashayekhi F, Rasti M, Khoshdel Z, Owji AA. Expression levels of the tyrosine hydroxylase gene and histone modifications around its promoter in the locus coeruleus and ventral tegmental area of rats during forced abstinence from morphine. Eur Addict Res. 2018;24(6):304–311. doi: 10.1159/000495362
  104. Phuc Le P, Friedman JR, Schug J, et al. Glucocorticoid receptor-dependent gene regulatory networks. PLoS Genet. 2005;1(2):e16. doi: 10.1371/journal.pgen.0010016
  105. Lindley SE, Bengoechea TG, Schatzberg AF, Wong DL. Glucocorticoid effects on mesotelencephalic dopamine neurotransmission. Neuropsychopharmacology. 1999;21(3):399–407. doi: 10.1016/S0893-133X(98)00103-1
  106. Ho-Van-Hap A, Babineau LM, Berlinguet L. Hormonal action on monoamine oxidase activity in rats. Can J Biochem. 1967;45(3): 355–362. doi: 10.1139/o67-042
  107. Caesar PM, Collins GG, Sandler M. Catecholamine metabolism and monoamine oxidase activity in adrenalectomized rats. Biochem Pharmacol. 1970;19(3):921–926. doi: 10.1016/0006-2952(70)90255-8
  108. Parvez H, Parvez S. The regulation of monoamine oxidase activity by adrenal cortical steroids. Acta Endocrinol (Copenh). 1973;73(3):509–517. doi: 10.1530/acta.0.0730509
  109. Rothschild AJ, Langlais PJ, Schatzberg AF, et al. The effects of a single acute dose of dexamethasone on monoamine and metabolite levels in rat brain. Life Sci. 1985;36(26):2491–2501. doi: 10.1016/0024-3205(85)90145-6
  110. Veals JW, Korduba CA, Symchowicz S. Effect of dexamethasone on monoamine oxidase inhibiton by iproniazid in rat brain. Eur J Pharmacol. 1977;41(3):291–299. doi: 10.1016/0014-2999(77)90322-3
  111. Iversen LL, Salt PJ. Inhibition of catecholamine Uptake-2 by steroids in the isolated rat heart. Br J Pharmacol. 1970;40(3): 528–530. doi: 10.1111/j.1476-5381.1970.tb10637.x
  112. Williams PB, Hudgins PM. Actions of hydrocortisone, desoxycorticosterone acetate and progesterone on 14C-norepinephrine uptake and metabolism by rabbit aorta. Pharmacology. 1973;9(5): 262–269. doi: 10.1159/000136394
  113. Gilad GM, Rabey JM, Gilad VH. Presynaptic effects of glucocorticoids on dopaminergic and cholinergic synaptosomes. Implications for rapid endocrine-neural interactions in stress. Life Sci. 1987;40(25):2401–2408. doi: 10.1016/0024-3205(87)90754-5
  114. Shabanov PD, Lebedev AA, Pavlenko VP. Gormony gipofizarno-nadpochechnikovoi sistemy v mekhanizmakh mozgovogo podkrepleniya. Reviews on Clinical Pharmacology and Drug Therapy. 2003;2(2):35–51. (In Russ.)
  115. Selye H. Stress: The Physiology and the Pathology of Exposure to Stress. Montreal: Acta Medica Publication, 1950.
  116. Sugama S, Kakinuma Y. Loss of dopaminergic neurons occurs in the ventral tegmental area and hypothalamus of rats following chronic stress: Possible pathogenetic loci for depression involved in Parkinson’s disease. Neurosci Res. 2016;111:48–55. doi: 10.1016/j.neures.2016.04.008
  117. Kaska S, Brunk R, Kechner M, Mazei-Robison M. Regulation of cytoskeletal remodeling proteins in the ventral tegmental area by morphine, stress, and TORC2. FASEB J. 2017;31(S1):985.12. doi: 10.1096/fasebj.31.1_supplement.985.12
  118. Douma EH, de Kloet ER. Stress-induced plasticity and functioning of ventral tegmental dopamine neurons. Neurosci Biobehav Rev. 2020;108:48–77. doi: 10.1016/j.neubiorev.2019.10.015
  119. Krishnan V, Han MH, Graham DL, et al. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007;131(2):391–404. doi: 10.1016/j.cell.2007.09.018
  120. Qu Y, Yang C, Ren Q, et al. Regional differences in dendritic spine density confer resilience to chronic social defeat stress. Acta Neuropsychiatr. 2018;30(2):117–122. doi: 10.1017/neu.2017.16
  121. Holly EN, Miczek KA. Ventral tegmental area dopamine revisited: effects of acute and repeated stress. Psychopharmacology (Berl). 2016;233(2):163–186. doi: 10.1007/s00213-015-4151-3
  122. Ungless MA, Magill PJ, Bolam JP. Uniform inhibition of dopamine neurons in the ventral tegmental area by aversive stimuli. Science. 2004;303(5666):2040–2042. doi: 10.1126/science.1093360
  123. Brischoux F, Chakraborty S, Brierley DI, Ungless MA. Phasic excitation of dopamine neurons in ventral VTA by noxious stimuli. Proc Natl Acad Sci USA. 2009;106(12):4894–4899. doi: 10.1073/pnas.0811507106
  124. Navratilova E, Xie JY, Okun A, et al. Pain relief produces negative reinforcement through activation of mesolimbic reward-valuation circuitry. Proc Natl Acad Sci USA. 2012;109(50):20709–20713. doi: 10.1073/pnas.1214605109
  125. Cohen JY, Haesler S, Vong L, et al. Neuron-type-specific signals for reward and punishment in the ventral tegmental area. Nature. 2012;482(7383):85–88. doi: 10.1038/nature10754
  126. Lammel S, Lim BK, Malenka RC. Reward and aversion in a heterogeneous midbrain dopamine system. Neuropharmacology. 2014;76 Pt B(0 0):351–359. doi: 10.1016/j.neuropharm.2013.03.019
  127. Neurobiological mechanisms of the rewars and punishment systems in the brain afteractivation of nucleus accumbens. Reviews on Clinical Pharmacology and Drug Therapy. 2013;11(3):3–9. (In Russ.)
  128. Valentino RJ, Van Bockstaele E. Endogenous opioids: opposing stress with a cost. F1000Prime Rep. 2015;7:58. doi: 10.12703/P7-58
  129. Fields HL, Margolis EB. Understanding opioid reward. Trends Neurosci. 2015;38(4):217–225. doi: 10.1016/j.tins.2015.01.002
  130. Le Merrer J, Becker JA, Befort K, Kieffer BL. Reward processing by the opioid system in the brain. Physiol Rev. 2009;89(4): 1379–1412. doi: 10.1152/physrev.00005.2009
  131. Toubia T, Khalife T. The endogenous opioid system: role and dysfunction caused by opioid therapy. Clin Obstet Gynecol. 2019;62(1):3–10. doi: 10.1097/GRF.0000000000000409
  132. Devine DP, Wise RA. Self-administration of morphine, DAMGO, and DPDPE into the ventral tegmental area of rats. J Neurosci. 1994;14(4):1978–1984. doi: 10.1523/JNEUROSCI.14-04-01978.1994
  133. Kudo T, Konno K, Uchigashima M, et al. GABAergic neurons in the ventral tegmental area receive dual GABA/enkephalin-mediated inhibitory inputs from the bed nucleus of the stria terminalis. Eur J Neurosci. 2014;39(11):1796–1809. doi: 10.1111/ejn.12503
  134. James A, Williams J. Basic opioid pharmacology an update. Br J Pain. 2020;14(2):115–121. doi: 10.1177/2049463720911986
  135. Pasternak GW. Mu opioid pharmacology: 40 years to the promised land. Adv Pharmacol. 2018;82:261–291. doi: 10.1016/bs.apha.2017.09.006
  136. Mercer AJ, Hentges ST, Meshul CK, Low MJ. Unraveling the central proopiomelanocortin neural circuits. Front Neurosci. 2013;7:19. doi: 10.3389/fnins.2013.00019
  137. Qiu J, Wagner EJ, Rønnekleiv OK, Kelly MJ. Insulin and leptin excite anorexigenic pro-opiomelanocortin neurones via activation of TRPC5 channels. J Neuroendocrinol. 2018;30(2):10.1111/jne.12501. doi: 10.1111/jne.12501
  138. Ghamari-Langroudi M, Colmers WF, Cone RD. PYY3-36 inhibits the action potential firing activity of POMC neurons of arcuate nucleus through postsynaptic Y2 receptors. Cell Metab. 2005;2(3):191–199. doi: 10.1016/j.cmet.2005.08.003
  139. Chen SR, Chen H, Zhou JJ, et al. Ghrelin receptors mediate ghrelin-induced excitation of agouti-related protein/neuropeptide Y but not pro-opiomelanocortin neurons. J Neurochem. 2017;142(4):512–520. doi: 10.1111/jnc.14080
  140. Romero-Picó A, Vázquez MJ, González-Touceda D, et al. Hypothalamic κ-opioid receptor modulates the orexigenic effect of ghrelin. Neuropsychopharmacology. 2013;38(7):1296–1307. doi: 10.1038/npp.2013.28
  141. Bodnar RJ. Endogenous opioid modulation of food intake and body weight: Implications for opioid influences upon motivation and addiction. Peptides. 2019;116:42–62. doi: 10.1016/j.peptides.2019.04.00
  142. Zheng H, Patterson LM, Berthoud HR. Orexin signaling in the ventral tegmental area is required for high-fat appetite induced by opioid stimulation of the nucleus accumbens. J Neurosci. 2007;27(41):11075–11082. doi: 10.1523/JNEUROSCI.3542-07.2007
  143. Barnes MJ, Primeaux SD, Bray GA. Food deprivation increases the mRNA expression of micro-opioid receptors in the ventral medial hypothalamus and arcuate nucleus. Am J Physiol Regul Integr Comp Physiol. 2008;295(5):R1385–R1390. doi: 10.1152/ajpregu.00030.2008
  144. Skibicka KP, Shirazi RH, Hansson C, Dickson SL. Ghrelin interacts with neuropeptide Y Y1 and opioid receptors to increase food reward. Endocrinology. 2012;153(3):1194–1205. doi: 10.1210/en.2011-1606
  145. Melis M, Gessa GL, Diana M. Different mechanisms for dopaminergic excitation induced by opiates and cannabinoids in the rat midbrain. Prog Neuropsychopharmacol Biol Psychiatry. 2000;24(6): 993–1006. doi: 10.1016/s0278-5846(00)00119-6
  146. Spanagel R, Herz A, Shippenberg TS. Opposing tonically active endogenous opioid systems modulate the mesolimbic dopaminergic pathway. Proc Natl Acad Sci USA. 1992;89(6):2046–2050. doi: 10.1073/pnas.89.6.2046
  147. Wenzel JM, Cheer JF. Endocannabinoid regulation of reward and reinforcement through interaction with dopamine and endogenous opioid signaling. Neuropsychopharmacology. 2018;43(1): 103–115. doi: 10.1038/npp.2017.126
  148. Everett TJ, Gomez DM, Hamilton LR, Oleson EB. Endocannabinoid modulation of dopamine release during reward seeking, interval timing, and avoidance. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2021;104:110031. doi: 10.1016/j.pnpbp.2020.110031
  149. Hayward MD, Pintar JE, Low MJ. Selective reward deficit in mice lacking beta-endorphin and enkephalin. J Neurosci. 2002;22(18):8251–8258. doi: 10.1523/JNEUROSCI.22-18-08251.2002
  150. Kola B, Hubina E, Tucci SA, et al. Cannabinoids and ghrelin have both central and peripheral metabolic and cardiac effects via AMP-activated protein kinase. J Biol Chem. 2005;280(26):25196–25201. doi: 10.1074/jbc.C500175200
  151. Al Massadi O, Nogueiras R, Dieguez C, Girault JA. Ghrelin and food reward. Neuropharmacology. 2019;148:131–138. doi: 10.1016/j.neuropharm.2019.01.001
  152. Howlett AC, Barth F, Bonner TI, et al. International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54(2):161–202. doi: 10.1124/pr.54.2.161
  153. Hua T, Vemuri K, Pu M, et al. Crystal structure of the human cannabinoid receptor CB1. Cell. 2016;167(3):750–762.e14. doi: 10.1016/j.cell.2016.10.004
  154. Piazza PV, Cota D, Marsicano G. The CB1 Receptor as the cornerstone of exostasis. Neuron. 2017;93(6):1252–1274. doi: 10.1016/j.neuron.2017.02.002
  155. Kola B, Farkas I, Christ-Crain M, et al. The orexigenic effect of ghrelin is mediated through central activation of the endogenous cannabinoid system. PLoS One. 2008;3(3): e1797. doi: 10.1371/journal.pone.0001797
  156. Kirkham TC, Williams CM, Fezza F, Di Marzo V. Endocannabinoid levels in rat limbic forebrain and hypothalamus in relation to fasting, feeding and satiation: stimulation of eating by 2-arachidonoyl glycerol. Br J Pharmacol. 2002;136(4):550–557. doi: 10.1038/sj.bjp.0704767
  157. Di S, Malcher-Lopes R, Halmos KC, Tasker JG. Nongenomic glucocorticoid inhibition via endocannabinoid release in the hypothalamus: a fast feedback mechanism. J Neurosci. 2003;23(12): 4850–4857. doi: 10.1523/JNEUROSCI.23-12-04850.2003
  158. Di S, Malcher-Lopes R, Marcheselli VL, et al. Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of glutamate and gamma-aminobutyric acid inputs to hypothalamic magnocellular neurons. Endocrinology. 2005;146(10):4292–4301. doi: 10.1210/en.2005-0610
  159. Tucci SA, Rogers EK, Korbonits M, Kirkham TC. The cannabinoid CB1 receptor antagonist SR141716 blocks the orexigenic effects of intrahypothalamic ghrelin. Br J Pharmacol. 2004;143(5):520–523. doi: 10.1038/sj.bjp.0705968
  160. Kirkham TC. Cannabinoids and appetite: food craving and food pleasure. Int Rev Psychiatry. 2009;21(2):163–171. doi: 10.1080/09540260902782810
  161. French ED. delta9-Tetrahydrocannabinol excites rat VTA dopamine neurons through activation of cannabinoid CB1 but not opioid receptors. Neurosci Lett. 1997;226(3):159–162. doi: 10.1016/s0304-3940(97)00278-4
  162. Solinas M, Justinova Z, Goldberg SR, Tanda G. Anandamide administration alone and after inhibition of fatty acid amide hydrolase (FAAH) increases dopamine levels in the nucleus accumbens shell in rats. J Neurochem. 2006;98(2):408–419. doi: 10.1111/j.1471-4159.2006.03880.x
  163. Melis T, Succu S, Sanna F, et al. The cannabinoid antagonist SR141716A (Rimonabant) reduces the increase of extra-cellular dopamine release in the rat nucleus accumbens induced by a novel high palatable food. Neurosci Lett. 2007;419(3):231–235. doi: 10.1016/j.neulet.2007.04.012
  164. Oleson EB, Beckert MV, Morra JT, et al. Endocannabinoids shape accumbal encoding of cue-motivated behavior via CB1 receptor activation in the ventral tegmentum. Neuron. 2012;73(2):360–373. doi: 10.1016/j.neuron.2011.11.018
  165. Sustkova-Fiserova M, Charalambous C, Havlickova T, et al. Alterations in rat accumbens endocannabinoid and GABA content during fentanyl treatment: the role of ghrelin. Int J Mol Sci. 2017;18(11):2486. doi: 10.3390/ijms18112486
  166. Kalafateli AL, Vallöf D, Jörnulf JW, et al. A cannabinoid receptor antagonist attenuates ghrelin-induced activation of the mesolimbic dopamine system in mice. Physiol Behav. 2018;184:211–219. doi: 10.1016/j.physbeh.2017.12.005
  167. Gómez-Cañas M, Rodríguez-Cueto C, Satta V., et al. Endocannabinoid-Binding Receptors as Drug Targets. Methods in Molecular Biology. 2022;(2576):67–94. doi: 10.1007/978-1-0716-2728-0_6
  168. Busquets-Garcia A, Bains J, Marsicano G. CB1 Receptor Signaling in the Brain: Extracting Specificity from Ubiquity. Neuropsychopharmacology. 2018;43(1):4–20. doi: 10.1038/npp.2017.206
  169. Schultz W. Dopamine reward prediction-error signalling: a two-component response. Nat Rev Neurosci. 2016;17(3):183–195. doi: 10.1038/nrn.2015.26
  170. Abizaid A, Liu ZW, Andrews ZB, et al. Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite. J Clin Invest. 2006;116(12):3229–3239. doi: 10.1172/JCI29867
  171. Skibicka KP, Hansson C, Egecioglu E, Dickson SL. Role of ghrelin in food reward: impact of ghrelin on sucrose self-administration and mesolimbic dopamine and acetylcholine receptor gene expression. Addict Biol. 2012;17(1):95–107. doi: 10.1111/j.1369-1600.2010.00294.x
  172. Shi L, Bian X, Qu Z, et al. Peptide hormone ghrelin enhances neuronal excitability by inhibition of Kv7/KCNQ channels. Nat Commun. 2013;4:1435. doi: 10.1038/ncomms2439
  173. Wellman M, Abizaid A. Growth Hormone Secretagogue Receptor Dimers: A New Pharmacological Target. eNeuro. 2015;2(2): ENEURO.0053–14.2015. doi: 10.1523/ENEURO.0053-14.2015
  174. Cornejo MP, Mustafá ER, Barrile F, et al. The intriguing ligand-dependent and ligand-independent actions of the growth hormone secretagogue receptor on reward-related behaviors. Neurosci Biobehav Rev. 2021;120:401–416. doi: 10.1016/j.neubiorev.2020.10.017
  175. Hunt DL, Castillo PE. Synaptic plasticity of NMDA receptors: mechanisms and functional implications. Curr Opin Neurobiol. 2012;22(3):496–508. doi: 10.1016/j.conb.2012.01.007
  176. Volianskis A, France G, Jensen MS, et al. Long-term potentiation and the role of N-methyl-D-aspartate receptors. Brain Res. 2015;1621:5–16. doi: 10.1016/j.brainres.2015.01.016
  177. Diering GH, Huganir RL. The AMPA receptor code of synaptic plasticity. Neuron. 2018;100(2):314–329. doi: 10.1016/j.neuron.2018.10.018
  178. Charlety PJ, Grenhoff J, Chergui K, et al. Burst firing of mesencephalic dopamine neurons is inhibited by somatodendritic application of kynurenate. Acta Physiol Scand. 1991;142(1):105–112. doi: 10.1111/j.1748-1716.1991.tb09134.x
  179. Engberg G, Kling-Petersen T, Nissbrandt H. GABAB-receptor activation alters the firing pattern of dopamine neurons in the rat substantia nigra. Synapse. 1993;15(3):229–238. doi: 10.1002/syn.890150308
  180. Borgland SL, Chang SJ, Bowers MS, et al. Orexin A/hypocretin-1 selectively promotes motivation for positive reinforcers. J Neurosci. 2009;29(36):11215–11225. doi: 10.1523/JNEUROSCI.6096-08.2009
  181. Doane DF, Lawson MA, Meade JR, et al. Orexin-induced feeding requires NMDA receptor activation in the perifornical region of the lateral hypothalamus. Am J Physiol Regul Integr Comp Physiol. 2007;293(3): R1022–R1026. doi: 10.1152/ajpregu.00282.2007
  182. Jerlhag E, Egecioglu E, Dickson SL, Engel JA. Glutamatergic regulation of ghrelin-induced activation of the mesolimbic dopamine system. Addict Biol. 2011;16(1):82–91. doi: 10.1111/j.1369-1600.2010.00231.x
  183. Bouarab C, Thompson B, Polter AM. VTA GABA Neurons at the interface of stress and reward. Front Neural Circuits. 2019;13:78. doi: 10.3389/fncir.2019.00078
  184. Ostroumov A, Thomas AM, Kimmey BA, et al. Stress increases ethanol self-administration via a shift toward excitatory GABA signaling in the ventral tegmental area. Neuron. 2016;92(2):493–504. doi: 10.1016/j.neuron.2016.09.029
  185. Niehaus JL, Murali M, Kauer JA. Drugs of abuse and stress impair LTP at inhibitory synapses in the ventral tegmental area. Eur J Neurosci. 2010;32(1):108–117. doi: 10.1111/j.1460-9568.2010.07256.x
  186. Nugent FS, Penick EC, Kauer JA. Opioids block long-term potentiation of inhibitory synapses. Nature. 2007;446(7139):1086–1090. doi: 10.1038/nature05726
  187. Tung LW, Lu GL, Lee YH, et al. Orexins contribute to restraint stress-induced cocaine relapse by endocannabinoid-mediated disinhibition of dopaminergic neurons. Nat Commun. 2016;7:12199. doi: 10.1038/ncomms12199
  188. Hsu TM, Suarez AN, Kanoski SE. Ghrelin: A link between memory and ingestive behavior. Physiol Behav. 2016;162:10–17. doi: 10.1016/j.physbeh.2016.03.039
  189. Serrenho D, Santos SD, Carvalho AL. The role of ghrelin in regulating synaptic function and plasticity of feeding-associated circuits. Front Cell Neurosci. 2019;13:205. doi: 10.3389/fncel.2019.00205
  190. Hainmueller T, Bartos M. Parallel emergence of stable and dynamic memory engrams in the hippocampus. Nature. 2018;558(7709):292–296. doi: 10.1038/s41586-018-0191-2
  191. Diano S, Farr SA, Benoit SC, et al. Ghrelin controls hippocampal spine synapse density and memory performance. Nat Neurosci. 2006;9(3):381–388. doi: 10.1038/nn1656
  192. Carlini VP, Varas MM, Cragnolini AB, et al. Differential role of the hippocampus, amygdala, and dorsal raphe nucleus in regulating feeding, memory, and anxiety-like behavioral responses to ghrelin. Biochem Biophys Res Commun. 2004;313(3):635–641. doi: 10.1016/j.bbrc.2003.11.150
  193. Chen L, Xing T, Wang M, et al. Local infusion of ghrelin enhanced hippocampal synaptic plasticity and spatial memory through activation of phosphoinositide 3-kinase in the dentate gyrus of adult rats. Eur J Neurosci. 2011;33(2):266–275. doi: 10.1111/j.1460-9568.2010.07491.x
  194. Davis JF, Choi DL, Clegg DJ, Benoit SC. Signaling through the ghrelin receptor modulates hippocampal function and meal anticipation in mice. Physiol Behav. 2011;103(1):39–43. doi: 10.1016/j.physbeh.2010.10.017
  195. Albarran-Zeckler RG, Brantley AF, Smith RG. Growth hormone secretagogue receptor (GHS-R1a) knockout mice exhibit improved spatial memory and deficits in contextual memory. Behav Brain Res. 2012;232(1):13–19. doi: 10.1016/j.bbr.2012.03.012
  196. Nicoll RA. A brief history of long-term potentiation. Neuron. 2017;93(2):281–290. doi: 10.1016/j.neuron.2016.12.015
  197. Ribeiro LF, Catarino T, Santos SD, et al. Ghrelin triggers the synaptic incorporation of AMPA receptors in the hippocampus. Proc Natl Acad Sci USA. 2014;111(1):E149–E158. doi: 10.1073/pnas.1313798111
  198. Berrout L, Isokawa M. Ghrelin promotes reorganization of dendritic spines in cultured rat hippocampal slices. Neurosci Lett. 2012;516(2):280–284. doi: 10.1016/j.neulet.2012.04.009
  199. Kern A, Mavrikaki M, Ullrich C, et al. Hippocampal dopamine/drd1 signaling dependent on the ghrelin receptor. Cell. 2015;163(5):1176–1190. doi: 10.1016/j.cell.2015.10.062
  200. Martínez Damonte V, Rodríguez SS, Raingo J. Growth hormone secretagogue receptor constitutive activity impairs voltage-gated calcium channel-dependent inhibitory neurotransmission in hippocampal neurons. J Physiol. 2018;596(22):5415–5428. doi: 10.1113/JP276256
  201. Kanoski SE, Fortin SM, Ricks KM, Grill HJ. Ghrelin signaling in the ventral hippocampus stimulates learned and motivational aspects of feeding via PI3K-Akt signaling. Biol Psychiatry. 2013;73(9): 915–923. doi: 10.1016/j.biopsych.2012.07.002
  202. Quraishi SA, Paladini CA. Chapter 18. Plasticity in Dopamine Neurons. Steiner H., Tseng K.Y., editors. Handbook of Basal Ganglia Structure and Function (2nd ed.). Elsevier, 2017. 1036 p.
  203. Chevaleyre V, Castillo PE. Heterosynaptic LTD of hippocampal GABAergic synapses: a novel role of endocannabinoids in regulating excitability. Neuron. 2003;38(3):461–472. doi: 10.1016/s0896-6273(03)00235-6
  204. Chevaleyre V, Castillo PE. Endocannabinoid-mediated metaplasticity in the hippocampus. Neuron. 2004;43(6):871–881. doi: 10.1016/j.neuron.2004.08.03

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