Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

The role of PPAR-γ in memory deficits induced by prenatal and lactation alcohol exposure in mice

Abstract

Patients diagnosed with fetal alcohol spectrum disorder (FASD) show persistent cognitive disabilities, including memory deficits. However, the neurobiological substrates underlying these deficits remain unclear. Here, we show that prenatal and lactation alcohol exposure (PLAE) in mice induces FASD-like memory impairments. This is accompanied by a reduction of N-acylethanolamines (NAEs) and peroxisome proliferator-activated receptor gamma (PPAR-γ) in the hippocampus specifically in a childhood-like period (at post-natal day (PD) 25). To determine their role in memory deficits, two pharmacological approaches were performed during this specific period of early life. Thus, memory performance was tested after the repeated administration (from PD25 to PD34) of: i) URB597, to increase NAEs, with GW9662, a PPAR-γ antagonist; ii) pioglitazone, a PPAR-γ agonist. We observed that URB597 suppresses PLAE-induced memory deficits through a PPAR-γ dependent mechanism, since its effects are prevented by GW9662. Direct PPAR-γ activation, using pioglitazone, also ameliorates memory impairments. Lastly, to further investigate the region and cellular specificity, we demonstrate that an early overexpression of PPAR-γ, by means of a viral vector, in hippocampal astrocytes mitigates memory deficits induced by PLAE. Together, our data reveal that disruptions of PPAR-γ signaling during neurodevelopment contribute to PLAE-induced memory dysfunction. In turn, PPAR-γ activation during a childhood-like period is a promising therapeutic approach for memory deficits in the context of early alcohol exposure. Thus, these findings contribute to the gaining insight into the mechanisms that might underlie memory impairments in FASD patients.

This is a preview of subscription content, access via your institution

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Alcohol consumption by dams during gestation and lactation.
Fig. 2: Hippocampal alterations in the expanded ECS induced by PLAE.
Fig. 3: Endogenous or exogenous PPAR-γ activation ameliorates memory impairments in PLAE mice.
Fig. 4: PLAE reduces astrocytic PPAR-γ primarily in CA1 of the HPC.
Fig. 5: Astrocytic PPAR-γ upregulation in dorsal HPC rescues memory deficits induced by PLAE.

References

  1. Wilhoit LF, Scott DA, Simecka BA. Fetal alcohol spectrum disorders: characteristics, complications, and treatment. Community Ment Health J. 2017;53:711–8.

    Article  PubMed  Google Scholar 

  2. Kodituwakku PW. Neurocognitive profile in children with fetal alcohol spectrum disorders. Dev Disabil Res Rev. 2009;15:218.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Cantacorps L, Alfonso-Loeches S, Moscoso-Castro M, Cuitavi J, Gracia-Rubio I, López-Arnau R, et al. Maternal alcohol binge drinking induces persistent neuroinflammation associated with myelin damage and behavioural dysfunctions in offspring mice. Neuropharmacology. 2017;123:368–84.

    Article  CAS  PubMed  Google Scholar 

  4. Rubert G, Miñana R, Pascual M, Guerri C. Ethanol exposure during embryogenesis decreases the radial glial progenitor pool and affects the generation of neurons and astrocytes. J Neurosci Res. 2006;84:483–96.

    Article  CAS  PubMed  Google Scholar 

  5. Miller MW. Effect of pre- or postnatal exposure to ethanol on the total number of neurons in the principal sensory nucleus of the trigeminal nerve: cell proliferation and neuronal death. Alcohol Clin Exp Res. 1995;19:1359–63.

    Article  CAS  PubMed  Google Scholar 

  6. Ikonomidou C, Bittigau P, Ishimaru MJ, Wozniak DF, Koch C, Genz K, et al. Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome. Science. 2000;287:1056–60.

    Article  CAS  PubMed  Google Scholar 

  7. Fontaine CJ, Patten AR, Sickmann HM, Helfer JL, Christie BR. Effects of pre-natal alcohol exposure on hippocampal synaptic plasticity: sex, age and methodological considerations. Neurosci Biobehav Rev. 2016;64:12–34.

    Article  CAS  PubMed  Google Scholar 

  8. Cantacorps L, González-Pardo H, Arias JL, Valverde O, Conejo NM. Altered brain functional connectivity and behaviour in a mouse model of maternal alcohol binge-drinking. Prog Neuro-Psychopharmacol Biol Psychiatry. 2018;84:237–49.

    Article  CAS  Google Scholar 

  9. García-Baos A, Puig-Reyne X, García-Algar Ó, Valverde O. Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model. Biomed Pharmacother. 2021;141:111813.

    Article  PubMed  Google Scholar 

  10. Drew PD, Kane CJM. Fetal alcohol spectrum disorders and neuroimmune changes. Int Rev Neurobiol. 2014;118:41–80.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Hausknecht K, Shen Y-L, Wang R-X, Haj-Dahmane S, Shen R-Y. Prenatal ethanol exposure persistently alters endocannabinoid signaling and endocannabinoid-mediated excitatory synaptic plasticity in ventral tegmental area dopamine neurons. J Neurosci. 2017;37:5798–808.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Cristino L, Bisogno T, Di Marzo V. Cannabinoids and the expanded endocannabinoid system in neurological disorders. Nat Rev Neurol. 2019. https://doi.org/10.1038/s41582-019-0284-z.

  13. Gomes TM, Dias da Silva D, Carmo H, Carvalho F, Silva JP. Epigenetics and the endocannabinoid system signaling: An intricate interplay modulating neurodevelopment. Pharmacol Res. 2020;162:105237.

  14. Gómez M, Hernández M, Fernández-Ruiz J. Cannabinoid signaling system: does it play a function in cell proliferation and migration, neuritic elongation and guidance and synaptogenesis during brain ontogenesis? Cell Adhes Migr. 2008;2:246.

    Article  Google Scholar 

  15. O’Sullivan SE. An update on PPAR activation by cannabinoids. Br J Pharm. 2016;173:1899–910.

    Article  Google Scholar 

  16. Iannotti FA, Vitale RM. The endocannabinoid system and PPARs: focus on their signalling crosstalk, action and transcriptional regulation. Cells. 2021;10:1–22.

    Article  Google Scholar 

  17. Kota BP, Huang THW, Roufogalis BD. An overview on biological mechanisms of PPARs. Pharm Res. 2005;51:85–94.

    Article  CAS  Google Scholar 

  18. Wagner K-D, Wagner N, Guo J, Wu J, He Q, Zhang M, et al. The potential role of PPARs in the fetal origins of adult disease. Cells. 2022;11:3474.

    Article  Google Scholar 

  19. D’angelo M, Castelli V, Catanesi M, Antonosante A, Dominguez-Benot R, Ippoliti R, et al. PPARγ and cognitive performance. Mol Sci. 2019. https://doi.org/10.3390/ijms20205068.

  20. Zhao Q, Wang Q, Wang J, Tang M, Huang S, Peng K, et al. Maternal immune activation-induced PPARγ-dependent dysfunction of microglia associated with neurogenic impairment and aberrant postnatal behaviors in offspring. Neurobiol Dis. 2019;125:1–13.

    Article  PubMed  Google Scholar 

  21. Liu WC, Wu CW, Fu MH, Tain YL, Liang CK, Hung CY, et al. Maternal high fructose-induced hippocampal neuroinflammation in the adult female offspring via PPARγ-NF-κB signaling. J Nutr Biochem. 2020;81:108378.

  22. Panlilio LV, Justinova Z, Goldberg SR. Inhibition of FAAH and activation of PPAR: new approaches to the treatment of cognitive dysfunction and drug addiction. Pharm Ther. 2013;138:84–102.

    Article  CAS  Google Scholar 

  23. Rubio M, McHugh D, Fernández-Ruiz J, Bradshaw H, Walker JM. Short-term exposure to alcohol in rats affects brain levels of anandamide, other N-acylethanolamines and 2-arachidonoyl-glycerol. Neurosci Lett. 2007;421:270–4.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Basavarajappa BS, Joshi V, Shivakumar M, Subbanna S. Distinct functions of endogenous cannabinoid system in alcohol abuse disorders. Br J Pharm. 2019;176:3085–109.

    CAS  Google Scholar 

  25. Subbanna S, Shivakumar M, Psychoyos D, Xie S, Basavarajappa BS. Anandamide-CB1 receptor signaling contributes to postnatal ethanol-induced neonatal neurodegeneration, adult synaptic, and memory deficits. J Neurosci. 2013;33:6350–66.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Gasparyan A, Navarro D, Navarrete F, Austrich-Olivares A, Scoma ER, Hambardikar VD, et al. Cannabidiol repairs behavioral and brain disturbances in a model of fetal alcohol spectrum disorder. Pharm Res. 2023;188:106655.

    Article  CAS  Google Scholar 

  27. Koren G, Cohen R, Sachs O. Use of cannabis in fetal alcohol spectrum disorder. Cannabis Cannabinoid Res. 2020;6:74–6: https://doi.org/10.1089/can.2019.0056.

  28. Koren G, Cohen R. Medicinal use of cannabis in children and pregnant women. Rambam Maimonides Med J. 2020;11:1–5.

  29. Tiwari V, Chopra K. Resveratrol prevents alcohol-induced cognitive deficits and brain damage by blocking inflammatory signaling and cell death cascade in neonatal rat brain. J Neurochem. 2011;117:678–90.

    CAS  PubMed  Google Scholar 

  30. Drew PD, Johnson JW, Douglas JC, Phelan KD, Kane CJM. Pioglitazone blocks ethanol induction of microglial activation and immune responses in the hippocampus, cerebellum, and cerebral cortex in a mouse model of fetal alcohol spectrum disorders. Alcohol Clin Exp Res. 2015;39:445–54.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Kane CJM, Phelan KD, Drew PD. Neuroimmune mechanisms in fetal alcohol spectrum disorder. Dev Neurobiol. 2012;72:1302.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Perez-Catalan NA, Doe CQ, Ackerman SD. The role of astrocyte‐mediated plasticity in neural circuit development and function. Neural Dev. 2021;16:1–14.

    Article  PubMed  PubMed Central  Google Scholar 

  33. Farhy-Tselnicker I, Allen NJ. Astrocytes, neurons, synapses: a tripartite view on cortical circuit development. Neural Dev. 2018;13:1–12.

    Article  Google Scholar 

  34. Liddelow SA, Barres BA. Reactive astrocytes: production, function, and therapeutic potential. Immunity. 2017;46:957–67.

    Article  CAS  PubMed  Google Scholar 

  35. Kane CJM, Drew PD. Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders. J Neurosci Res. 2021;99:1973–85.

    Article  CAS  PubMed  Google Scholar 

  36. Giordano G, Guizzetti M, Dao K, Mattison HA, Costa LG. Ethanol impairs muscarinic receptor-induced neuritogenesis in rat hippocampal slices: role of astrocytes and extracellular matrix proteins. Biochem Pharm. 2011;82:1792–9.

    Article  CAS  PubMed  Google Scholar 

  37. Guizzetti M, Moore NH, Giordano G, VanDeMark KL, Costa LG. Ethanol inhibits neuritogenesis induced by astrocyte muscarinic receptors. Glia. 2010;58:1395.

    Article  PubMed  PubMed Central  Google Scholar 

  38. Wang Y, Fu AKY, Ip NY. Instructive roles of astrocytes in hippocampal synaptic plasticity: neuronal activity-dependent regulatory mechanisms. FEBS J. 2022;289:2202–18.

    Article  CAS  PubMed  Google Scholar 

  39. Medina AE. Fetal alcohol spectrum disorders and abnormal neuronal plasticity. Neuroscientist. 2011;17:274–87.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Patten AR, Sickmann HM, Dyer RA, Innis SM, Christie BR. Omega-3 fatty acids can reverse the long-term deficits in hippocampal synaptic plasticity caused by prenatal ethanol exposure. Neurosci Lett. 2013;551:7–11.

    Article  CAS  PubMed  Google Scholar 

  41. Chaboub LS, Deneen B. Astrocyte form and function in the developing CNS. Semin Pediatr Neurol. 2013;20:230–5.

    Article  PubMed  Google Scholar 

  42. Semple BD, Blomgren K, Gimlin K, Ferriero DM, Noble-Haeusslein LJ. Brain development in rodents and humans: identifying benchmarks of maturation and vulnerability to injury across species. Prog Neurobiol. 2013;106-7:1–16.

    Article  Google Scholar 

  43. Barceló-Coblijn G, Wold LE, Ren J, Murphy EJ. Prenatal ethanol exposure increases brain cholesterol content in adult rats. Lipids. 2013;48:1059–68.

    Article  PubMed  Google Scholar 

  44. Wen Z, Kim HY. Alterations in hippocampal phospholipid profile by prenatal exposure to ethanol. J Neurochem. 2004;89:1368–77.

    Article  CAS  PubMed  Google Scholar 

  45. Walter L, Franklin A, Witting A, Möller T, Stella N. Astrocytes in culture produce anandamide and other acylethanolamides. J Biol Chem. 2002;277:20869–76.

    Article  CAS  PubMed  Google Scholar 

  46. Moosecker S, Pissioti A, Leidmaa E, Harb MR, Dioli C, Gassen NC, et al. Brain expression, physiological regulation and role in motivation and associative learning of peroxisome proliferator-activated receptor γ. Neuroscience. 2021;479:91–106.

    Article  CAS  PubMed  Google Scholar 

  47. Warden A, Truitt J, Merriman M, Ponomareva O, Jameson K, Ferguson LB, et al. Localization of PPAR isotypes in the adult mouse and human brain. Sci Rep. 2016;6:27618.

  48. Realini N, Vigano’ D, Guidali C, Zamberletti E, Rubino T, Parolaro D. Chronic URB597 treatment at adulthood reverted most depressive-like symptoms induced by adolescent exposure to THC in female rats. Neuropharmacology. 2011;60:235–43.

    Article  CAS  PubMed  Google Scholar 

  49. Bellozi PMQ, Pelição R, Santos MC, Lima IVA, Saliba SW, Vieira ÉLM, et al. URB597 ameliorates the deleterious effects induced by binge alcohol consumption in adolescent rats. Neurosci Lett. 2019;711:134408.

  50. Rivera P, Fernández-Arjona M, del M, Silva-Peña D, Blanco E, Vargas A, et al. Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure. Biochem Pharm. 2018;157:244–57.

    Article  CAS  PubMed  Google Scholar 

  51. Fidelman S, Mizrachi Zer-Aviv T, Lange R, Hillard CJ, Akirav I. Chronic treatment with URB597 ameliorates post-stress symptoms in a rat model of PTSD. Eur Neuropsychopharmacol. 2018;28:630–42.

    Article  CAS  PubMed  Google Scholar 

  52. Kubota N, Terauchi Y, Kubota T, Kumagai H, Itoh S, Satoh H, et al. Pioglitazone ameliorates insulin resistance and diabetes by both adiponectin-dependent and -independent pathways *. J Biol Chem. 2006;281:8748–55.

    Article  CAS  PubMed  Google Scholar 

  53. Santos DFS, Donahue RR, Laird DE, Oliveira MCG, Taylor BK. The PPARγ agonist pioglitazone produces a female-predominant inhibition of hyperalgesia associated with surgical incision, peripheral nerve injury, and painful diabetic neuropathy. Neuropharmacology. 2022;205:108907.

    Article  CAS  PubMed  Google Scholar 

  54. Dasu MR, Park S, Devaraj S, Jialal I. Pioglitazone inhibits toll-like receptor expression and activity in human monocytes and db/db mice. Endocrinology. 2009;150:3457–64.

    Article  CAS  PubMed  Google Scholar 

  55. Collino M, Patel NSA, Lawrence KM, Collin M, Latchman DS, Yaqoob MM, et al. The selective PPARgamma antagonist GW9662 reverses the protection of LPS in a model of renal ischemia-reperfusion. Kidney Int. 2005;68:529–36.

    Article  CAS  PubMed  Google Scholar 

  56. Han Y, Wang J, Zhao Q, Xie X, Song R, Xiao Y, et al. Pioglitazone alleviates maternal sleep deprivation-induced cognitive deficits in male rat offspring by enhancing microglia-mediated neurogenesis. Brain Behav Immun. 2020;87:568–78.

    Article  CAS  PubMed  Google Scholar 

  57. Baumann A, Burger K, Brandt A, Staltner R, Jung F, Rajcic D, et al. GW9662, a peroxisome proliferator-activated receptor gamma antagonist, attenuates the development of non-alcoholic fatty liver disease. Metabolism. 2022;133:155233.

    Article  CAS  PubMed  Google Scholar 

  58. Bentley GR. Hydration as a limiting factor in lactation. J Hum Biol. 1998;10:151–61.

    Article  CAS  Google Scholar 

  59. Rhodes JS, Best K, Belknap JK, Finn DA, Crabbe JC. Evaluation of a simple model of ethanol drinking to intoxication in C57BL/6J mice. Physiol Behav. 2005;84:53–63.

    Article  CAS  PubMed  Google Scholar 

  60. Drinking Levels Defined | National Institute on Alcohol Abuse and Alcoholism (NIAAA). https://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/moderate-binge-drinking.

  61. Basavarajappa B, Basavarajappa SB. Fetal alcohol spectrum disorder: potential role of endocannabinoids signaling. Brain Sci. 2015;5:456–93.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Tsuboi K, Uyama T, Okamoto Y, Ueda N. Endocannabinoids and related N-acylethanolamines: biological activities and metabolism. Inflamm Regen. 2018;38:28.

  63. Govindarajulu M, Pinky PD, Bloemer J, Ghanei N, Suppiramaniam V, Amin R. Signaling Mechanisms of Selective PPARγ Modulators in Alzheimer’s Disease. PPAR Res. 2018;2018:2010675.

  64. Pizcueta P, Vergara C, Emanuele M, Vilalta A, Rodríguez-Pascau L, Martinell M. Development of PPARγ agonists for the treatment of neuroinflammatory and neurodegenerative diseases: leriglitazone as a promising candidate. Int J Mol Sci. 2023;24:3201.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  65. DeVito LM, Eichenbaum H. Distinct contributions of the hippocampus and medial prefrontal cortex to the ‘what-where-when’ components of episodic-like memory in mice. Behav Brain Res. 2010;215:318–25.

    Article  PubMed  Google Scholar 

  66. Bird CM, Burgess N. The hippocampus and memory: insights from spatial processing. Nat Rev Neurosci. 2008;9:182–94.

    Article  CAS  PubMed  Google Scholar 

  67. Trindade P, Hampton B, Manhães AC, Medina AE. Developmental alcohol exposure leads to a persistent change on astrocyte secretome. J Neurochem. 2016;137:730.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  68. Guizzetti M, Zhang X, Goeke C, Gavin DP. Glia and neurodevelopment: focus on fetal alcohol spectrum disorders. Front Pediatr. 2014;2:123.

    Article  PubMed  PubMed Central  Google Scholar 

  69. Wilhelm CJ, Guizzetti M. Fetal alcohol spectrum disorders: an overview from the glia perspective. Front Integr Neurosci. 2016;9:65.

    Article  PubMed  PubMed Central  Google Scholar 

  70. Cantacorps L, Montagud-Romero S, Valverde O. Curcumin treatment attenuates alcohol-induced alterations in a mouse model of foetal alcohol spectrum disorders. Prog Neuropsychopharmacol Biol Psychiatry. 2020;100:109899.

  71. Zizzo G, Cohen PL. The PPAR-γ antagonist GW9662 elicits differentiation of M2c-like cells and upregulation of the MerTK/Gas6 axis: a key role for PPAR-γ in human macrophage polarization. J Inflamm. 2011;2011. https://doi.org/10.1186/s12950-015-0081-4.

  72. Chistyakov DV, Astakhova AA, Goriainov SV, Sergeeva MG. Comparison of PPAR ligands as modulators of resolution of inflammation, via their influence on cytokines and oxylipins release in astrocytes. Int J Mol Sci. 2020;21:9577.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Dello Russo C, Gavrilyuk V, Weinberg G, Almeida A, Bolanos JP, Palmer J, et al. Peroxisome proliferator-activated receptor γ thiazolidinedione agonists increase glucose metabolism in astrocytes. J Biol Chem. 2003;278:5828–36.

    Article  CAS  PubMed  Google Scholar 

  74. Corona JC, Duchen MR. PPARγ as a therapeutic target to rescue mitochondrial function in neurological disease. Free Radic Biol Med. 2016;100:153.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  75. Miglio G, Rosa AC, Rattazzi L, Collino M, Lombardi G, Fantozzi R. PPARgamma stimulation promotes mitochondrial biogenesis and prevents glucose deprivation-induced neuronal cell loss. Neurochem Int. 2009;55:496–504.

    Article  CAS  PubMed  Google Scholar 

  76. Zehnder T, Petrelli F, Romanos J, De Oliveira Figueiredo EC, Lewis TL, Déglon N, et al. Mitochondrial biogenesis in developing astrocytes regulates astrocyte maturation and synapse formation. Cell Rep. 2021;35:108952.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

This work was supported by the Ministerio de Economia y Competitividad (#PID2019-104077RB-100 - MCIN/AEI/10.13039/501100011033), Ministerio de Sanidad (Plan Nacional sobre Drogas #2018/007 and ISCIII-Feder-RIAPAd-RICORS #RD21/0009/001) by the EU NextGeneration and by the Generalitat de Catalunya, AGAUR (#2021SGR00485). AG-B received a FI-AGAUR grant from the Generalitat de Catalunya (#2019FI_B0081). IG-L obtained a grant from the Ministerio de Ciencia e Innovación (#PRE2020-091923) The Department of Medicine and Health Sciences (UPF) is a “Unidad de Excelencia María de Maeztu” funded by the AEI (#CEX2018-000792-M). OV is recipient of an ICREA Academia Award (Institució Catalana de Recerca i Estudis Avançats, Generalitat de Catalunya). The authors wish to thank Xavier Puig-Reyne for the technical support.

Author information

Authors and Affiliations

Authors

Contributions

AGB and OV were responsible for the study concept and design. AGB and IGL carried out the behavioral experiments (DID test). AGB conducted the pharmacological and genetic manipulations and the posterior behavioral experiments (memory tests), as well as the RT-qPCR and IHC assays. AGB, FS and OV analyzed and interpreted the data. AP and RT carried out the LC-MS/MS studies and analyses. AGB, IGL, AP, and OV drafted the manuscript. All authors critically reviewed the content of the manuscript.

Corresponding author

Correspondence to Olga Valverde.

Ethics declarations

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and Permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Garcia-Baos, A., Pastor, A., Gallego-Landin, I. et al. The role of PPAR-γ in memory deficits induced by prenatal and lactation alcohol exposure in mice. Mol Psychiatry (2023). https://doi.org/10.1038/s41380-023-02191-z

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1038/s41380-023-02191-z

Search

Quick links