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Alterations in brain derived neurotrophic factor (BDNF) signalling, which regulates synaptic function through the activation of full-length tropomyosin-related kinase B receptors (TrkB-FL), are implicated in the aetiology of schizophrenia, as is N-methyl-D-aspartate receptor (NMDA-R) hypofunction. However, whether NMDA-R hypofunction contributes to the disrupted BDNF signalling seen in patients remains unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>The purpose of this study was to characterise BDNF signalling and function in a preclinical rodent model relevant to schizophrenia induced by prolonged NMDA-R hypofunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Using the subchronic phencyclidine (PCP) model, we performed electrophysiology approaches, molecular characterisation and behavioural analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>The data showed that prolonged NMDA-R antagonism, induced by subchronic PCP treatment, impairs long-term potentiation (LTP) and the facilitatory effect of BDNF upon LTP in the medial prefrontal cortex (PFC) of adult mice. Additionally, TrkB-FL receptor expression is decreased in the PFC of these animals. By contrast, these changes were not present in the hippocampus of PCP-treated mice. Moreover, BDNF levels were not altered in the hippocampus or PFC of PCP-treated mice. Interestingly, these observations are paralleled by impaired performance in PFC-dependent cognitive tests in mice treated with PCP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Overall, these data suggest that NMDA-R hypofunction induces dysfunctional BDNF signalling in the PFC, but not in the hippocampus, which may contribute to the PFC-dependent cognitive deficits seen in the subchronic PCP model. Additionally, these data suggest that targeting BDNF signalling may be a mechanism to improve PFC-dependent cognitive dysfunction in schizophrenia.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/02698811211008560","type":"journal-article","created":{"date-parts":[[2021,5,19]],"date-time":"2021-05-19T06:49:14Z","timestamp":1621406954000},"page":"730-743","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":21,"title":["Sustained NMDA receptor hypofunction impairs brain-derived neurotropic factor signalling in the PFC, but not in the hippocampus, and disturbs PFC-dependent cognition in mice"],"prefix":"10.1177","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9151-7149","authenticated-orcid":false,"given":"Sara R","family":"Tanqueiro","sequence":"first","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de Medicina Molecular Jo\u00e3o Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco M","family":"Mouro","sequence":"additional","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de Medicina Molecular Jo\u00e3o Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catarina B","family":"Ferreira","sequence":"additional","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de Medicina Molecular Jo\u00e3o Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9line F","family":"Freitas","sequence":"additional","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de Medicina Molecular Jo\u00e3o Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo\u00e3o","family":"Fonseca-Gomes","sequence":"additional","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de Medicina Molecular Jo\u00e3o Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederico","family":"Sim\u00f5es do Couto","sequence":"additional","affiliation":[{"name":"Instituto de Farmacologia e Neuroci\u00eancias, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal"},{"name":"Instituto de 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