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The kynurenine pathway has emerged as a target for addiction treatment through its modulation of glutamatergic and dopaminergic neurotransmission. This study investigates the effects of kynurenine 3\u2010monooxygenase (KMO) inhibition on fentanyl self\u2010administration in rats.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Adult male rats received the KMO inhibitor, Ro 61\u20108048 during fentanyl self\u2010administration. Responding was assessed across acquisition, maintenance, extinction and reinstatement. The involvement of nicotinic acetylcholine receptor \u03b17 subunit (\n                      <jats:italic>\u03b1<\/jats:italic>\n                      7nAChR) was investigated using the positive allosteric modulator PNU\u2010120596. Sucrose self\u2010administration, locomotor activity and rotarod performance were also evaluated. Kynurenine pathway metabolites were quantified in plasma and nucleus accumbens using ultra\u2010performance liquid chromatography\u2010mass spectrometry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Ro 61\u20108048 reduced fentanyl intake and active lever responding across all addiction phases. These effects were associated with increased kynurenic acid (KYNA) levels and altered kynurenine pathway metabolite profiles. PNU\u2010120596 did not prevent Ro 61\u20108048 effects, indicating an\n                      <jats:italic>\u03b1<\/jats:italic>\n                      7nAChR\u2010independent mechanism. Although Ro 61\u20108048 reduced sucrose self\u2010administration and spontaneous locomotor activity, it did not affect rotarod performance, progressive ratio breakpoints nor did it produce aversive behaviour suggesting that KMO inhibition modulates the reinforcing strength of both drug and natural rewards, rather than inducing general behavioural suppression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>KMO inhibition with Ro 61\u20108048 robustly attenuates fentanyl\u2010directed behaviour and affects kynurenine pathway metabolism beyond a shift towards KYNA production. These findings support KMO inhibition as a potential therapeutic strategy for opioid use disorder and warrant further investigation into its underlying mechanisms and translational potential.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70549","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T23:55:57Z","timestamp":1782258957000},"page":"5458-5475","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Inhibition of kynurenine 3\u2010monooxygenase (KMO) reduces fentanyl and sucrose intake and relapse\u2010like behaviour in rats"],"prefix":"10.1111","volume":"183","author":[{"given":"Carlos","family":"N\u00fa\u00f1ez\u2010de la Calle","sequence":"first","affiliation":[{"name":"Departamento de Farmacolog\u00eda y Toxicolog\u00eda, Facultad de Medicina Universidad Complutense  Madrid Spain"},{"name":"Instituto de Investigaci\u00f3n Sanitaria Hospital 12 de Octubre 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