Physiol Behav. 2026 Sep 10:115501. doi: 10.1016/j.physbeh.2026.115501. Online ahead of print.
ABSTRACT
Nitric oxide (NO) and dopaminergic/glutamatergic signaling may contribute to central control of feed intake, but the nature of their interactions in avian species remains unclear. This study examined potential roles of these systems in modulating food consumption in 5‑day‑old male Ross 308 broiler chicks. A total of 480 male Ross 308 chicks were used in ten experiments, each with four treatment groups (n = 12 per group). Chicks received intracerebroventricular (ICV) administration of L‑arginine (NO precursor), L‑NAME (NOS inhibitor), MK‑801 (NMDA antagonist), MSPG (metabotropic glutamate antagonist), SCH23390 (D1 antagonist) and AMI‑193 (D2 antagonist), alone or in combination. Feed intake was measured at 30, 60 and 120 min after injection. L-arginine and L-NAME reduced feed intake at selected doses and observation times, although the magnitude and duration of the responses varied across doses and time points, indicating that pharmacological manipulation of central nitrergic signaling produced non-linear feeding responses under the present experimental conditions. L‑arginine‑induced hypophagia was attenuated by MK‑801, whereas MK‑801 alone did not alter intake. MSPG alone reduced feed intake but did not significantly alter L-arginine- or L-NAME-induced hypophagia when co-administered with either treatment. D1 blockade attenuated L‑arginine‑induced hypophagia, but did not significantly modify L-NAME-induced hypophagia, whereas D2 blockade did not significantly modify the hypophagic responses to either treatment. These findings provide behavioral pharmacological evidence consistent with context-dependent contributions of glutamatergic and dopaminergic signaling to nitrergic-associated feeding responses in male broiler chicks. NMDA and D1 receptor signaling may contribute to L‑arginine‑induced hypophagia, whereas L-NAME-induced hypophagia was enhanced by NMDA receptor blockade but was not significantly modified by metabotropic glutamate, D1, or D2 receptor blockade under the present conditions. However, the present acute ICV pharmacological approach does not establish the underlying physiological or cellular mechanisms, which require direct neurochemical and molecular investigation.
PMID:42722222 | DOI:10.1016/j.physbeh.2026.115501
