© 2022,Turk Hijyen ve Deneysel Biyoloji Dergisi. All Rights Reserved.Objective: Thiamine deficiency (TD) during the developmental period is a very rare condition in the developed countries but it is becoming more frequent worldwide because of worsened socioeconomic status in some communities. Thiamine has many metabolic and structural functions in the brain especially in the developmental period. Postnatal TD may cause long-lasting effects in the brain. Chronic TD causes hearning deficit but the effects of postnatal TD to the central auditory processing during adulthood have not been investigated sufficiently. The loudness dependence of auditory evoked potentials (LDAEP) provides a well established marker of the central serotonin activity. Besides, paired-click responses (PRs) are associated with glutamatergic/ GABAergic transmission. İnvestigating these responses and underlying oscillations that reflect the neuronal correlate of auditory processing provides important information about auditory changes due to TD condition. Methods: Rats were divided into two groups as follows; Control whose dams fed with normal diet (C), thiamine deficient whose dams fed with thiamine_deficient diet during postnatal period (TD). In adulthood, we recorded AEPs and PRs and analyzed LDAEP, components and spectral changes to unravel the network alterations. Results: The N1/P2 responses for two loadest stimulus were significantly increased in the TD group versus the C group. In parallel, higher LDAEP value was obtained in the TD group. As gamma level was significantly attenuated in the TD group, elevated theta/alpha response was observed in the TD group compared with the C group. For PRs, higher N1 response to second stimuli and lower suppression rate detected in the TD group. Concomitant increment of theta responses to second stimuli was observed in the TD group. Conclusion: Postnatal TD causes degenerative changes with long-term implications observed in auditory network dynamics which could be partly explained by altered serotonergic and glutamatergic/GABAergic transmission.