Rationale: Whether the underlying neurochemical basis of sensori(motor) gating is exclusively the result of mammalian brain evolution is not known.

Objective: The effects of ketamine (KET), benztropine (BTP), apomorphine (APO), methylphenidatehydrochloride (AMP) and haloperidol (HAL) on sensorimotor gating of the acoustic startle and gating of auditory input into the telelencephalon was assessed in a within-subject design in pigeons (Columba livia) using the prepulse inhibition (PPI) paradigm.

Methods: The startle blink reflex was recorded using EMG electrodes which were chronically implanted into the adjoining Musculus palpepralis superior et inferior, Musculus elevator palpebralis superior, and Musculus nictitantis. Thalamic gating was recorded using electrodes which were chronically implanted into the nucleus ovoidalis thalami and the neostriatum caudale (field L), respectively.

Results: KET, APO and AMP disrupted dose-dependently sensorimotor gating. The effect of APO and AMP was blocked by HAL. PPI disruption following BTP did not reach statistical significance. KET disrupted thalamic gating and increased prepulse-induced inhibition in field L. By contrast, AMP increased thalamic and decreased field L inhibition of field potentials when preceded by a pre-stimulus. Both effects were antagonised by HAL thus providing preliminary evidence for a D2-mediated auditory gating mechanism in the thalamus. However, while the effect of APO at the thalamic level was similar to AMP, prepulse-induced inhibition of field L activity was enhanced. This may be explained by concurrent D1-mediated telencephalic inhibition.

Conclusion: It is concluded that thalamic gating is modulated by a dopaminergic/glutamatergic mechanism. The findings also confirm the notion of an homologous neurochemical basis of sensorimotor gating in mammals and birds.