Pharmacology of sensory gating in the ascending auditory system of the pigeon (Columba livia)

Rationale: Whether the underlying neurochemical basis of sensori(motor) gat ing is exclusively the result of mammalian brain evolution is not known. Ob jective: 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 telel encephalon was assessed in a within-subject design in pigeons (Columba livi a) 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 elev ator palpebralis superior, and Musculus nictitantis. Thalamic gating was re corded using electrodes which were chronically implanted into the nucleus o voidalis thalami and the neostriatum caudale (field L), respectively. Resul ts: KET, APO and AMP disrupted dose-dependently sensorimotor gating. The ef fect of APO and AMP was blocked by HAL. PPI disruption following BTP did no t reach statistical significance. KET disrupted thalamic gating and increas ed prepulse-induced inhibition in field L. By contrast, AMP increased thala mic and decreased field L inhibition of field potentials when preceded by a pre-stimulus. Both effects were antagonised by HAL thus providing prelimin ary evidence for a D-2-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 e xplained by concurrent D-1-mediated telencephalic inhibition. Conclusion: I t is concluded that thalamic gating is modulated by a dopaminergic/glutamat ergic mechanism. The findings also confirm the notion of an homologous neur ochemical basis of sensorimotor gating in mammals and birds.