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.