QUINOLINIC ACID LESIONS OF THE VENTRAL STRIATUM REDUCE SENSORIMOTOR GATING OFACOUSTIC STARTLE IN RATS

The startle reflex is inhibited when the startling stimulus is precede d 30-500 ms by a weak noise or 'prepulse'. While the primary startle c ircuit is organized at or below the pens, the amount of 'prepulse inhi bition' (PPI) is modulated by forebrain activity and is reduced in cer tain neuropsychiatric disorders. The reduction of PPI in these disorde rs is thought to reflect disturbances in sensorimotor inhibition which underlie an inability to 'gate' irrelevant sensory, motor or cognitiv e information. PPI is altered by pharmacologic manipulations of the ve ntral striatum, which is thought to modulate PPI via sequential effere nt projections through the ventral pallidum and pontine reticular form ation. In the present study, we assessed the effects of cellular lesio ns of the ventral striatum (VS) on PPI. Quinolinic acid lesions of the VS significantly reduced PPI and increased startle amplitude; however , changes in PPI and startle amplitude were not significantly correlat ed within rats. Infusion of the GABA agonist muscimol into ventral str iatal terminal fields in the ventral pallidum significantly restored P PI in VS-lesioned rats, but did not reverse lesion effects on startle amplitude. It was verified that muscimol infusions were made into an a rea which receives direct VS innervation, using ventral pallidal injec tions of the retrograde tracer Nuclear yellow in VS sham-lesioned rats . Cells in the ventral striatum appear to modulate sensorimotor gating of the startle reflex via a GABAergic innervation of the ventral pall idum.