GLYCINE AND GABA INFLUENCE BINAURAL PROCESSING IN THE INFERIOR COLLICULUS OF THE MOUSTACHE BAT

1. The mammalian inferior colliculus contains large populations of bin aural cells that are excited by stimulation of the contralateral ear a nd are inhibited by stimulation of the ipsilateral ear, and are called excitatory/inhibitory (EI) cells. Neurons with EI properties are init ially created in the lateral superior olive (LSO), which, in turn, sen ds strong bilateral projections to the inferior colliculus. The questi ons that we address in this report are 1) whether the inhibition evoke d by stimulation of the ipsilateral ear occurs at the inferior collicu lus or whether it occurs in a lower nucleus, presumably the LSO; and 2 ) if the ipsilaterally evoked inhibition occurs at the inferior collic ulus, is the inhibition a consequence of glycinergic innervation or is it a consequence of GABAergic innervation. To study these questions, we recorded from 61 EI neurons in the inferior colliculus of the musta che bat before and during the iontophoretic application of the glycine receptor antagonist, strychnine. We also tested the effects of the ga mma-aminobutyric acid-A (GABA(A)) receptor antagonist, bicuculline, on 38 of the 61 neurons that were tested with strychnine. The main findi ng is that glycinergic or GABAergic inhibition, or both, contribute to the ipsilaterally evoked inhibition in similar to 50% of the EI neuro ns in the inferior colliculus. 2. Strychnine and bicuculline had diffe rent effects on the magnitude of the spike counts evoked by stimulatio n of the contralateral (excitatory) ear. On average, strychnine caused the maximum spike count evoked by contralateral stimulation to increa se by only 23%. The relatively small effects of strychnine on response magnitude are in marked contrast to the effects of bicuculline, which usually caused much larger increases in spike counts. For example, al though strychnine caused spike counts to more than double in similar t o 25% of the collicular neurons, bicuculline caused a doubling of the spike count in similar to 60% of the cells. 3. The inhibitory influenc es of ipsilateral stimulation were evaluated by driving the neurons wi th a fixed intensity at the contralateral ear and then documenting the reductions in spike counts due to the presentation of progressively h igher intensities at the ipsilateral ear. In 64% of the neurons sample d, blocking glycinergic inhibition with strychnine had little or no ef fect on the ipsilaterally evoked inhibition. These cells remained as s trongly inhibited during the application of strychnine as they did bef ore its application. In addition, the ipsilateral intensity that produ ced complete or nearly complete spike suppression in the predrug condi tion was also unchanged by strychnine. 4. In 36% of the neurons, stryc hnine markedly reduced the degree of ipsilaterally evoked spike suppre ssion. In five of these neurons, there was a complete elimination of t he ipsilateral inhibition: these neurons were transformed from strongl y inhibited EI neurons into monaural neurons. 5. The influence of both strychnine and bicuculline was tested sequentially in 38 neurons. In about one-half of these cells, (53%, 20/38) the ipsilaterally evoked i nhibition was unaffected by either drug. In 10 other units (26%), both drugs substantially reduced or eliminated the ipsilaterally evoked in hibition. In most of these cells, both bicuculline and strychnine redu ced the ipsilaterally evoked inhibition to a similar degree. In the re maining eight cells studied with both drugs (21%), the ipsilaterally e voked inhibition was reduced or eliminated by one of the drugs, but no t by both. 6. These results show that both glycinergic and GABAergic p rojections influence the ipsilaterally evoked inhibition in about one- half of the EI neurons in the inferior colliculus. The glycinergic inh ibition elicited by ipsilateral stimulation is most likely due to proj ections from the ipsilateral lateral superior olive, whereas the GABAe rgic inhibition evoked by ipsilateral stimulation is most likely cause d by the projections from the contralateral dorsal nucleus of the late ral lemniscus.