Changes in the length and organization of nucleus laminaris dendrites after unilateral otocyst ablation in chick embryos

To evaluate the contributions of the ear and acoustic stimulation to the structural development of central auditory neurons, the right otocyst was surgically destroyed in chick embryos on the third day of incubation. This pro‐cedure prevents the formation of the inner ear and acousticovestibular nerve and thus removes the dominant afferent synaptic input to nucleus magnocellularis (NM). Subsequently, nucleus laminaris (NL), which receives afferent synaptic input to its dorsal dendrites from the ipsilateral NM and afferents to its ventral dendrites from the contralateral NM, was studied on both sides of the brain in Golgi preparations. By embryonic day 17, the total lengths of the individual NL dendritic fields connected to the right NM (i.e., the manipulated dendrites) were decreased by an average of 44% as compared to those NL dendrites connected to the left NM (i.e., the unmanipulated dendrites). The mean length of the unman‐ipulated dendrites in experimental animals, however, did not differ from average dendritic length in normal control embryos. The amount of dendritic length lost by a NL neuron was strongly correlated with the length of the unmanipulated dendrites on the opposite side of the same neuron and with that neuron's position within NL. The lengths of dorsal and ventral dendrites on individual neurons were at least as highly correlated in experimental as in normal control animals. Correlation of dendrite length with the position of measured neurons within NL indicated that the large rostromedial‐to‐caudolateral gradient of increasing den‐drite length present in the normal NL is also found in the manipulated dendrites in experimental animals. Regression and correlation analyses relating the length of dendrites to their longitudinal cross‐sectional area revealed that there was no difference in mean dendritic diameter between the manipulated and unmani‐pulated dendrites in experimental animals. The findings of a high dorsal‐ventral length correlation in experimental animals and a normal spatial gradient of dendritic length among the manipulated dendrites suggests two explanations. Either (1) acoustically evoked synaptic activity is not essential for the develop‐ment of these two aspects of dendritic organization, or (2) the normal NM afferents to the unmanipulated dendrites of each NL neuron in an animal with one ablated otocyst can, under the influence of acoustically driven activity, control develop‐ment of the manipulated dendrites. These alternate hypotheses can be tested experimentally.