Lordosis-disrupting tectal lesions alter midbrain unit somatosensory responsiveness in hamsters

Previous research has shown that bilateral deep tectal lesions in golden hamsters abolish the lordosis response, whereas unilateral lesions selectively impair lordosis elicitation by contralateral flank stimulation. The present study analyzed the neural basis of these lesion effects by assessing the somatosensory responsiveness of midbrain neurons in three groups of urethane-anesthetized hamsters: animals with lordosis-abolishing bilateral tectal lesions, animals with lordosis-impairing unilateral lesions, and intact animals. Animals with bilateral lesions differed from the other groups in three aspects of unit sensory responsiveness by showing: (1) the highest percentage of neurons responsive to somatic stimulation, (2) the highest incidence of unit responsiveness to flank stimulation, and (3) the greatest proportion of responsive neurons in the ventral tegmentum. Hamsters with unilateral lesions showed basically normal unit responsiveness apart from elevated unit response to face stimulation. The results suggest that bilateral tectal lesions may eliminate lordosis by the combined effects of enhanced ventral tegmental somatosensory responsiveness and tectal destruction. Unilateral lesions appear to impair lordosis without changing the somatosensory excitability of remaining midbrain neurons.