Nucleus Isthmi and Optic Tectum in Frogs
Our laboratory has been investigating the role of nucleus isthmi in tectally mediated visual information processing. We have found that unilateral ablation of n. isthmi results in a contralateral monocular scotoma. Within the scotoma the animal does not respond to visually presented prey or threat stimuli. The size of the scotoma is dependent on the volume of n. isthmi ablated. When the entire nucleus is ablated there is no recovery of function within the scotoma for up to 11 months. Unilateral injection into n. isthmi of the excitatory neurotoxin ibotenic acid results in a temporary loss of responses to visually presented prey in the contralateral monocular field. Normal responses return within 1 to 2 weeks. Bilateral ablation of n. isthmi results in loss of responsiveness to visually presented prey and threat stimuli in the entire visual field. After 4 to 5 weeks there is a return of responsiveness in the binocular field. Nucleus isthmi fibers are the predominant non-retinal extrinsic input to the superficial tectal layers. The contralaterally projecting isthmo-tectal fibers cross in the posterior part of the optic chiasm. When this part is transected, the animal no longer responds to visually presented threat stimuli but responds normally to visually presented prey stimuli. Nucleus isthmi is virtually the only cholinergic input to the tectum. There is evidence from other laboratories that some retino-tectal fibers contain membrane bound acetylcholine receptors. Thus, n. isthmi might directly modify retinal input. Our evidence is compatible with the model of Arbib & House with n. isthmi playing a role in prey localization.
KeywordsOptic Chiasm Optic Tectum Threat Stimulus ChAT Activity Ibotenic Acid
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