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In anurans, visual prey information is filtered in the retina and processed in interacting pretectal and tectal retinal projection fields. Neuropeptide Y is involved in pretecto-tectal inhibition. Information related to prey and its location in space is transmitted to the bulbar/spinal motor pattern generating systems by ensembles of efferent tectal and tegmental neurons. This basic stimulus-response (S-R) mediating circuit is influenced by forebrain loops. It is suggested that ventral striatum and lateral thalamic nucleus participate in a loop responsible for gating S-R. The hippocampal pallium modifies S-R via the anterior thalamus with regard to previous experience. Dopaminergic modulation influences prey-catching strategies.

Previous studies on the dopaminergic modulation of visuomotor functions in amphibians showed that the dopamine agonist apomorphine (APO) alters prey-catching strategies. After systemic administration of APO in common toads Bufo bufo, prey-oriented turning and locomotion was attenuated whereas snapping toward prey was facilitated in a dose dependent manner. With systemic APO administration, toads which had previously been hunting, that is pursuing prey, behaved in a waiting position, that is sitting motionless and waiting for prey. This suggests that APO facilitates the ingestive component and inhibits the orientational and locomotory components of prey capture. To help unravel the cerebral sites of action of APO, the present study employs the ¹⁴C-2-deoxyglucose method to compare the rate of local glucose utilization in 41 brain structures. The retinal projection fields – e.g. superficial optic tectum, pretectal nuclei, and anterior dorsal thalamic nucleus – showed an elevation in glucose utilization due to APO-induced increases in retinal output. The medial tectal layers and the ventral striatum, both involved in visuomotor functions related to prey-oriented turning and locomotion, displayed APO-induced decreases in glucose utilization. APO-induced increases in glucose utilization were observed in the medial reticular formation and the hypoglossal nucleus which participate in the motor pattern generation of snapping. APO-induced increases in glucose utilization were also detected in the nucleus accumbens and the ventral tegmentum (mesolimbic system) as well as in the ventromedial pallium (‘primordium hippocampi’) and the septum, both of which belonging to the limbic system. These structures contribute to motivational level control and may be responsible for the APO-induced elevation of the snapping rate. Various other structures revealed APO-induced increases in glucose utilization. These structures include the olfactory bulb, lateral pallium, suprachiasmatic nucleus, nucleus of the periventricular organ, and the nucleus of the solitary tract. The lateral amygdala displayed APO-induced decreases in glucose utilization. The APO-induced alterations in local cerebral glucose utilization are evaluated with reference to the distribution of dopaminergic structures, and this is compared with similar data obtained in the rat by other authors. A neural network explaining the APO-induced behavioral syndrome in the common toad is discussed.

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This study confirms for a phylogenetically basal terrestrial vertebrate that dopaminergic modulations interfere with the visually directed appetitive and consummatory feeding behaviors orienting and snapping, respectively. (1) In common toads Bufo bufo, intralymphatic administration of the dopamine D2/D1-receptor agonist apomorphine led to a dose-dependent facilitation of prey-snapping in response to moving objects. The snapping activity reached a maximum 15-35 min after apomorphine injection. (2) To changes in configurational stimulus features, the basic pattern of discrimination was maintained; however, the acuity of discrimination was reduced due to the high snapping response level. (3) The apomorphine-induced facilitation of snapping was accompanied by a suppression of prey-oriented lunging and turning. Toads snapped only if prey occurred frontally in the visual field at a relatively short distance. The snapping behavior was fixed in its form and stereotyped regarding its immediate release. (4) About 90 min after apomorphine administration, prey-oriented turning behavior was restored and displayed a facilitatory rebound. (5) In comparative experiments with the species B. marinus, both prey-oriented turning and snapping responses were suppressed by apomorphine in a dose-dependent manner. (6) After pre-treatment with the dopamine antagonist haloperidol, apomorphine showed no measurable effect on the visual release of prey orienting or snapping. (7) The results contribute to the sensorimotor and the motivation hypothesis of dopamine function proposed for higher vertebrates and stimulate a comparative discussion of anatomic homologies and functional analogies.