Browsing by Subject "Toads -- Behavior"
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Item Association of habituation with endogenous alpha-melanocyte-stimulating hormone in the brain of the toad, Bufo cognatus(Texas Tech University, 1995-05) Kim, YoungsooSeveral lines of evidence indicate that, in mammalian and nonmammalian vertebrates, alpha-melanocyte- stimulating hormone (a-MSH) acts as a neurotransmitter/neuromodulator within the brain to enhance learning and memory. Although a great deal is known about the pharmacological effects of a-MSH peptides on learning, virtually nothing is known about the physiological role of endogenous a-MSH neurons in learning behavior. I used a simple behavioral model of learning, habituation of prey-catching behavior in the toad Bufo cognatus, to examine whether learning behavior is associated with alterations in the activity of melanotropin cells in the brain and pituitary gland. Changes in the tissue concentration of a-MSH in specific brain areas were used to gauge changes in the synthetic/secretory actions of brain a-MSH cells. The distribution of a-MSH and adrenocorticotropin (ACTH) in the brain of the toad was examined by immunocytochemistry using the avidin biotinylated-peroxidase technique. Pro-opiomelanocortin (POMC) perikarya were detected in the ventral infundibular nucleus and the lateral hypothalamic nucleus. The cells projected their fibers toward brain areas that included the ventral telencephalon, the ventral hypothalamus, the tectum and pretectal area, the brainstem, and the spinal cord. Intense immunoreactive staining was observed in the olfactory nucleus and the nucleus accumbens, the medial anterior thalamus, the preoptic nuclei, and the infundibulum. The immunocytochemical localization of a-MSH-immunoreactivity in the brain of B. cognatus was confirmed by biochemical studies. First, heterologous radioimmunoassay of a-MSH in the toad was validated by the demonstration of parallelism between serially diluted brain extracts and plasma and synthetic a-MSH. a-MSH concentration was highest in the caudal thalamus and retrochiasmatic hypothalamus, followed by the caudal telencephalon and preoptic area, the rostral telencephalon, the brainstem and the optic tectum. With one exception, there were no significant differences at any time point between control and habituated animals. However, significant changes in brain a-MSH content were observed within each group over time. In the brains of both habituated and control animals, a-MSH content was increased in the hypothalamic and the preoptic areas and decreased in the telencephalic area and the brainstem. My immunocytochemical and biochemical findings suggest that, aside fi'om its hormonal activity in the control of melanosome dispersion, a- MSH may play a role as a neurotransmitter and/or neuromodulator in the toad brain. Furthermore, it seems that the habituation of prey-catching behavior is not associated with changes in the activity of a-MSH levels in the brain and the plasma of toads. Prolonged confinement might cause alterations in the activity of neuronal and pituitary POMC cells.Item Influence of ACTH/MSH peptides and corticosterone of habituation of prey catching behavior in the toad, Bufo cognatus(Texas Tech University, 1995-08) Carpenter, Anne MarieThe effect of adrenocorticotropin and melanotropin peptides, corticosterone, and the a-MSH antagonist, U-76188E, was studied on the acquisition and extinction of the prey-catching behavior in the toad, Bufo cognatus. Male toads were injected with corticosterone, porcine ACTH[l-39], a-MSH, (Nle4-D-Phe7)a-MSH, desacetyl- a-MSH, ACTH[4-10], a-MSH antagonist (U-76188E), or control vehicle 30 min prior to acquisition. ACTH[l-39], ACTH[4-10] and a-MSH significantly decreased the number of turning reactions during acquisition in relation to controls. The effect of these peptides was rapid, occurring within the first 20 min of acquisition. Corticosterone caused a significant decrease in the number of turning reactions, although this effect was not observed until 40 min after the onset of testing. (Nle^4-DPhe^ 7) a-MSH and des-acetyl-a-MSH did not influence acquisition. The a-MSH antagonist (U-76188E) abolished the behavioral response to a-MSH during acquisition, but did not significantly influence extinction. ACTH[ 1-391 was the only peptide to delay extinction. These data suggest that the ability of ACTH to facilitate acquisition is independent of interrenal corticosterone secretion. Furthermore, it appears that minor structural differences can dramatically influence the ability of ACTH/MSH peptides to modulate learning and memory processes in toads.