Journal of comparative and physiological psychology最新文献

The probability of proboscis extension to a water posttest is increased by prior sucrose stimulation. This phenomenon, termed the central excitatory state (CES), first described in Phormia regina, has now been characterized in Drosophila melanogaster. Drosophila's CES (a) decays over time and (b) is a function of sucrose concentration. THe test for CES also measures water responsiveness, a component of proboscis extension operationally independent of CES. Control experiments confirmed that CES-dependent proboscis extension is not an artifact due to restimulation of sucrose residues and that the neural junctures involved are centrally located.

The relation between dehydration and suckling behavior was determined in weanling rats 14, 20, and 23 days of age. After 15 days of age, intracellular and extracellular dehydration sharply reduced both the number of rats that suckled and the amount of milk consumed. Rehydration returned both behaviors to control levels. Thus, during the weaning period, the internal determinants of suckling are not homologous with those of drinking but are more homologous with those governing feeding.

The functional relation between restricted damage to ventral primary somatosensory neocortex and the ability of rats to acquire conditioned taste aversion (CTA( was examined by a combination of behavioral and neurohistological techniques. Lesions confined exclusively to the established gustatory neocortex (GN) did not disrupt CTA acquisition, nor did lesions confined to suprarhinal cortical areas ventral to the GN. Lesions that encroached on dorsal prepiriform and insular cortices produced CTA acquisition deficits and damaged a large proportion of efferent projections to the prefrontal and precentral neocortex. In a second experiment, lesions of dorsal prepiriform and insular cortices did not modify taste preference-aversion threshold to any of the four taste modalities. It is concluded tha ventral somatosensory neocortical fields, including the established GN, do not mediate CTA acquisition and that rhinal cortices ventral and posterior to the GN are preferentially involved in associative learning for tastes and illness.

p-Chloroamphetamine (PCA), which releases serotonin (5-HT) stores in brain regions, injected (5 mg/kg, ip) into male rats 40 min prior to the presentation of four inescapable shocks (.065 W) in the right-hand compartment of a normal shuttle box resulted in a profound fear-retention deficit as characterized by the total loss of the freezing and immobility posture that is normally the aftermath of shock presentation; zimelidine (10 mg/kg) 60 min before PCA completely blocked the disruption of fear. The "PCA effect" on fear retention was found at the 2.5 mg/kg but not quite at the 1.25 mg/kg dose, and when PCA (5 mg/kg) had been injected at least 8 hr before conditioning. The selective 5-HT uptake inhibitors zimelidine and fluoxetine, but not the noradrenaline (NA) uptake inhibitor desipramine, blocked the PCA effect, as did the 5-HT antagonist methergoline, but not the selective dopamine antagonist pimozide. A total retention impairment with a conditioning-testing delay of just 60 min was also evidenced, and the administration of PCA up to 2 hr before fear-retention testing also produced the retention deficit; these findings suggest some "retrieval failure." The 5-HT specificity of the PCA effect on fear retention was established by the demonstration that 5-HT-depleted rats (PCA, 2 X 10 mg/kg), but not NA-depleted rats, showed a nearly complete blockade of the fear-retention deficit. These experiments describe a role for 5-HT in both memory storage and retrieval processes.

Rats with bilateral dorsal hippocampal lesions were impaired when tested on standard (non-cued) versions of the radial arm maze, but other hippocampal groups performed almost as well as cortical and operated control groups when salient visual cues were added to each arm. Preoperative training on the non-cued, but not the cued, maze interfered with the benefits of postoperatively cuing hippocampal groups. Control groups performed equally well under all cuing and training conditions. Procedures that eliminated response sequencing did not affect performance of hippocampal or control groups. The results were interpreted as reflecting hippocampal involvement in mediating spatial cues but not necessarily along the lines predicted by cognitive map theory. It is suggested that deficits animals with hippocampal lesions represent one manifestation of a general impairment in processing information.

Extensive damage to the mesencephalic reticular formation (MRF) in rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. Animals with MRF lesions, although initially neither more nor less responsive than controls, could not attain as low a long-term asymptote of habituation as could control animals with repeated presentations of an auditory stimulus. Changing the quality of the auditory stimulus abolished the asymptotic difference in responsiveness. With repeated presentations of the second auditory stimulus, control animals again reached a significantly lower long-term habituation asymptote than did animals with MRF lesions. The course of long-term habituation for the two groups suggested a disruption of an extrinsic, inhibitory habituation process by the lesions. The effects of MRF lesions were specific to the acoustic startle response. Control animals and those with lesions showed comparable response levels, short-term habituation, and long-term habituation of the lick suppression response. responsiveness and habituation to tactile stimuli were comparable for the two groups in both lick suppression and startle response measures.

The capacity for taste cues to modulate the food intake of ventromedial hypothalamic (VMH) and normal rats was examined. Rats with a chronically indwelling gastric cannula sham fed (cannula open) or normally fed (cannula closed) liquid diets varying in sucrose content. Throughout the study VMH rats were maintained at control body weight levels. The results identified two major aspects of the relationship between palatability and feeding. First, for both groups, the discrepancy in consumption between sham and normal feeding situations depended on the sweetness of the diet. The implications of this finding for studies using sham feeding to assess putative feeding control signals are discussed. Second, VMH lesions were demonstrated to exaggerate the sensory control of food intake. Under sham-feeding conditions, increases in the sweetness of the diet led to disproportionately large increments of food intake in VMH animals relative to controls. These data support the existence of a finickiness component in the VMH syndrome and allude to the nature of the physiological disturbance underlying this behavior change.

Neuronal unit activity was recorded from auditory nuclei, and dorsal hippocampus, and the cerebellum in rabbits behaviorally detecting a threshold-level constant intensity white noise stimulus. Stimulus-evoked neuronal unit activity was present and identical on both detection and nondetection trials in auditory nuclei but was dichotomous in the hippocampus and in the cerebellum, the latter two systems predicting the occurrence of behavioral detection. It is concluded that the behavioral absolute auditory threshold is not determined by differential activation of neurons in the primary auditory relay nuclei.