Weakly electric fish generate electric current and use hundreds of voltage sensors on the surface of their body to navigate and locate food. Experiments (von der Emde and Fetz 2007 J. Exp. Biol. 210 3082-95) show that they can discriminate between differently shaped conducting or insulating objects by using electrosensing. One approach to electrically identify and characterize the object with a lower computational cost rather than full shape reconstruction is to use the first order polarization tensor (PT) of the object. In this paper, by considering experimental work on Peters' elephantnose fish Gnathonemus petersii, we investigate the possible role of the first order PT in the ability of the fish to discriminate between objects of different shapes. We also suggest some experiments that might be performed to further investigate the role of the first order PT in electrosensing fish. Finally, we speculate on the possibility of electrical cloaking or camouflage in prey of electrosensing fish and what might be learnt from the fish in human remote sensing.
Alongside difficulties with communication and social interaction, autism is often accompanied by unusual sensory and perceptual experiences including enhanced visual performance on tasks that involve separating local parts from global context. This superiority may be the result of atypical integrative processing, involving feedback and lateral connections between visual neurons. The current study investigated the integrity of these connections in autistic adults by examining two psychophysics tasks that rely on these processes - collinear facilitation and contour integration. The relative contribution of feedback and lateral connectivity was studied by altering the timing of the target relative to the flankers in the collinear facilitation task, in 16 autistic and 16 non-autistic adults. There were no significant differences in facilitation between the autistic and non-autistic groups, indicating that for this task and participant sample, lateral and feedback connectivity appear relatively intact in autistic individuals. Contour integration was examined in a different group of 20 autistic and 18 non-autistic individuals, for open and closed contours to assess the closure effect (improved detection of closed compared to open contours). Autistic individuals showed a reduced closure effect at both short (150 ms) and longer (500 ms) stimulus presentation durations that was driven by better performance of the autistic group for the open contours. These results suggest that reduced closure in a simple contour detection paradigm is unlikely to be due to slower global processing. Reduced closure has implications for understanding sensory overload by contributing to reduced figure-ground segregation of salient visual features.
Various lines of evidence suggest a role in cognition for the endogenous neuropeptide, neurotensin, involving an interaction with the central nervous system cholinergic pathways. A preliminary study has shown that central administration of neurotensin enhances spatial and nonspatial working memory in the presence of scopolamine, a muscarinic receptor antagonist which induces memory deficits. Utilizing similar methods, the present study employed a two-trial novel object discrimination task to determine the acute effect of a neurotensin peptide analogue with improved metabolic stability, PD149163, on recognition memory in Lister hooded rats. Consistent with previous findings with neurotensin, animals receiving an intracerebroventricular injection of PD149163 (3 microg) significantly discriminated the novel from familiar object during the choice trial. In addition, a similar dose of PD149163 restored the scopolamine-induced deficit in novelty recognition. The restoration effect on scopolamine-induced amnesia produced by PD149163 was blocked by SR142948A, a nonselective neurotensin receptor antagonist, at a dose of 1 mg/kg (intraperitonial) but not at 0.1 mg/kg. In conclusion, the present results confirm a role for neurotensin in mediating memory processes, possibly via central cholinergic mechanisms.