No abstract

Visual activity after eye-opening influences feature map structure in primary visual cortex (V1). For instance, rearing cats in an environment of stripes of one orientation yields an over-representation of that orientation in V1. However, whether such changes also affect the higher-order statistics of orientation maps is unknown. A statistical bias of orientation maps in normally raised animals is that the probability of the angular difference in orientation preference between each pair of points in the cortex depends on the angle of the line joining those points relative to a fixed but arbitrary set of axes. Natural images show an analogous statistical bias; however, whether this drives the development of comparable structure in V1 is unknown. We examined these statistics for normal, stripe-reared and dark-reared cats, and found that the biases present were not consistently related to those present in the input, or to genetic relationships. We compared these results with two computational models of orientation map development, an analytical model and a Hebbian model. The analytical model failed to reproduce the experimentally observed statistics. In the Hebbian model, while orientation difference statistics could be strongly driven by the input, statistics similar to those seen in experimental maps arose only when symmetry breaking was allowed to occur spontaneously. These results suggest that these statistical biases of orientation maps arise primarily spontaneously, rather than being governed by either input statistics or genetic mechanisms.

Androstadienone is a steroid found in human sweat and other secretions. It has been widely proposed as a candidate for a human pheromone. As an odorant it possesses some unique properties. Here we demonstrate that, firstly, there is a very wide range of thresholds in the human population, and they are not normally distributed. Secondly, repetitive exposure causes a decrease in detection threshold of more than four orders of magnitude, and thirdly, accompanying this sensitization process is a change in the perceived odor quality. Those with low to intermediate sensitivities ascribe to it a wide range of odor descriptors across the hedonic scale, but as these individuals become sensitized, their description changes to predominantly putrid. We propose that this change in odor quality reflects the presence of at least two receptor populations for androstadienone; a low-affinity receptor conveying pleasant odor qualities and a high-affinity receptor mediating unpleasant odor qualities. We further propose that repetitive exposure results in the increased expression of the high-affinity receptor thereby shifting the balance of perception to the negative end of the hedonic scale.

Although the basis of our knowledge of experience-dependent plasticity comes from studies on carnivores and primates, studies examining the physiological and molecular mechanisms that underlie development and plasticity have increasingly employed mice. We have used several common rearing paradigms, such as dark-rearing and monocular deprivation (MD), to examine the timing of the physiological and molecular changes to altered experience in the cat primary visual cortex. Dark-rearing from birth or for 1 week starting at 4 weeks of age produced a similar reduction in the amplitude of responses measured through intrinsic signal imaging and a reduction in orientation selectivity. One week of visual experience following dark-rearing until 4 weeks of age yielded normal responses in both amplitude and orientation selectivity. The depression of deprived-eye responses was similar in magnitude after 2 and 7 days of MD. In contrast, non-deprived-eye responses almost doubled in magnitude after 7 days compared with 2 days of MD. These changes in the functional properties of primary visual cortex neurons were mirrored by specific changes in synaptic protein expression. Changes in proteins such as the NR2A and NR2B subunits of the N-methyl-D-aspartate receptor, postsynaptic density protein 95, alpha-CA(2+) /calmodulin-dependent protein kinase II (αCaMKII), and GABA(A) α1a indicated that the levels of sensory activity regulated mechanisms associated with both excitatory (NR2A and NR2B) and inhibitory (GABA(A) α1a) transmission so as to maintain response homeostasis. Additionally, we found that MD regulated the AMPA receptor glutamate (GluR1) subunit as well as signalling molecules (αCaMKII and synaptic Ras GTPase activating protein, SynGAP) downstream of N-methyl-D-aspartate receptors. Proteins in a common signalling pathway appeared to have similar developmental expression profiles that were broadly similar between cats and rodents.