Cortical Maps: Data and Models

How are the complex maps for orientation selectivity (OS) created in the primary visual cortex (V1)? Rodents and rabbits have a random distribution of OS preferences across V1 while in cats, ferrets, and all primates cells with similar OS preferences cluster together into relatively wide cortical columns. Given other clear similarities in the organization of the visual pathways, why is it that maps coding OS preferences are so radically different? Prominent models have been created of cortical OS mapping that incorporate Hebbian plasticity, intracortical interactions, and the properties of growing axons. However, these models suggest that the maps arise primarily through intracortical interactions. Here we focus on several other features of the visual system and brain that may influence V1 structure. These are: eye divergence, the total number of cells in V1, the thalamocortical networks, the topography of the retina and phylogeny. We outline the evidence for and against these factors contributing to map formation. One promising theory is that the central-to-peripheral ratio (CP ratio) of retinal cell density can be used to predict whether or not a species has pinwheel maps. Animals with high CP ratios (>7) have orientation columns while those with low CP ratios (<4) have random OS maps. The CP ratio is related to the total number of cells in cortex, which also appears to be a reasonable contributing factor. However, while these factors correlate with map structure to some extent, there is a gray area where certain species do not fit elegantly into the theory. A problem with the existing literature is that OS maps have been investigated in only a small number of mammals, from a small fraction of the mammalian phylogenetic tree. We suggest four species (agouti, fruit bat, sheep, and wallaby) that have a range of interesting characteristics, which sit at intermediate locations between primates and rodents, that make them good targets for filling in the missing gaps in the literature. We make predictions about the map structures of these species based on the organization of their brains and visual systems and, in doing so, set possible paths for future research.

Manipulations that enhance neuroplasticity may inadvertently create opportunities for maladaptation. We have previously used passive exposures to non-traumatic white noise to open windows of plasticity in the adult rat auditory cortex and induce frequency-specific functional reorganizations of the tonotopic map. However, similar reorganizations in the central auditory pathway are thought to contribute to the generation of hearing disorders such as tinnitus and hyperacusis. Here, we investigate whether noise-induced reorganizations are accompanied by electrophysiological or behavioral evidence of tinnitus or hyperacusis in adult Long-Evans rats. We used a 2-week passive exposure to moderate-intensity (70 dB SPL) broadband white noise to reopen a critical period for spectral tuning such that a second 1-week exposure to 7 kHz tone pips produced an expansion of the 7 kHz frequency region in the primary auditory cortex (A1). We demonstrate for the first time that this expansion also takes place in the ventral auditory field (VAF). Sound exposure also led to spontaneous and sound-evoked hyperactivity in the anterior auditory field (AAF). Rats were assessed for behavioral evidence of tinnitus or hyperacusis using gap and tone prepulse inhibition of the acoustic startle response. We found that sound exposure did not affect gap-prepulse inhibition. However, sound exposure led to an improvement in prepulse inhibition when the prepulse was a 7 kHz tone, showing that exposed rats had enhanced sensorimotor gating for the exposure frequency. Together, our electrophysiological and behavioral results provide evidence of hyperacusis but not tinnitus in sound-exposed animals. Our findings demonstrate that periods of prolonged noise exposure may open windows of plasticity that can also be understood as windows of vulnerability, potentially increasing the likelihood for maladaptive plasticity to take place.