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In the hall of animal oddities, the reindeer (Rangifer tarandus) is the only mammal with a color-shifting tapetum lucidum and the only ruminant with a lichen-dominated diet. These puzzling traits coexist with yet another enigma--ocular media that transmit up to 60% of ultraviolet (UV) light, enough to excite the cones responsible for color vision. It is unclear why any day-active circum-Arctic mammal would benefit from UV visual sensitivity, but it could improve detection of UV-absorbing lichens against a background of UV-reflecting snows, especially during the extended twilight hours of winter. To explore this idea and advance our understanding of reindeer visual ecology, we recorded the reflectance spectra of several ground-growing (terricolous), shrubby (fruticose) lichens in the diets of reindeer living in Cairngorms National Park, Scotland.

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A working hypothesis is put forward in this article that the contralateral organization of the human nervous system appears to function like a quantum unfolded holographic apparatus by appearing to invert and reverse quantum unfolded visual and non-visual spatial information. As such, the three-dimensional contralateral organization would be an artifactual representation of the underlying dynamics of a fundamentally two-dimensional universe. According to the holographic principle, nothing that is experienced as three-dimensional could have been processed in a three-dimensional brain. Everything we would experience at a two-dimensional level would appear as a three-dimensional holographic representation, including the architecture of our brains. Various research observations reported elsewhere are reviewed and interpreted here as they may be related in a process that is fundamental to the underlying two-dimensional dynamics of the contralateral organization. The classic holographic method and characteristics of image formation contained by a holograph are described as they relate to the working hypothesis. The double-slit experiment is described and its relevance to the working hypothesis.

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In insects and mammals, olfactory experience in early life alters olfactory behavior and function in later life. In the vinegar fly Drosophila, flies chronically exposed to a high concentration of a monomolecular odor exhibit reduced behavioral aversion to the familiar odor when it is reencountered. This change in olfactory behavior has been attributed to selective decreases in the sensitivity of second-order olfactory projection neurons (PNs) in the antennal lobe that respond to the overrepresented odor. However, since odorant compounds do not occur at similarly high concentrations in natural sources, the role of odor experience-dependent plasticity in natural environments is unclear. Here, we investigated olfactory plasticity in the antennal lobe of flies chronically exposed to odors at concentrations that are typically encountered in natural odor sources. These stimuli were chosen to each strongly and selectively excite a single class of primary olfactory receptor neuron (ORN), thus facilitating a rigorous assessment of the selectivity of olfactory plasticity for PNs directly excited by overrepresented stimuli. Unexpectedly, we found that chronic exposure to three such odors did not result in decreased PN sensitivity but rather mildly increased responses to weak stimuli in most PN types. Odor-evoked PN activity in response to stronger stimuli was mostly unaffected by odor experience. When present, plasticity was observed broadly in multiple PN types and thus was not selective for PNs receiving direct input from the chronically active ORNs. We further investigated the DL5 olfactory coding channel and found that chronic odor-mediated excitation of its input ORNs did not affect PN intrinsic properties, local inhibitory innervation, ORN responses or ORN-PN synaptic strength; however, broad-acting lateral excitation evoked by some odors was increased. These results show that PN odor coding is only mildly affected by strong persistent activation of a single olfactory input, highlighting the stability of early stages of insect olfactory processing to significant perturbations in the sensory environment.

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An animal's umwelt, comprising its perception of the sensory environment, which is inherently subjective, can change across the lifespan in accordance with major life events. In mammals, the onset of motherhood, in particular, is associated with a neural and sensory plasticity that alters a mother's detection and use of sensory information such as infant-related sensory stimuli. Although the literature surrounding mammalian mothers is well established, very few studies have addressed the effects of parenthood on sensory plasticity in mammalian fathers. In this review, we summarize the major findings on the effects of parenthood on behavioural and neural responses to sensory stimuli from pups in rodent mothers, with a focus on the olfactory, auditory, and somatosensory systems, as well as multisensory integration. We also review the available literature on sensory plasticity in rodent fathers. Finally, we discuss the importance of sensory plasticity for effective parental care, hormonal modulation of plasticity, and an exploration of temporal, ecological, and life-history considerations of sensory plasticity associated with parenthood. The changes in processing and/or perception of sensory stimuli associated with the onset of parental care may have both transient and long-lasting effects on parental behaviour and cognition in both mothers and fathers; as such, several promising areas of study, such as on the molecular/genetic, neurochemical, and experiential underpinnings of parenthood-related sensory plasticity, as well as determinants of interspecific variation, remain potential avenues for further exploration.

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In mammals, learning circuits play an essential role in energy balance by creating associations between sensory cues and the rewarding qualities of food. This process is altered by diet-induced obesity, but the causes and mechanisms are poorly understood. Here, we exploited the relative simplicity and wealth of knowledge about the D. melanogaster reinforcement learning network, the mushroom body, in order to study the relationship between the dietary environment, dopamine-induced plasticity, and food associations. We show flies that are fed a high-sugar diet cannot make associations between sensory cues and the rewarding properties of sugar. This deficit was caused by diet exposure, not fat accumulation, and specifically by lower dopamine-induced plasticity onto mushroom body output neurons (MBONs) during learning. Importantly, food memories dynamically tune the output of MBONs during eating, which instead remains fixed in sugar-diet animals. Interestingly, manipulating the activity of MBONs influenced eating and fat mass, depending on the diet. Altogether, this work advances our fundamental understanding of the mechanisms, causes, and consequences of the dietary environment on reinforcement learning and ingestive behavior.

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Elevated sugar consumption is associated with an increased risk for metabolic diseases. Whereas evidence from humans, rodents, and insects suggests that dietary sucrose modifies sweet taste sensation, understanding of peripheral nerve or taste bud alterations is sparse. To address this, male rats were given access to 30% liquid sucrose for 4 weeks (sucrose rats). Neurophysiological responses of the chorda tympani (CT) nerve to lingual stimulation with sugars, other taste qualities, touch, and cold were then compared with controls (access to water only). Morphological and immunohistochemical analyses of fungiform papillae and taste buds were also conducted. Sucrose rats had substantially decreased CT responses to 0.15-2.0 M sucrose compared with controls. In contrast, effects were not observed for glucose, fructose, maltose, Na saccharin, NaCl, organic acid, or umami, touch, or cold stimuli. Whereas taste bud number, size, and innervation volume were unaffected, the number of PLCß2+ taste bud cells in the fungiform papilla was reduced in sucrose rats. Notably, the replacement of sucrose with water resulted in a complete recovery of all phenotypes over 4 weeks. The work reveals the selective and modality-specific effects of sucrose consumption on peripheral taste nerve responses and taste bud cells, with implications for nutrition and metabolic disease risk. VIDEO ABSTRACT.

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Our ears capture sound from all directions but do not encode directional information explicitly. Instead, subtle acoustic features associated with unique sound source locations must be learned through experience. Surprisingly, aspects of this mapping process remain highly plastic throughout adulthood: Adult human listeners can accommodate acutely modified acoustic inputs ("new ears") over a period of a few weeks to recover near-normal sound localization, and this process can be accelerated with explicit training. Here we evaluated the extent of such plasticity given only transient exposure to distorted inputs. Distortions were produced via earplugs, which severely degrade sound localization performance, constraining their usability in real-world settings that require accurate directional hearing. Localization was measured over a period of ten weeks. Provision of feedback via simple paired auditory and visual stimuli led to a rapid decrease in the occurrence of large errors (responses >|±30°| from target) despite only once-weekly exposure to the altered inputs. Moreover, training effects generalized to untrained sound source locations. Lesser but qualitatively similar improvements were observed in a group of subjects that did not receive explicit feedback. In total, data demonstrate that even transient exposure to altered spatial acoustic information is sufficient for meaningful perceptual improvement (i.e., chronic exposure is not required), offering insight on the nature and time course of perceptual learning in the context of spatial hearing. Data also suggest that the large and potentially hazardous errors in localization caused by earplugs can be mitigated with appropriate training, offering a practical means to increase their usability.

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Chemosensory systems are critical for evaluating the caloric value and potential toxicity of food. While animals can discriminate between thousands of odors, much less is known about the discriminative capabilities of taste systems. Fats and sugars represent calorically potent and attractive food sources that contribute to hedonic feeding. Despite the differences in nutritional value between fats and sugars, the ability of the taste system to discriminate between different rewarding tastants is thought to be limited. In Drosophila, taste neurons expressing the ionotropic receptor 56d (IR56d) are required for reflexive behavioral responses to the medium-chain fatty acid, hexanoic acid. Here, we tested whether flies can discriminate between different classes of fatty acids using an aversive memory assay. Our results indicate that flies are able to discriminate medium-chain fatty acids from both short- and long-chain fatty acids, but not from other medium-chain fatty acids. While IR56d neurons are broadly responsive to short-, medium-, and long-chain fatty acids, genetic deletion of IR56d selectively disrupts response to medium-chain fatty acids. Further, IR56d+ GR64f+ neurons are necessary for proboscis extension response (PER) to medium-chain fatty acids, but both IR56d and GR64f neurons are dispensable for PER to short- and long-chain fatty acids, indicating the involvement of one or more other classes of neurons. Together, these findings reveal that IR56d is selectively required for medium-chain fatty acid taste, and discrimination of fatty acids occurs through differential receptor activation in shared populations of neurons. Our study uncovers a capacity for the taste system to encode tastant identity within a taste category.

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Animals must encode fundamental physical relationships in their brains. A heron plunging its head underwater to skewer a fish must correct for light refraction, an archerfish shooting down an insect must "consider" gravity, and an echolocating bat that is attacking prey must account for the speed of sound in order to assess its distance. Do animals learn these relations or are they encoded innately and can they adjust them as adults are all open questions. We addressed this question by shifting the speed of sound and assessing the sensory behavior of a bat species that naturally experiences different speeds of sound. We found that both newborn pups and adults are unable to adjust to this shift, suggesting that the speed of sound is innately encoded in the bat brain. Moreover, our results suggest that bats encode the world in terms of time and do not translate time into distance. Our results shed light on the evolution of innate and flexible sensory perception.

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Vertebrate rod and cone photoreceptors detect light via a specialized organelle called the outer segment. This structure is packed with light-sensitive molecules known as visual pigments that consist of a G-protein-coupled, seven-transmembrane protein known as opsin, and a chromophore prosthetic group, either 11-cis retinal ('A1') or 11-cis 3,4-didehydroretinal ('A2'). The enzyme cyp27c1 converts A1 into A2 in the retinal pigment epithelium. Replacing A1 with A2 in a visual pigment red-shifts its spectral sensitivity and broadens its bandwidth of absorption at the expense of decreased photosensitivity and increased thermal noise. The use of vitamin A2-based visual pigments is strongly associated with the occupation of aquatic habitats in which the ambient light is red-shifted. By modulating the A1/A2 ratio in the retina, an organism can dynamically tune the spectral sensitivity of the visual system to better match the predominant wavelengths of light in its environment. As many as a quarter of all vertebrate species utilize A2, at least during a part of their life cycle or under certain environmental conditions. A2 utilization therefore represents an important and widespread mechanism of sensory plasticity. This review provides an up-to-date account of the A1/A2 chromophore exchange system.

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Nociception and its plasticity are essential biological processes controlling adaptive behavioral responses in animals. These processes are also linked to different pain conditions in human and have received considerable attention, notably via studies in rodent models and the use of heat-evoked withdrawal behavior assays as a readout of unpleasant experience. More recently, invertebrates have also emerged as useful complementary models, with their own set of advantages, including their amenability to genetic manipulations, the accessibility and relative simplicity of their nervous system and ethical concerns linked to animal suffering. Like humans, the nematode Caenorhabditis elegans (C. elegans) can detect noxious heat and produce avoidance responses such as reversals. Here, we present a methodology suitable for the high-throughput analysis of C. elegans heat-evoked reversals and the adaptation to repeated stimuli. We introduce two platforms: the INFERNO (for infrared-evoked reversal analysis platform), allowing the quantification of the thermal sensitivity in a petri dish containing a large population (> 100 animals), and the ThermINATOR (for thermal adaptation multiplexed induction platform), allowing the mass-adaptation of up to 18 worm populations at the same time. We show that wild type animals progressively desensitize in response to repeated noxious heat pulses. Furthermore, analyzing the phenotype of mutant animals, we show that the mechanisms underlying baseline sensitivity and adaptation, respectively, are supported by genetically separable molecular pathways. In conclusion, the presented method enables the high-throughput evaluation of thermal avoidance in C. elegans and will contribute to accelerate studies in the field with this invertebrate model.

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Previous work has shown that motor learning is associated with changes to both movements and to the somatosensory perception of limb position. In an earlier study that motivates the current work, it appeared that following washout trials, movements did not return to baseline but rather were aligned with associated changes to sensed limb position. Here, we provide a systematic test of this relationship, examining the idea that adaptation-related changes to sensed limb position and to the path of the limb are linked, not only after washout trials but at all stages of the adaptation process. We used a force-field adaptation paradigm followed by washout trials in which subjects performed movements without visual feedback of the limb. Tests of sensed limb position were conducted at each phase of adaptation, specifically before and after baseline movements in a null field, after force-field adaptation, and following washout trials in a null field. As in previous work, sensed limb position changed in association with force-field adaptation. At each stage of adaptation, we observed a correlation between the sensed limb position and associated path of the limb. At a group level, there were differences between the clockwise and counter-clockwise conditions. However, whenever there were changes in sensed limb position, movements following washout did not return to baseline. This suggests that adaptation in sensory and motor systems is not independent processes but rather sensorimotor adaptation is linked to sensory change. Sensory change and limb movement remain in alignment throughout adaptation such that the path of the limb is aligned with the altered sense of limb position.

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Humans can learn to use acoustic echoes to detect and classify objects. Echolocators typically use tongue clicks to induce these echoes, and there is some evidence that higher spectral frequency content of an echolocator's tongue click is associated with better echolocation performance. This may be explained by the intensity of the echoes. The current study tested experimentally (a) if emissions with higher spectral frequencies lead to better performance for target detection, and (b) if this is mediated by echo intensity. Participants listened to sound recordings that contained an emission and sometimes an echo from an object. The peak spectral frequency of the emission was varied between 3.5 and 4.5 kHz. Participants judged whether they heard the object in these recordings and did the same under conditions in which the intensity of the echoes had been digitally equated. Participants performed better using emissions with higher spectral frequencies, but this advantage was eliminated when the intensity of the echoes was equated. These results demonstrate that emissions with higher spectral frequencies can benefit echolocation performance in conditions where they lead to an increase in echo intensity. The findings suggest that people who train to echolocate should be instructed to make emissions (e.g. mouth clicks) with higher spectral frequency content.

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Normal aging is associated with a number of smell impairments that are paralleled by age-dependent changes in the peripheral olfactory system, including decreases in olfactory sensory neurons (OSNs) and in the regenerative capacity of the epithelium. Thus, an age-dependent degradation of sensory input to the brain is one proposed mechanism for the loss of olfactory function in older populations. Here, we tested this hypothesis by performing in vivo optical neurophysiology in 6-, 12-, 18-, and 24-month-old mice. We visualized odor-evoked neurotransmitter release from populations of OSNs into olfactory bulb glomeruli, and found that these sensory inputs are actually quite stable during normal aging. Specifically, the magnitude and number of odor-evoked glomerular responses were comparable across all ages, and there was no effect of age on the sensitivity of OSN responses to odors or on the neural discriminability of different sensory maps. These results suggest that the brain's olfactory bulbs do not receive deteriorated input during aging and that local bulbar circuitry might adapt to maintain stable nerve input.

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Generalization of fear from previously threatening stimuli to novel but related stimuli can be beneficial, but if fear overgeneralizes to inappropriate situations it can produce maladaptive behaviors and contribute to pathological anxiety. Appropriate fear learning can selectively facilitate early sensory processing of threat-predictive stimuli, but it is unknown if fear generalization has similarly generalized neurosensory consequences. We performed in vivo optical neurophysiology to visualize odor-evoked neural activity in populations of periglomerular interneurons in the olfactory bulb 1 day before, 1 day after, and 1 month after each mouse underwent an olfactory fear conditioning paradigm designed to promote generalized fear of odors. Behavioral and neurophysiological changes were assessed in response to a panel of odors that varied in similarity to the threat-predictive odor at each time point. After conditioning, all odors evoked similar levels of freezing behavior, regardless of similarity to the threat-predictive odor. Freezing significantly correlated with large changes in odor-evoked periglomerular cell activity, including a robust, generalized facilitation of the response to all odors, broadened odor tuning, and increased neural responses to lower odor concentrations. These generalized effects occurred within 24 h of a single conditioning session, persisted for at least 1 month, and were detectable even in the first moments of the brain's response to odors. The finding that generalized fear includes altered early sensory processing of not only the threat-predictive stimulus but also novel though categorically-similar stimuli may have important implications for the etiology and treatment of anxiety disorders with sensory sequelae.

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Insect antenna is a multisensory organ, each modality of which can be modulated by biogenic amines. Octopamine (OA) and its metabolic precursor tyramine (TA) affect activity of antennal olfactory receptor neurons. There is some evidence that dopamine (DA) modulates gustatory neurons. Serotonin can serve as a neurotransmitter in some afferent mechanosensory neurons and both as a neurotransmitter and neurohormone in efferent fibers targeted at the antennal vessel and mechanosensory organs. As a neurohormone, serotonin affects the generation of the transepithelial potential by sensillar accessory cells. Other possible targets of biogenic amines in insect antennae are hygro- and thermosensory neurons and epithelial cells. We suggest that the insect antenna is partially autonomous in the sense that biologically active substances entering its hemolymph may exert their effects and be cleared from this compartment without affecting other body parts.

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Many philosophers use findings about sensory substitution devices in the grand debate about how we should individuate the senses. The big question is this: Is "vision" assisted by (tactile) sensory substitution really vision? Or is it tactile perception? Or some sui generis novel form of perception? My claim is that sensory substitution assisted "vision" is neither vision nor tactile perception, because it is not perception at all. It is mental imagery: visual mental imagery triggered by tactile sensory stimulation. But it is a special form of mental imagery that is triggered by corresponding sensory stimulation in a different sense modality, which I call "multimodal mental imagery."

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Breathing is a vital homeostatic behavior and must be precisely regulated throughout life. Clinical conditions commonly associated with inflammation, undermine respiratory function may involve plasticity in respiratory control circuits to compensate and maintain adequate ventilation. Alternatively, other clinical conditions may evoke maladaptive plasticity. Yet, we have only recently begun to understand the effects of inflammation on respiratory plasticity. Here, we review some of common models used to investigate the effects of inflammation and discuss the impact of inflammation on nociception, chemosensory plasticity, medullary respiratory centers, motor plasticity in motor neurons and respiratory frequency, and adaptation to high altitude. We provide new data suggesting glial cells contribute to CNS inflammatory gene expression after 24h of sustained hypoxia and inflammation induced by 8h of intermittent hypoxia inhibits long-term facilitation of respiratory frequency. We also discuss how inflammation can have opposite effects on the capacity for plasticity, whereby it is necessary for increases in the hypoxic ventilatory response with sustained hypoxia, but inhibits phrenic long term facilitation after intermittent hypoxia. This review highlights gaps in our knowledge about the effects of inflammation on respiratory control (development, age, and sex differences). In summary, data to date suggest plasticity can be either adaptive or maladaptive and understanding how inflammation alters the respiratory system is crucial for development of better therapeutic interventions to promote breathing and for utilization of plasticity as a clinical treatment.

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Sensory experience has a profound effect on neocortical neurons. Passive stimulation of whiskers or sensory deprivation from whiskers can induce long-lasting changes in neuronal responses or modify the receptive field in adult animals. We recorded barrel cortical neurons in urethane-anesthetized rats in layers 2/3 or 5/6 to determine if repetitive stimulation would induce long-lasting response facilitation. Air-puff stimulation (20-ms duration, 40 pulses at 0.5-8Hz) was applied to a single whisker. This repetitive stimulation increased tactile responses in layers 2/3 and 5/6 for 60min. Moreover, the functional coupling (coherence) between the sensory stimulus and the neural response also increased after the repetitive stimulation in neurons showing response facilitation. The long-lasting response facilitation was due to activation of N-methyl-d-aspartate (NMDA) receptors because it was reduced by APV ((2R)-amino-5-phosphonovaleric acid, (2R)-amino-5-phosphonopentanoate) and MK801 application. Inactivation of layer 2/3 also blocked response facilitation in layer 5/6, suggesting that layer 2/3 may be fundamental in this synaptic plasticity processes. Moreover, i.p. injection of eserine augmented the number of layer 2/3 neurons expressing long-lasting response facilitation; this effect was blocked by atropine, suggesting that muscarinic receptor activation favors the induction of the response facilitation. Our data indicate that physiologically repetitive stimulation of a single whisker at the frequency at which rats move their whiskers during exploration of the environment induces long-lasting response facilitation improving sensory processing.

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The organism's ability to adapt to the changing sensory environment is due in part to the ability of the nervous system to change with experience. Input and synapse specific Hebbian plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), are critical for sculpting the nervous system to wire its circuit in tune with the environment and for storing memories. However, these synaptic plasticity mechanisms are innately unstable and require another mode of plasticity that maintains homeostasis to allow neurons to function within a desired dynamic range. Several modes of homeostatic adaptation are known, some of which work at the synaptic level. This review will focus on the known mechanisms of experience-induced homeostatic synaptic plasticity in the neocortex and their potential function in sensory cortex plasticity. This article is part of the Special Issue entitled 'Homeostatic Synaptic Plasticity'.

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