Neural circuit mechanisms for pattern detection and feature combination in olfactory cortex

Odors are initially encoded in the brain as a set of distinct physicochemical characteristics but are ultimately perceived as a unified sensory object--a "smell." It remains unclear how chemical features encoded by diverse odorant receptors and segregated glomeruli in the main olfactory bulb (MOB) are assembled into integrated cortical representations. Combining patterned optical microstimulation of MOB with in vivo electrophysiological recordings in anterior piriform cortex (PCx), we assessed how cortical neurons decode complex activity patterns distributed across MOB glomeruli. PCx firing was insensitive to single-glomerulus photostimulation. Instead, individual cells reported higher-order combinations of coactive glomeruli resembling odor-evoked sensory maps. Intracellular recordings revealed a corresponding circuit architecture providing each cortical neuron with weak synaptic input from a distinct subpopulation of MOB glomeruli. PCx neurons thus detect specific glomerular ensembles, providing an explicit neural representation of chemical feature combinations that are the hallmark of complex odor stimuli.     

Neural mechanisms for color perception in the primary visual cortex

New neurophysiological results show the existence of multiple transformations of color signals in the primary visual cortex (V1) in macaque monkey. These different color mechanisms may contribute separately to the perception of color boundaries and colored regions. Many cells in V1 respond to color and to black-white (luminance) patterns. These neurons are spatially selective and could provide signals about boundaries between differently colored regions. Other V1 neurons that prefer color over luminance respond without much spatial selectivity to colored stimuli, and could be the neural basis for the response to local color modulation within a region. How these different types of color cells combine inputs from cone photoreceptors is what gives them their different spatial selectivities for color.     

Neural mechanisms in the anterior olfactory nucleus of the rabbit and their possible relevance to localization of an olfactory source

Extracellular recordings were obtained from 40 Anterior OlfactoryNucleus (A.O.N.) units in response to birhinal olfactory stimulations.The units located in the A.O.N. pars dorsalis responded differentlyaccording to the time interval between the onsets of right andleft puffs during birhinal olfactory stimulation. On the contrary,the greater part of the units located in the A.O.N. pars ventraliswas not sensitive to time intervals variations. These data indicatethe ability of some A.O.N. cells to encode temporal characteristicsof an olfactory stimulation.     

Psychophysical and behavioral characteristics of olfactory adaptation

Sensory adaptation allows organisms to reach behavioral equilibrium with the ambient environment and respond primarily to changes in stimulation. Given its functional significance, it is not surprising that adaptation in the olfactory system exhibits many of the same characteristics as adaptation in other sensory systems, including vision. Repeated or prolonged exposure to an odorant typically leads to stimulus-specific decreases in olfactory sensitivity to that odorant, but sensitivity recovers over time in the absence of further exposure. Psychophysical analysis shows that olfactory adaptation results in elevations in odor thresholds and in reduced responsiveness to suprathreshold stimulation. Further, the magnitude of the decrease and the time course of adaptation and recovery are dependent on the concentration of the odor and on the duration of exposure. It is generally agreed that olfactory adaptation can occur at multiple levels in the olfactory system and can involve both peripheral (receptor level) and more central (post-receptor) components. Evidence for peripheral and central involvement comes from studies showing that monorhinal stimulation results in adaptation in both the ipsilateral and contralateral nostril, although the degree of adaptation in the ipsilateral nostril is more profound and recovery is slower. Additional evidence for central involvement comes from studies that have found relatively small decreases in peripheral response following repeated stimulation despite substantial reductions in perceived intensity. Most psychophysical studies of adaptation, however, have not differentiated the peripheral and central processes. Although relatively few in number, studies of the parametric features of olfactory adaptation in both vertebrate (e.g. rat) and invertebrate (e.g. Drosophila, Caenorhabditis elegans) animal models appear to replicate the findings in psychophysical studies of adult humans. Despite the broad overall similarity of olfactory adaptation to adaptation in other sensory systems, olfactory adaptation exhibits some unique features. Adaptation in olfaction has been shown to be very long-lasting in some cases and may be modulated by the contribution of pre-neural events and physico-chemical properties of the odorant molecules that govern diffusion to receptor sites and post-receptor clearance.     

Distortion of olfactory perception: diagnosis and treatment

Clinically, olfaction can fail in any of three ways: (i) decreased sensitivity (hyposmia, anosmia) and two types of distortion (dysosmia); (ii) distorted quality of an odorant stimulation (troposmia); (iii) perceived odor when no odorant is present (phantosmia, hallucination). The distortions are usually much more upsetting to a person's quality of life than a simple loss. An ipsilatersal loss of olfactory sensitivity is often identified in the nostril with any type of olfactory distortion. The pathophysiology of a stimulated distortion (troposmia) is likely a decreased number of functioning olfactory primary neurons so that an incomplete characterization of the odorant is made. In phantosmia, two possible causations include an abnormal signal or inhibition from the primary olfactory neurons or peripheral olfactory or trigeminal signals that "trigger" a central process. The clinician's goal is to carefully define the problem (e.g. taste versus smell, real versus perceived, one versus two nostrils), to perform the appropriate examination and testing and to provide therapy if possible. Treatment includes assurance with no active therapy (because many of these will naturally resolve), topical medications, systemic medications, anesthesia to parts of the nose and, rarely, referral for surgical excision of olfactory neurons. Endoscopic transnasal operations have the advantage of treating phantosmia and sometimes allowing a return of olfactory ability after the operation.     

Measures of human olfactory perception during pregnancy

Although considerable anecdotal evidence suggests that pregnancy affects olfactory sensitivity, scientific evidence is limited and inconclusive. Whereas hedonic ratings are affected by pregnancy, odor identification is not. The aim of the current study was to examine odor perception in women across pregnancy and in the postpartum period. One hundred nonsmoking women who were pregnant, postpartum, or had never been pregnant were tested on the University of Pennsylvania Smell Identification Test (UPSIT). Intensity ratings and scratch patterns were collected as potential indicators of sensitivity, and participants rated the odors' pleasantness. Participants also rated their own sense of smell. Mean UPSIT scores did not differ significantly across groups indicating no difference in odor identification. Trends in planned comparisons suggested that in the first trimester, odors were rated as more intense and less pleasant. In the first trimester, women scratched the odor strips significantly fewer times. Consistent with previous reports, 90% of pregnant women reported that specific odors smelled less pleasant and 60% reported that some odors smelled more pleasant. Although nearly two-thirds of pregnant women rated their olfactory sensitivity to be enhanced during pregnancy and overall pregnant women's self-rated olfactory sensitivity was higher than controls', self-ratings were not correlated with UPSIT scores nor odor intensity ratings. These results suggest that these and previous findings may reflect the fact that the effect of pregnancy on olfaction is small and inconsistent.     

The effect of emotion and personality on olfactory perception

It is well established that both the emotional tone of sensory stimuli and the personality characteristics of an individual can bias sensory perception. What has largely been unexplored is whether the current emotional state of an individual has a similar effect, and how it works together with other factors. Here we carry out a comprehensive study to examine how olfactory perception is affected by the emotional tone of the stimuli, and the personality and current emotional state of the individual. Subjects reported experiencing happiness, sadness, negativity/hostility and neutrality when exposed to corresponding emotionally themed video clips, and in each case, smelled a suprathreshold pleasant, an unpleasant and a neutral odorant. The time taken for the subject to detect each odorant and the olfactory intensity were recorded. We found that women detected the pleasant odorant faster than the neutral one. In addition, personality modulated reaction time and olfactory intensity, such that neurotic and anxious individuals were selectively biased toward affective rather than neutral odorants. Finally, current emotional state augmented intensity in men but not in women, and differentially influenced the response time. These findings provided new insights into the effects of emotion and personality on olfactory perception.     

Investigation of breathing parameters during odor perception and olfactory imagery

Compared with visual and auditory imagery, little is known aboutolfactory imagery. There is evidence that respiration may bealtered by both olfactory perception and olfactory imagery.In order to investigate this relationship, breathing parameters(respiratory minute volume, respiratory amplitude, and breathingrate) in human subjects during olfactory perception and olfactoryimagery were investigated. Fifty-six subjects having normalolfactory function were tested. Nasal respiration was measuredusing a respiratory pressure sensor. Using an experimental blockdesign, we alternately presented odors or asked the subjectsto imagine a given smell. Four different pleasant odors wereused: banana, rose, coffee, and lemon odor. We detected a significantincrease in respiratory minute volume between olfactory perceptionand the baseline condition as well as between olfactory imageryand baseline condition. Additionally we found significant differencesin the respiratory amplitude between imagery and baseline conditionand between odor and imagery condition. Differences in the breathingrate between olfactory perception, olfactory imagery, and baselinewere not statistically significant. We conclude from our resultsthat olfactory perception and olfactory imagery both have effectson the human respiratory profile and that these effects arebased on a common underlying mechanism.     

Neural mechanisms of emesis

Emesis is a reflex, developed to different degrees in different species, that allows an animal to rid itself of ingested toxins or poisons. The reflex can be elicited either by direct neuronal connections from visceral afferent fibers, especially those from the gastrointestinal tract, or from humoral factors. Emesis from humoral factors depends on the integrity of the area postrema; neurons in the area postrema have excitatory receptors for emetic agents. Emesis from gastrointestinal afferents does not depend on the area postrema, but probably the reflex is triggered by projections to some part of the nucleus tractus solitarius. As with a variety of other complex motor functions regulated by the brain stem, it is likely that the sequence of muscle excitation and inhibition is controlled by a central pattern generator located in the nucleus tractus solitarius, and that information from humoral factors via the area postrema and visceral afferents via the vagus nerve converge at this point. This central pattern generator, like those for motor functions such as swallowing, presumably projects to the various motor nuclei, perhaps through interneuronal pathways, to elicit the sequential excitation and inhibition that controls the reflex.     

Neural mechanisms of aggression

Unchecked aggression and violence exact a significant toll on human societies. Aggression is an umbrella term for behaviours that are intended to inflict harm. These behaviours evolved as adaptations to deal with competition, but when expressed out of context, they can have destructive consequences. Uncontrolled aggression has several components, such as impaired recognition of social cues and enhanced impulsivity. Molecular approaches to the study of aggression have revealed biological signals that mediate the components of aggressive behaviour. These signals may provide targets for therapeutic intervention for individuals with extreme aggressive outbursts. This Review summarizes the complex interactions between genes, biological signals, neural circuits and the environment that influence the development and expression of aggressive behaviour.     

Neural mechanisms of imitation

Recent advances in our knowledge of the neural mechanisms of imitation suggest that there is a core circuitry of imitation comprising the superior temporal sulcus and the 'mirror neuron system', which consists of the posterior inferior frontal gyrus and adjacent ventral premotor cortex, as well as the rostral inferior parietal lobule. This core circuitry communicates with other neural systems according to the type of imitation performed. Imitative learning is supported by interaction of the core circuitry of imitation with the dorsolateral prefrontal cortex and perhaps motor preparation areas--namely, the mesial frontal, dorsal premotor and superior parietal areas. By contrast, imitation as a form of social mirroring is supported by interaction of the core circuitry of imitation with the limbic system.     

Central mechanisms of tactile shape perception

Studies show that while the cortical mechanisms of two-dimensional (2D) form and motion processing are similar in touch and vision, the mechanisms of three-dimensional (3D) shape processing are different. 2D form and motion are processed in areas 3b and 1 of SI cortex by neurons with receptive fields (RFs) composed of excitatory and inhibitory subregions. 3D shape is processed in area 2 and SII and relies on the integration of cutaneous and proprioceptive inputs. The RFs of SII neurons vary in size and shape with heterogeneous structures consisting of orientation-tuned fingerpads mixed with untuned excitatory or inhibitory fingerpads. Furthermore, the sensitivity of the neurons to cutaneous inputs changes with hand conformation. We hypothesize that these RFs are the kernels underlying tactile object recognition.