Neural correlates of saccadic suppression in humans

When you look into a mirror and move your eyes left to right, you will see that you cannot observe your own eye movements. This demonstrates the phenomenon of saccadic suppression: during saccadic eye movements, visual sensitivity is much reduced. Given that humans make more than 100,000 eye movements each day, it is clear why suppression is needed: without it, the motion on the retina would prevent us from seeing anything at all. Psychophysical data show that suppression is stimulus selective: it is strongest for the kind of stimuli that preferentially activate magnocellular thalamic neurons. This has led to the hypothesis that saccadic suppression selectively targets the magnocellular stream. We used fMRI to find brain areas with a stimulus-selective suppression of the BOLD signal that matches the psychophysical data. We found such a neural correlate of saccadic suppression in the dorsal stream (hMT+, V7) and in ventral area V4. These areas receive magnocellular input; hence our findings are consistent with the magnocellular hypothesis. The range of effects in our data and in single cell data, however, argues against a single thalamic mechanism that suppresses all cortical input. Instead, we speculate that saccadic suppression relies on multiple mechanisms operating in different cortical areas.     

Neural correlates of the contents of visual awareness in humans

The immediacy and directness of our subjective visual experience belies the complexity of the neural mechanisms involved, which remain incompletely understood. This review focuses on how the subjective contents of human visual awareness are encoded in neural activity. Empirical evidence to date suggests that no single brain area is both necessary and sufficient for consciousness. Instead, necessary and sufficient conditions appear to involve both activation of a distributed representation of the visual scene in primary visual cortex and ventral visual areas, plus parietal and frontal activity. The key empirical focus is now on characterizing qualitative differences in the type of neural activity in these areas underlying conscious and unconscious processing. To this end, recent progress in developing novel approaches to accurately decoding the contents of consciousness from brief samples of neural activity show great promise.     

Neural correlates of chromatic motion perception.

A variety of psychophysical and neurophysiological studies suggest that chromatic motion perception in the primate brain may be performed outside the classical motion processing pathway. We addressed this provocative proposal directly by assessing the sensitivity of neurons in motion area MT to moving colored stimuli while simultaneously determining perceptual sensitivity in nonhuman primate observers. The results of these studies demonstrate a strong correspondence between neuronal and perceptual measures. Our findings testify that area MT is indeed a principal component of the neuronal substrate for color-based motion processing.     

Fixed breathing frequency decreases end-tidal PCO2 in humans.

We tested the effect of a fixed breathing frequency on the partial pressure of CO2 in the end-tidal air (PETCO2) in resting healthy subjects. In the first experiment, three different rates of breathing were dictated: the same frequency of breathing as the subject's control one (1f), a double frequency (2f), and half of the control frequency (0.5f). 10 min dictate of 1f and 2f induced a decrease of PETCO2. The dictate of 0.5f had no significant effect on PETCO2. In the second experiment, 1f was dictated for 30 min, inducing a decrease of PETCO2 throughout the duration of the dictate. These results demonstrate that fixing the breathing frequency by the dictate affects the chemostatic control of ventilation.     

Cardiovascular control during voluntary static exercise in humans with tetraplegia.

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.     

Neural control of breathing: a system analysis.

A model of the neural control of quiet breathing in an anaesthetised and tracheostomised laboratory animal is presented. The loop consisting of the brain generator with its respiratory "master function", the phrenic command, the aerodynamics of the lungs and the volume information carried by the vagus nerves is described in mathematical terms. Computer model experiments are presented and compared with corresponding physiological situations. The stability of the model is demonstrated.     

Neural correlates of decisions

Once considered the province of philosophy and the behavioral sciences, the process of making decisions has received increasing scrutiny from neurobiologists. Recent research suggests that sensory judgements unfold through the gradual accumulation of neuronal signals in sensory-motor pathways, favoring one alternative over others. Stored representations of the outcome of prior actions activate neurons in many of these same areas during decision-making. The challenge for neurobiologists lies in deciphering how signals from these disparate areas are integrated to form a single behavioral choice and the mechanisms responsible for selecting the appropriate information upon which decisions should be informed in particular contexts.     

Neural correlates of hate

In this work, we address an important but unexplored topic, namely the neural correlates of hate. In a block-design fMRI study, we scanned 17 normal human subjects while they viewed the face of a person they hated and also faces of acquaintances for whom they had neutral feelings. A hate score was obtained for the object of hate for each subject and this was used as a covariate in a between-subject random effects analysis. Viewing a hated face resulted in increased activity in the medial frontal gyrus, right putamen, bilaterally in premotor cortex, in the frontal pole and bilaterally in the medial insula. We also found three areas where activation correlated linearly with the declared level of hatred, the right insula, right premotor cortex and the right fronto-medial gyrus. One area of deactivation was found in the right superior frontal gyrus. The study thus shows that there is a unique pattern of activity in the brain in the context of hate. Though distinct from the pattern of activity that correlates with romantic love, this pattern nevertheless shares two areas with the latter, namely the putamen and the insula.     

Hemodynamic and biochemical effects of 100% oxygen breathing in humans.

High concentrations of inspired oxygen have been reported to have significant hemodynamic effects that may be related to increased free radical production. If oxygen therapy increases free radical production, it may also modify hemodynamic responses to a nitric oxide donor. Twenty-nine healthy male volunteers were studied using randomized, double-blind, placebo-controlled, crossover designs to determine whether oxygen therapy is associated with hemodynamic and forearm vascular effects. We measured hemodynamic parameters and forearm vascular responses before and 1 h after exposure to 100% oxygen versus medical air. Plasma 8-iso-PGF2alpha and plasma vitamin C were measured to assess the biochemical effects of oxygen administration. Hemodynamic measurements were also made following the acute administration of sublingual nitroglycerin. Oxygen therapy caused no significant change in blood pressure, plasma 8-iso-PGF2alpha, or vitamin C. Oxygen did cause a significant reduction in heart rate and forearm blood flow, and an increase in peripheral vascular resistance. Oxygen caused no change in the hemodynamic response to nitroglycerin. Therefore, in healthy young adults, therapy with 100% oxygen does not affect blood pressure, despite causing an increase in vascular resistance, is not associated with evidence of increased free radical injury, and does not affect the hemodynamic responses to nitroglycerin.     

Some mechanisms of voluntary control of walking in humans

The electrical activities of some muscles of the lower extremities have been studied by the method of presentation of an acoustic signal for a change in walking speed. It has been established that the motor response to a signal has two stages, at which (1) the ratio of muscle activities facilitating acceleration or deceleration of walking is formed and (2) the muscle activity corresponding to the new rate of locomotion is set. The latent period of the first stage of the motor response depends on the temporal relationship of the signal and the phase of muscle activity: it is minimum if the signal coincides with the phase of activity and maximum if the signal is given in the phase of bioelectric silence. It may be supposed that the voluntary control of the locomotion rate is related to at least two types of cortical effects: cyclic and acyclic. The former determine the transition from one speed of walking to another through changing human body posture characteristics (probably, they influence interneurons and motoneurons of reflex arcs); the latter, the characteristics of the new mode of the locomotor cycle by affecting the functional state of the interneurons and motoneurons of the spinal generator of stepping movements.     

Time course of ozone-induced changes in breathing pattern in healthy exercising humans.

We examined the time course of O3-induced changes in breathing pattern in 97 healthy human subjects (70 men and 27 women). One- to five-minute averages of breathing frequency (f(B)) and minute ventilation (Ve) were used to generate plots of cumulative breaths and cumulative exposure volume vs. time and cumulative exposure volume vs. cumulative breaths. Analysis revealed a three-phase response; delay, no response detected; onset, f(B) began to increase; response, f(B) stabilized. Regression analysis was used to identify four parameters: time to onset, number of breaths at onset, cumulative inhaled dose of ozone at onset of O3-induced tachypnea, and the percent change in f(B). The effect of altering O3 concentration, Ve, atropine treatment, and indomethacin treatment were examined. We found that the lower the O3 concentration, the greater the number of breaths at onset of tachypnea at a fixed ventilation, whereas number of breaths at onset of tachypnea remains unchanged when Ve is altered and O3 concentration is fixed. The cumulative inhaled dose of O3 at onset of tachypnea remained constant and showed no relationship with the magnitude of percent change in f(B). Atropine did not affect any of the derived parameters, whereas indomethacin did not affect time to onset, number of breaths at onset, or cumulative inhaled dose of O3 at onset of tachypnea but did attenuate percent change in f(B). The results are discussed in the context of dose response and intrinsic mechanisms of action.     

Neural correlates of frog calling

Summary A tissue bath incorporating a screen for support of the specimen and an air-lift pump to circulate saline across the screen was designed to provide maximum exposure of isolated frog brainstems ofRana pipiens pipiens to oxygenated saline (Fig. 1). Normal neural correlates of electrically-evoked mating calling were recorded from the region of the pretrigeminal nucleus and the laryngeal nerve in the isolated brainstem (Fig. 3A) and isolated hemi-brainstem (Fig. 2) of the Northern leopard frog. Conspicuous slow-wave activity in the region of the pretrigeminal nucleus supports the possibility that this may be an important integrative area for calling. It appears that the pretrigeminal region is not able, independently, to generate the pulses of the vocal phase of calling. Synchronizing and reinforcing inter-connections between the calling mechanisms of the two sides were identified. The data are summarized in a revised model of mating calling (Fig. 7).This work was supported by NINDS grant NS-06673. The electronic equipment was set up and maintained by Mr. Wayne R. Hudson. I am grateful to Dr. William Van Meter for suggesting the Sylgard for the pinning block and to Dr. Patricia Gallagher for suggesting the saline solution of Phillis and Tebcis.     

Neural correlates of frog calling. Masculinization by androgens

Neural correlates of mating calling can be recorded from isolated brainstems of male, Northern leopard frogs after the circuits for this behavior have been triggered by electrical stimulation of the preoptic area. Correlates can be evoked reliably and by a stimulus of low amplitude. However, such correlates can be evoked only rarely from female brainstems, and then only by a much larger stimulus. The sensitivity to triggering in female brainstems can be masculinized by previous treatment of the intact frog with testosterone propionate or dihydrotestosterone, but not by estradiol benzoate. This suggests that the action of the androgens is direct and does not require aromatization to estrogens. Comparisons with other studies suggest that the androgen effect may be mainly on posterior parts of the calling circuits (i.e., call pattern generator or motoneurons), rather than on the preoptic area trigger of the generator.     

Neural correlates of associative training in Hermissenda

Hair cells in Hermissenda respond to illumination of the ipsilateral and contralateral eyes. These responses are modified by associative training of the animal. The observed electrophysiological changes appear to result from changes in the photoreceptors' synaptic input to the hair cells.     

Neural control of breathing: insights from genetic mouse models.

Recent studies described the in vivo ventilatory phenotype of mutant newborn mice with targeted deletions of genes involved in the organization and development of the respiratory-neuron network. Whole body flow barometric plethysmography is the noninvasive method of choice for studying unrestrained newborn mice. Breathing-pattern abnormalities with apneas occur in mutant newborn mice that lack genes involved in the development and modulation of rhythmogenesis. Studies of deficits in ventilatory responses to hypercapnia and/or hypoxia helped to identify genes involved in chemosensitivity to oxygen and carbon dioxide. Combined studies in mutant newborn mice and in humans have shed light on the pathogenesis of genetically determined respiratory-control abnormalities such as congenital central hypoventilation syndrome, Rett syndrome, and Prader-Willi syndrome. The development of mouse models has opened up the field of research into new treatments for respiratory-control disorders in humans.