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Activation of lateral extrastriate areas during orthographic processing of Japanese characters studied with fMRI.

We investigated the early orthographic processing in the occipital cortex using Japanese morphogram by functional magnetic resonance imaging. Kanji (Japanese morphogram) is one system of character used in the Japanese language, each character of which has a specific meaning and pronunciations. To ensure that the effects of the general visual properties of Kanji were excluded from Kanji-related activation, we created strict control stimuli, the "scrambled Kanji" that had the same luminance, contrast, and retinotopical size as those of the original Kanji. In the Kanji vs scrambled Kanji task, we found significant activation in the left inferior occipital gyrus. However, we found no activation in earlier visual cortices, including the primary visual cortex, indicating that the scrambled Kanji served as an effective control stimulus for this task. In the Kanji vs blank screen task, much more areas, including earlier visual cortices, were activated. The activation that we found in the Kanji vs scrambled Kanji task was compatible with the results of previous studies of English letter strings by other groups, suggesting that the left inferior occipital gyrus plays an essential role in orthographic processing common to these two different writing systems.

Arousal↗

[Evaluation of time resolution of the primary motor cortex by a single paradigm using a stimulation system].

Many researchers are investigating brain function by using a block paradigm in fMRI measurement. However, time resolution has been limited because the block paradigm employed data collection by consecutive image acquisition after stimulation began. Because of this problem, the evaluation of early brain activity was not adequate. Therefore, a system that was able to take imaging from a high time dependence to stimulation in real time was necessary to evaluate early brain activity. It is necessary to obtain controlled image taking by an MRI device with an external trigger by creating a sequence design in the system controlling stimulation and a sequence designed to achieve the above. The execution of a single paradigm by the originally designed sequence thus becomes possible, and arbitrarily setting all processes from stimulation to image taking is possible. It is thought that the practical use of the single paradigm designed by the control system of stimulation enables real-time imaging for stimulation and provides time-dependent data. From this, evaluation of brain activity of the primary motor cortex is possible in the early stage by event-related data collection. In addition, "sank," a relative decrement in PO(2) was also an initial stage of BOLD, that is, an initial dip occurs as a transitory signal change by using a single paradigm that synchronizes with the control system of stimulation for the evaluation of early brain activity. Moreover, it is thought that taking images by a single paradigm that is synchronized with the control system of stimulation is indispensable for time and spatial elucidation of detailed brain activity, to evaluate hyper brain function. Therefore, the brain activity in the primary visual cortex at the early stage was clarified in this study by using a single paradigm designed to synchronize with the control system of stimulation by single-shot EPI.

Adult↗

Localization of [3H]nicotine, [3H]cytisine, [3H]epibatidine, and [125I]alpha-bungarotoxin binding sites in the brain of Macaca mulatta.

We determined the localization of [(3)H]nicotine, [(3)H]cytisine, [(3)H]epibatidine, and [(125)I]alpha-bungarotoxin binding sites in the brain of rhesus monkey by means of receptor autoradiography. The labelings by [(3)H]nicotine, [(3)H]cytisine, and [(3)H]epibatidine were highly concordant, except for epibatidine. Layer IV of some cortical areas, most thalamic nuclei, and presubiculum displayed high levels of labeling for the three ligands. Moderate levels of binding were detected in the subiculum, the septum, and the mesencephalon. Low levels were present in layers I-II and VI of the cortex, the cornu Ammonis, the dentate gyrus, and the amygdala. In addition, the level of epibatidine labeling was very high in the epithalamic nuclei and the interpeduncular nucleus, whereas labeling by nicotine and cytisine was very weak in the same regions. The distribution of [(125)I]alpha-bungarotoxin binding differed from the binding of the three agonists. The labeling was dense in layer I of most cortical areas, dentate gyrus, stratum lacunosum-moleculare of CA1 field, several thalamic nuclei, and medial habenula. A moderate labeling was found in layers V and VI of the prefrontal and frontal cortices, layer IV of primary visual cortex, amygdala, septum, hypothalamus, and some mesencenphalic nuclei. A weak signal was also detected in subiculum, claustrum, stratum oriens, and stratum lucidum of cornu Ammonis and also in some mesencephalic nuclei. The distribution of nicotine, cytisine, and epibatidine bindings corresponds broadly to the patterns observed in rodents, with the marked exception of the epithalamus. However, in monkey, those distributions match the distribution of alpha2 messenger RNA, rather than that of alpha4 transcripts as it exists in rodent brains. The distribution of the binding sites for alpha-bungarotoxin is larger in the brain of rhesus monkeys than in rodent brain, suggesting a more important role of alpha7 receptors in primates.

Alkaloids↗

Transplant of Schwann cells allows normal development of the visual cortex of dark-reared rats.

Visual experience is necessary for the correct development of the visual cortex. Dark-rearing from birth affects normal maturation of the functional properties of mammalian visual cortex: cortical cells show rapid habituation to repeated stimulation, decreased orientation selectivity, and enlarged receptive fields. Spatial resolution and response latency are also impaired. Recent experiments have demonstrated that visual deprivation reduces the expression of neurotrophins in the visual cortex. We formulated the hypothesis that visual experience drives the maturation of functional properties of the visual cortex by regulating cortical levels of neurotrophins. If this hypothesis is correct, exogenous supply of neurotrophins during dark-rearing from birth should prevent, or at least ameliorate, the effects of a lack of visual experience. Since Schwann cells are efficient biological minipumps of neurotrophic factors, we transplanted 1.0 or 1.5 x 10(6) Schwann cells or infused vehicle solution as a control into the lateral ventricles of 13 day old rats reared in total darkness from birth until the end of the critical period (postnatal day 45). Single-cell responses and visual-evoked potentials were recorded from the binocular zone of the primary visual cortex of each group. We found that in Schwann cell-transplanted animals all parameters tested were significantly improved upon those of dark-reared control rats and were in the range of normal adult values. Thus, Schwann cell transplant contributed to the normal development of visual response properties in the visual cortex, compensating for a complete absence of visual experience.

Animals↗

Negative BOLD in the visual cortex: evidence against blood stealing.

The positive BOLD (blood oxygen level-dependent) response elicited in human visual cortex by a localized visual stimulus is accompanied by a reduction in the BOLD response in regions of the visual cortex that represent unstimulated locations in the visual field. We have suggested previously that this negative BOLD reflects attention-related suppression of neural activity, but it might also be explained in terms of "blood stealing," i.e., hemodynamic changes that have no neural correlate. We distinguish two possible hemodynamic effects of this type: (1). blood flow reduction caused by locally reduced pressure in vessels that share their blood supply with nearby dilated vessels; and (2). blood flow reduction caused by active constriction of vessels under neural control. The first is ruled out as an explanation of negative BOLD by showing that a visual stimulus that stimulates primary visual cortex in one hemisphere can cause extensive suppression in the other hemisphere i.e., it is not a local phenomenon. Negative BOLD most likely reflects suppression of neural activity, but could also reflect an active blood flow control system.

Attention↗

Distribution of NADPH-diaphorase cells in visual and somatosensory cortex in four mammalian species.

The distribution of the well-labeled nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) Type I neurons was evaluated in the isocortex of four mammalian species: the Didelphis opossum, the Monodelphis opossum, the rat and the marmoset. In Didelphis opossum, laminar distribution was examined in tangential and non-tangential sections. The density increases from superficial to deep layers of the gray matter. In rats' tangential sections, infragranular and supragranular layers have higher density than layer IV. Cell density measurements in the visual and the somatosensory cortices were compared in tangential sections from flattened hemispheres of the four species. Somatosensory areas were identified histochemically in rat (barrel fields) and marmoset (S1 and S2/PV). In the opossums, areas S1 and S2/PV were identified by multiunit recording. Except in the rat, primary visual cortex (V1) was labeled histochemically by NADPHd and/or cytochrome oxidase. In the four species, cell density in somatosensory cortex was significantly higher than in visual cortex. Taken together these results demonstrate that NADPHd Type I neurons are not homogeneously distributed in the isocortex of these mammals. In conclusion, the tangential distribution of Type I neurons in the sensory areas examined, but not its laminar distribution, was similar in the four species. Given that rats, marmosets and opossums are distantly related species, and that the latter are considered to have more 'generalized' brains, it is conceivable that this pattern of tangential distribution of Type I neurons is a general feature of mammalian isocortex.

Afferent Pathways↗

No functional magnetic resonance imaging evidence for brightness and color filling-in in early human visual cortex.

The brightness and color of a surface depends on its contrast with nearby surfaces. For example, a gray surface can appear very light when surrounded by a black surface or dark when surrounded by a white surface. Some theories suggest that perceived surface brightness and color is represented explicitly by neural signals in cortical visual field maps; these neural signals are not initiated by the stimulus itself but rather by the contrast signals at the borders. Here, we use functional magnetic resonance imaging (fMRI) to search for such neural "filling-in" signals. Although we find the usual strong relationship between local contrast and fMRI response, when perceived brightness or color changes are induced by modulating a surrounding field, rather than the surface itself, we find there is no corresponding local modulation in primary visual cortex or other nearby retinotopic maps. Moreover, when we model the obtained fMRI responses, we find strong evidence for contributions of both local and long-range edge responses. We argue that such extended edge responses may be caused by neurons previously identified in neurophysiological studies as being brightness responsive, a characterization that may therefore need to be revised. We conclude that the visual field maps of human V1 and V2 do not contain filled-in, topographical representations of surface brightness and color.

Action Potentials↗

Retinal projections to the lateral posterior-pulvinar complex in intact and early visual cortex lesioned cats.

In intact cats, it is generally considered that the lateral posterior-pulvinar complex (LP-pulvinar) does not receive direct retinal terminals, with the exception of the retino-recipient zone known as the geniculate wing. There is, however, some evidence that early lesions of the visual cortex can occasionally induce the formation of novel retinal projections to the LP nucleus. Given the importance of knowing the connectivity pattern of the LP-pulvinar complex in intact and lesioned animals, we used the B fragment of cholera toxin, a sensitive anterograde tracer, to reinvestigate the retinal projections to the LP-pulvinar in normal cats and in cats with early unilateral lesions of the visual cortex (areas 17 and 18). Immunohistochemical localization of the toxin was performed to show the distribution and morphology of retinofugal terminals. A direct bilateral but predominantly contralateral retinal projection reached the caudal portion of LPl and LPm in the form of patches located mainly along its dorsomedial surface and many scattered terminals. The distribution of retinal projections to LP-pulvinar in intact and operated cats did not differ. Contrary to what had been previously reported, we found no evidence for lesion-induced sprouting of retinal axons in these higher-order thalamic nuclei. Retinal input to the LP-pulvinar might modulate visual responses driven by primary visual cortex or superior colliculus.

Animals↗

Experience-dependent plasticity in adult visual cortex.

Experience-dependent plasticity is a prominent feature of the mammalian visual cortex. Although such neural changes are most evident during development, adult cortical circuits can be modified by a variety of manipulations, such as perceptual learning and visual deprivation. Elucidating the underlying mechanisms at the cellular and synaptic levels is an essential step in understanding neural plasticity in the mature animal. Although developmental and adult plasticity share many common features, notable differences may be attributed to developmental cortical changes at multiple levels. These range from shifts in the molecular profiles of cortical neurons to changes in the spatiotemporal dynamics of network activity. In this review, we will discuss recent progress and remaining challenges in understanding adult visual plasticity, focusing on the primary visual cortex.

Animals↗

Voxel-based analysis of MRI detects abnormal visual cortex in children and adults with amblyopia.

Amblyopia, sometimes called "lazy eye," is a relatively common developmental visual disorder well characterized behaviorally; however, the neural substrates associated with amblyopia in humans remain unclear. We hypothesized that abnormalities in the cerebral cortex of subjects with amblyopia exist, possibly as a result of experience-dependent neuronal plasticity. Anatomic magnetic resonance imaging (MRI) and psychophysical vision testing was carried out on 74 subjects divided into two age ranges, 7-12 years and 18-35 years, and three diagnoses, strabismic amblyopia, anisometropic amblyopia, and normal vision. We report a behavioral impairment in contrast sensitivity for subjects with amblyopia, consistent with previous reports. When the high-resolution MRI brain images were analyzed quantitatively with optimized voxel-based morphometry, results indicated that adults and children with amblyopia have decreased gray matter volume in visual cortical regions, including the calcarine sulcus, known to contain primary visual cortex. This finding was confirmed with a separate region-of-interest analysis. For the children with amblyopia, additional gray matter reductions in parietal-occipital areas and ventral temporal cortex were detected, consistent with recent reports that amblyopia can result in spatial location and object processing deficits. These data are the first to provide possible neuroanatomic bases for the loss of binocularity and visual sensitivity in children and adults with amblyopia.

Adolescent↗

Orientation-specific adaptation in human visual cortex.

Nearly all methods for analyzing and interpreting functional magnetic resonance imaging (fMRI) data assume that the fMRI signal behaves in an approximately linear manner. However, it has been shown that the mean fMRI response to a pair of briefly presented visual stimuli is significantly smaller than would be expected from the response to a single stimulus. This smaller response could be the result of either a nonlinearity in the fMRI signal or neuronal adaptation. We tested the neuronal adaptation hypothesis by measuring the fMRI response to sequential pairs of sinusoidal gratings that had either the same or orthogonal orientation. The adaptation hypothesis predicts that brain areas with orientation-selective neurons should show a more linear response when the stimulus pair is orthogonal than when the pair is identical. Our results show no orientation-specific adaptation effects in primary visual cortex (V1) but increasing effects along the hierarchy of visual areas (V2, V3, and V4V). A psychophysical contrast detection experiment, using similar oriented gratings as adapters, shows evidence of orientation-specific adaptation in the visual system. These results have implications for the interpretation of rapid event-related fMRI experiments, as well as for recently developed methods that use adaptation as a tool to measure the response properties of underlying neuronal subpopulations.

Adaptation, Physiological↗

Human cerebral activation during steady-state visual-evoked responses.

Flicker stimuli of variable frequency (2-90 Hz) elicit a steady-state visual-evoked response (SSVER) in the electroencephalogram (EEG) with the same frequency as the stimulus. In humans, the amplitude of this response peaks at approximately 15 Hz, decreasing at higher stimulation frequencies. It was not known whether this peak response corresponds to increased synaptic activity in the visual cortex or to other mechanisms [for instance, the temporal coherence (phase summation) of evoked responses]. We studied the SSVER in 16 normal volunteers by means of visual stimulation at 14 different frequencies (from 5 to 60 Hz) while recording the EEG. In nine subjects of the group, we measured regional cerebral blood flow (rCBF) with positron emission tomography (PET)-H2(15)O at rest and during visual stimulation at five different frequencies: 5, 10, 15, 25, and 40 Hz. We confirmed that the amplitude of the SSVER in occipital regions peaks at 15 Hz stimulation. Applying to the PET rCBF data a contrast weighted by the amplitude of the SSVER, we determined that the primary visual cortex rCBF follows an activation pattern similar to the SSVER. This finding suggests that the amplitude of the SSVER corresponds to increased synaptic activity, specifically in Brodmann's area 17. Additionally, this study showed that visual stimulation at 40 Hz causes selective activation of the macular region of the visual cortex, and that a region in the dorsal aspect of the Crus I lobule of the left cerebellar hemisphere is activated during repetitive visual stimulation.

Adult↗

Visual input evokes transient and strong shunting inhibition in visual cortical neurons.

The function and nature of inhibition of neurons in the visual cortex have been the focus of both experimental and theoretical investigations. There are two ways in which inhibition can suppress synaptic excitation. In hyperpolarizing inhibition, negative and positive currents sum linearly to produce a net change in membrane potential. In contrast, shunting inhibition acts nonlinearly by causing an increase in membrane conductance; this divides the amplitude of the excitatory response. Visually evoked changes in membrane conductance have been reported to be nonsignificant or weak, supporting the hyperpolarization mode of inhibition. Here we present a new approach to studying inhibition that is based on in vivo whole-cell voltage clamping. This technique allows the continuous measurement of conductance dynamics during visual activation. We show, in neurons of cat primary visual cortex, that the response to optimally orientated flashed bars can increase the somatic input conductance to more than three times that of the resting state. The short latency of the visually evoked peak of conductance, and its apparent reversal potential suggest a dominant contribution from gamma-aminobutyric acid ((GABA)A) receptor-mediated synapses. We propose that nonlinear shunting inhibition may act during the initial stage of visual cortical processing, setting the balance between opponent 'On' and 'Off' responses in different locations of the visual receptive field.

Animals↗

Magnetic stimuli applied over motor and visual cortex: influence of coil position and field polarity on motor responses, phosphenes, and eye movements.

Transcranial magnetic stimulation was performed over the motor and visual cortex with the Novametrix 12-cm diameter stimulation coil. The influence of coil position on the size of electromyographic responses and on the intensity and position of phosphenes in the binocular visual field was studied. Furthermore, it was investigated whether stimulation over the visual cortex or over the frontal eye field evoked or disturbed eye movements. Coil position was recorded by constructing grids on the skull surface using extracranial bony landmarks, and was then related individually to underlying cerebral sulci by analysis of magnetic resonance images of the brain. Motor responses. Excitatory effects were maximal when the coil windings in the middle of the coil ring lay over the particular motor representation field of area 4. The response size depended on the direction of the coil currents passing over the motor cortex. For example, coil currents passing over the lateral part of the precentral gyrus from the front and transversely to the central sulcus elicited maximal responses in hand muscles. With the currents passing over the same area in the opposite direction, response amplitudes were much smaller, suggesting activation of different inputs to cortical motoneurons. Phosphenes. Fields of fixed, white and unstructured phosphens occurred in the lower half of the visual field when the coil center was placed about 7 cm anterior to the inion on the inion-nasion line. Counterclockwise or clockwise coil currents elicited phosphenes within the left or right lower quadrant of the binocular visual field, respectively, which could be attributed to an activation of the right or left primary visual cortex (area 17). The 'cortical' phosphenes moved with voluntary eye movements, but not during caloric and optokinetic nystagmus. Phosphenes resulting from an excitation of the optic nerve rather than the retina could be evoked by stimulation over frontal parts of the skull. Eye movements. The application of single magnetic field pulses over the frontal eye field or over the visual cortex did not elicit eye movements except for small vertical eye movements as part of a magnetically elicited blink.

Adolescent↗

Glucose hypometabolism in medial frontal cortex of patients with apraxia of lid opening.

PURPOSE: To determine whether regional cerebral functional abnormalities exist in patients with apraxia of lid opening (ALO). METHODS: Cerebral glucose metabolism was examined by positron emission tomography (PET) in 11 patients (8 women and 3 men, age 48-69 years); 10 with ALO accompanied by blepharospasm and 1 patient with pure ALO. Eleven normal volunteers (6 women and 5 men, age 45-66 years) were examined as controls. A comprehensive ophthalmological examination, magnetic resonance imaging (MRI), and PET were performed. The cerebral glucose metabolism was evaluated by the relative uptake of [fluorine-18]fluorodeoxyglucose by PET. The mean +/- two standard deviations of the normal controls was defined as the normal range for cerebral glucose metabolism. RESULTS: MRI revealed no particular lesion except for an infarction in the unilateral basal ganglia in two patients. Decreased glucose metabolism was observed in a wide area of the medial frontal lobe (six cases) and primary visual cortex (PVC) (four cases). Group multiple comparisons revealed a significant decrease ( P<0.0035) in the bilateral anterior cingulate gyrus, left supplementary motor area (SMA), and bilateral PVC. CONCLUSION: The results support the hypothesis that ALO is associated with hypofunction in the SMA and/or anterior cingulate gyrus.

Aged↗

Computational models of cortical visual processing.

The visual responses of neurons in the cerebral cortex were first adequately characterized in the 1960s by D. H. Hubel and T. N. Wiesel [(1962) J. Physiol. (London) 160, 106-154; (1968) J. Physiol. (London) 195, 215-243] using qualitative analyses based on simple geometric visual targets. Over the past 30 years, it has become common to consider the properties of these neurons by attempting to make formal descriptions of these transformations they execute on the visual image. Most such models have their roots in linear-systems approaches pioneered in the retina by C. Enroth-Cugell and J. R. Robson [(1966) J. Physiol. (London) 187, 517-552], but it is clear that purely linear models of cortical neurons are inadequate. We present two related models: one designed to account for the responses of simple cells in primary visual cortex (V1) and one designed to account for the responses of pattern direction selective cells in MT (or V5), an extrastriate visual area thought to be involved in the analysis of visual motion. These models share a common structure that operates in the same way on different kinds of input, and instantiate the widely held view that computational strategies are similar throughout the cerebral cortex. Implementations of these models for Macintosh microcomputers are available and can be used to explore the models' properties.

Computer Simulation↗

Distribution, morphology, and synaptic targets of corticothalamic terminals in the cat lateral posterior-pulvinar complex that originate from the posteromedial lateral suprasylvian cortex.

The lateral posterior (LP) nucleus is a higher order thalamic nucleus that is believed to play a key role in the transmission of visual information between cortical areas. Two types of cortical terminals have been identified in higher order nuclei, large (type II) and smaller (type I), which have been proposed to drive and modulate, respectively, the response properties of thalamic cells (Sherman and Guillery [1998] Proc. Natl. Acad. Sci. U. S. A. 95:7121-7126). The aim of this study was to assess and compare the relative contribution of driver and modulator inputs to the LP nucleus that originate from the posteromedial part of the lateral suprasylvian cortex (PMLS) and area 17. To achieve this goal, the anterograde tracers biotinylated dextran amine (BDA) or Phaseolus vulgaris leucoagglutinin (PHAL) were injected into area 17 or PMLS. Results indicate that area 17 injections preferentially labelled large terminals, whereas PMLS injections preferentially labelled small terminals. A detailed analysis of PMLS terminal morphology revealed at least four categories of terminals: small type I terminals (57%), medium-sized to large singletons (30%), large terminals in arrangements of intermediate complexity (8%), and large terminals that form arrangements resembling rosettes (5%). Ultrastructural analysis and postembedding immunocytochemical staining for gamma-aminobutyric acid (GABA) distinguished two types of labelled PMLS terminals: small profiles with round vesicles (RS profiles) that contacted mostly non-GABAergic dendrites outside of glomeruli and large profiles with round vesicles (RL profiles) that contacted non-GABAergic dendrites (55%) and GABAergic dendritic terminals (45%) in glomeruli. RL profiles likely include singleton, intermediate, and rosette terminals, although future studies are needed to establish definitively the relationship between light microscopic morphology and ultrastructural features. All terminals types appeared to be involved in reciprocal corticothalamocortical connections as a result of an intermingling of terminals labelled by anterograde transport and cells labelled by retrograde transport. In conclusion, our results indicate that the origin of the driver inputs reaching the LP nucleus is not restricted to the primary visual cortex and that extrastriate visual areas might also contribute to the basic organization of visual receptive fields of neurons in this higher order nucleus.

Animals↗

Constraints on the source of short-term motion adaptation in macaque area MT. I. the role of input and intrinsic mechanisms.

Neurons in area MT, a motion-sensitive area of extrastriate cortex, respond to a step of target velocity with a transient-sustained firing pattern. The transition from a high initial firing rate to a lower sustained rate occurs over a time course of 20-80 ms and is considered a form of short-term adaptation. The present paper asks whether adaptation is due to input-specific mechanisms such as short-term synaptic depression or if it results from intrinsic cellular mechanisms such as spike-rate adaptation. We assessed the contribution of input-specific mechanisms by using a condition/test paradigm to measure the spatial scale of adaptation. Conditioning and test stimuli were placed within MT receptive fields but were spatially segregated so that the two stimuli would activate different populations of inputs from the primary visual cortex (V1). Conditioning motion at one visual location caused a reduction of the transient firing to subsequent test motion at a second location. The adaptation field, estimated as the region of visual space where conditioning motion caused adaptation, was always larger than the MT receptive field. Use of the same stimulus configuration while recording from direction-selective neurons in V1 failed to demonstrate either adaptation or the transient-sustained response pattern that is the signature of short-term adaptation in MT. We conclude that the shift from transient to sustained firing in MT cells does not result from an input-specific mechanism applied to inputs from V1 because it operates over a wider range of the visual field than is covered by receptive fields of V1 neurons. We used a direct analysis of MT neuron spike trains for many repetitions of the same motion stimulus to assess the contribution to adaptation of intrinsic cellular mechanisms related to spiking. On a trial-by-trial basis, there was no correlation between number of spikes in the transient interval and the interval immediately after the transient period. This is opposite the prediction that there should be a correlation if spikes cause adaptation directly. Further, the transient was suppressed or extinguished, not delayed, in trials in which the neuron emitted zero spikes during the interval that showed a transient in average firing rate. We conclude that the transition from transient to sustained firing in neurons in area MT is caused by mechanisms that are neither input-specific nor controlled by the spiking of the adapting neuron. We propose that the short-term adaptation observed in area MT emerges from the intracortical circuit within MT.

Action Potentials↗