Increase In Receptive Field Size Research Articles

KiU-Net: Overcomplete Convolutional Architectures for Biomedical Image and Volumetric Segmentation.

Most methods for medical image segmentation use U-Net or its variants as they have been successful in most of the applications. After a detailed analysis of these "traditional" encoder-decoder based approaches, we observed that they perform poorly in detecting smaller structures and are unable to segment boundary regions precisely. This issue can be attributed to the increase in receptive field size as we go deeper into the encoder. The extra focus on learning high level features causes U-Net based approaches to learn less information about low-level features which are crucial for detecting small structures. To overcome this issue, we propose using an overcomplete convolutional architecture where we project the input image into a higher dimension such that we constrain the receptive field from increasing in the deep layers of the network. We design a new architecture for im- age segmentation- KiU-Net which has two branches: (1) an overcomplete convolutional network Kite-Net which learns to capture fine details and accurate edges of the input, and (2) U-Net which learns high level features. Furthermore, we also propose KiU-Net 3D which is a 3D convolutional architecture for volumetric segmentation. We perform a detailed study of KiU-Net by performing experiments on five different datasets covering various image modalities. We achieve a good performance with an additional benefit of fewer parameters and faster convergence. We also demonstrate that the extensions of KiU-Net based on residual blocks and dense blocks result in further performance improvements. Code: https://github.com/jeya-maria-jose/KiU-Net-pytorch.

Top-down feedback controls spatial summation and response amplitude in primate visual cortex

Sensory information travels along feedforward connections through a hierarchy of cortical areas, which, in turn, send feedback connections to lower-order areas. Feedback has been implicated in attention, expectation, and sensory context, but the mechanisms underlying these diverse feedback functions are unknown. Using specific optogenetic inactivation of feedback connections from the secondary visual area (V2), we show how feedback affects neural responses in the primate primary visual cortex (V1). Reducing feedback activity increases V1 cells’ receptive field (RF) size, decreases their responses to stimuli confined to the RF, and increases their responses to stimuli extending into the proximal surround, therefore reducing surround suppression. Moreover, stronger reduction of V2 feedback activity leads to progressive increase in RF size and decrease in response amplitude, an effect predicted by a recurrent network model. Our results indicate that feedback modulates RF size, surround suppression and response amplitude, similar to the modulatory effects of visual spatial attention.

Selectivity and Tolerance (“Invariance”) Both Increase as Visual Information Propagates from Cortical Area V4 to IT

Our ability to recognize objects despite large changes in position, size, and context is achieved through computations that are thought to increase both the shape selectivity and the tolerance ("invariance") of the visual representation at successive stages of the ventral pathway [visual cortical areas V1, V2, and V4 and inferior temporal cortex (IT)]. However, these ideas have proven difficult to test. Here, we consider how well population activity patterns at two stages of the ventral stream (V4 and IT) discriminate between, and generalize across, different images. We found that both V4 and IT encode natural images with similar fidelity, whereas the IT population is much more sensitive to controlled, statistical scrambling of those images. Scrambling sensitivity was proportional to receptive field (RF) size in both V4 and IT, suggesting that, on average, the number of visual feature conjunctions implemented by a V4 or IT neuron is directly related to its RF size. We also found that the IT population could better discriminate between objects across changes in position, scale, and context, thus directly demonstrating a V4-to-IT gain in tolerance. This tolerance gain could be accounted for by both a decrease in single-unit sensitivity to identity-preserving transformations (e.g., an increase in RF size) and an increase in the maintenance of rank-order object selectivity within the RF. These results demonstrate that, as visual information travels from V4 to IT, the population representation is reformatted to become more selective for feature conjunctions and more tolerant to identity preserving transformations, and they reveal the single-unit response properties that underlie that reformatting.

Stereo and motion Dmax in infants

These experiments compared the maximum displacement and disparity limits (Dmax) for apparent motion and stereopsis in random-dot displays in adult and 12-28 week-old infant subjects. Both stereo and motion Dmax increased during development, from about 0.3 deg in the youngest infants to 2 deg in adults. Some of the younger infants (12-14 weeks) did not give a stereo threshold, probably because stereopsis had not yet developed; but otherwise, the values of Dmax in the two domains were close to each other throughout the age range. These results suggest that both stereo and motion Dmax are limited by some common factor. Possible factors include receptive field sizes and internal noise. Simulations in which these were varied showed that while changes in both could contribute to the development of Dmax, only an increase in receptive field size can fully account for the rise in Dmax with age.

Inhomogeneous retino-cortical mapping is supported and stabilized with correlation-learning during self-motion

In primates, the area of primary visual cortex representing a fixed area of visual space decreases with increasing eccentricity. We identify visual situations to which this inhomogeneous retino-cortical mapping is well adapted and study their relevance during natural vision and development. We assume that cortical activations caused by stationary objects during self-motion along the direction of gaze travel on average with constant speed across the cortical surface, independent of retinal eccentricity. This is the case if the distribution of objects corresponds to an ellipsoid with the observer in its center. We apply the resulting flow field to train a simple network of pulse coding neurons with Hebbian learning and demonstrate that the density of learned receptive field centers is in close agreement with primate retino-cortical magnification. In addition, the model reproduces the increase of receptive field size and the decrease of its peak sensitivity with increasing eccentricity. Our results suggest that self-motion may have played an important role in the evolution of the visual system and that cortical magnification can be refined and stabilized by Hebbian learning mechanisms in ontogenesis under natural viewing conditions.

Spontaneous Retinal Activity Mediates Development of Ocular Dominance Columns and Binocular Receptive Fields in V1

The mechanisms that give rise to ocular dominance columns (ODCs) during development are controversial. Early experiments indicated a key role for retinal activity in ODC formation. However, later studies showed that in those early experiments, the retinal activity perturbation was initiated after ODCs had already formed. Moreover, recent studies concluded that early eye removals do not impact ODC segregation. Here we blocked spontaneous retinal activity during the very early stages of ODC development. This permanently disrupted the anatomical organization of ODCs and led to a dramatic increase in receptive field size for binocular cells in primary visual cortex. Our data suggest that early spontaneous retinal activity conveys crucial information about whether thalamocortical axons represent one or the other eye and that this activity mediates binocular competition important for shaping receptive fields in primary visual cortex.

Effects of a Cannabinoid Agonist on Spinal Nociceptive Neurons in a Rodent Model of Neuropathic Pain

The effects of the synthetic cannabinoid WIN 55,212-2 on heat-evoked firing of spinal wide dynamic range (WDR) neurons were examined in a rodent model of neuropathic pain. Fifty-eight WDR neurons (1 cell/animal) were recorded from the ipsilateral spinal dorsal horns of rats with chronic constriction injury (CCI) and sham-operated controls. Relative to sham-operated controls, neurons recorded in CCI rats showed elevations in spontaneous firing, noxious heat-evoked responses, and afterdischarge firing as well as increases in receptive field size. WIN 55,212-2 (0.0625, 0.125, and 0.25 mg/kg, intravenous) dose-dependently suppressed heat-evoked activity and decreased the receptive field areas of dorsal horn WDR neurons in both nerve injured and control rats with a greater inhibition in CCI rats. At the dose of 0.125 mg/kg iv, WIN 55,212-2 reversed the hyperalgesia produced by nerve injury. The effect of intravenous administration of WIN 55,212-2 appears to be centrally mediated because administration of the drug directly to the ligated nerve did not suppress the heat-evoked neuronal activity in CCI rats. Pretreatment with the cannabinoid CB(1) receptor antagonists SR141716A or AM251, but not the CB(2) antagonist SR144528, blocked the effects. These results provide a neural basis for reports of potent suppression by cannabinoids of the abnormal sensory responses that result from nerve injury.

Aberrant dendritic branching and sensory inputs in the superficial dorsal horn of mice lacking CaMKIIα autophosphorylation

Superficial dorsal horn neurones undergo marked structural and functional activity-dependent development during the early postnatal period, but little is known about the molecular mechanisms underlying these changes. Calcium signalling, through activation and autophosphorylation of CaMKII, has been shown to play a major role in the maturation of neuronal morphology and connectivity in the cortex. Here, we show that the normal structural and functional development of superficial dorsal horn neurones requires CaMKII autophosphorylation at the Thr286 residue. The dendritic branching of neurones from mice containing a point mutation at this site (T286A) was significantly increased compared with wild-type littermates. This was accompanied by significant increases in receptive field size, recorded from intact preparations. Whole-cell patch clamp recordings of superficial dorsal horn slices revealed a selective deficit in low-threshold A fibre-evoked synaptic input. These results show that CaMKII autophosphorylation is required for the normal development of spinal sensory circuits.

Expansion of visual receptive fields in experimental glaucoma

Glaucoma is a major cause of blindness and is characterized by death of retinal ganglion cells. In a rat model of glaucoma in which intraocular pressure is raised by cautery of episcleral veins, the somata and dendritic arbors of surviving retinal ganglion cells expand. To assess physiological consequences of this change, we have measured visual receptive-field size in a primary retinal target, the superior colliculus. Using multiunit recording, receptive-field sizes were measured for glaucomatous eyes and compared to both those measured for contralateral control eyes and to homolateral eyes of unoperated animals. Episcleral vein occlusion increased intraocular pressure. This was accompanied by a significant increase in receptive-field size across the superior colliculus. The expansion of receptive fields was proportional to both degree and duration of the increase of intraocular pressure. We suggest that this increase in the size of receptive fields of glaucomatous eyes may be related to the increase in the size of dendritic arbors of the surviving ganglion cells in retina.

NMDA receptor blockade in the superior colliculus increases receptive field size without altering velocity and size tuning.

Neonatal brain injury triggers compensatory processes that can be adaptive or detrimental, but little is known about the mechanisms of compensation or how they might affect the response properties of neurons within the injured region. We have studied this issue in a rodent model. Partial ablation of the hamster superior colliculus (SC) at birth results in a compressed but complete visual field map in the remaining SC and a compensatory conservation of receptive field (RF) size and stimulus velocity and size tuning. The circuit underlying stimulus tuning in this system or its preservation after brain lesions is not known. Our previous work has shown that N-methyl-d-aspartate (NMDA) receptors are necessary for the development and conservation of RF size after partial SC ablation. In this study, we examined whether NMDA receptor function is also necessary for the development and conservation of stimulus velocity and size tuning. We found that velocity and size tuning were unaffected by chronic postnatal blockade of NMDA receptors and the resulting increases in RF size. Thus NMDA receptors in the SC are not necessary for the development of stimulus velocity and size tuning or in the compensatory maintenance of these properties following brain damage. These results suggest that stimulus velocity and size tuning may arise in the retina or from NMDA receptor-independent circuitry intrinsic to SC. The lack of conflict between NMDA receptor activity-dependent and -independent processes may allow conservation of some RF properties while others change during injury-induced or evolutionary changes in afferent/target convergence.

Spatio–temporal plasticity of cortical receptive fields in response to repetitive visual stimulation in the adult cat

Many psychophysical experiments on perceptual learning in humans show increases of performance that are most probably based on functions of early visual cortical areas. Long-term plasticity of the primary visual cortex has so far been shown in vivo with the use of visual stimuli paired with electrical or pharmacological stimulation at the cellular level. Here, we report that plasticity in the adult visual cortex can be achieved by repetitive visual stimulation. First, spatial receptive field profiles of single units ( n=38) in area 17 or 18 of the anesthetized cat were determined with optimally oriented flashing light bars. Then a conditioning protocol was applied to induce associative synaptic plasticity. The receptive field center and an unresponsive region just outside the excitatory receptive field were synchronously stimulated (‘costimulation’, repetition rate 1 Hz; for 10–75 min). After costimulation the receptive field and its adjacent regions were mapped again. We observed specific increases of the receptive field size, changes of the receptive field subfield structure as well as shifts in response latency. In 37% of the cells the receptive field size increased specifically towards the stimulated side but not towards the non-stimulated opposite side of the receptive field. In addition, changes in the relative strength and size of the on and off subfield regions were observed. These specific alterations were dependent on the level of neuronal activity during costimulation. During recovery, the new responses dropped down to 120% of the preconditioning value on average within 103 min; however, the decay times significantly depended on the response magnitude after costimulation. In the temporal domain, the latency of new responses appeared to be strongly influenced by the latency of the response during costimulation. Twenty-nine percent of the units displayed no receptive field enlargement, most likely because the activity during costimulation was significantly lower than in the cases with enlarged receptive fields. An unspecific receptive field enlargement towards both the stimulated and non-stimulated side was observed in 34% of the tested cells. In contrast to the cells with specifically enlarged receptive fields, the unspecific increase of receptive field size was always accompanied by a strong increase of the general activity level. We conclude that the receptive field changes presumably took place by strengthening of synaptic inputs at the recorded cells in a Hebbian way as previously shown in the visual cortex in vitro and in vivo. The observed receptive field changes may be related to preattentive perceptual learning and could represent a basis of the ‘filling in’ of cortical scotomas obtained with specific training procedures in human patients suffering from visual cortex lesions.

Acute effect of an incision on mechanosensitive afferents in the plantar rat hindpaw.

The purpose of this study was to examine which primary afferent fibers are sensitized to mechanical stimuli after an experimental surgical incision to the glabrous skin of the rat hindpaw. Afferent fibers teased from the L(5) dorsal root or the tibial nerve were recorded in anesthetized rats. The mechanical response properties of each fiber were characterized before and 45 min after an incision (or sham procedure) within the mechanical receptive field. Sensitization is characterized by an expansion of the mechanical receptive field, an increase in background activity, an increase in response magnitude, or a decrease in response threshold. After incision, the background activity and response properties of Abeta-fibers (n = 9) to mechanical stimuli were unchanged. Four of 13 mechanosensitive Adelta-fibers exhibited sensitization after the incision; response threshold decreased, response magnitude increased, or receptive field size increased. Background activity of Adelta-fibers was not increased by the incision. Sensitization was observed in 4 of 18 mechanosensitive C-fibers 45 min after the incision. Background activity of C-fibers was not increased by the incision. In a group of mechanically insensitive afferent fibers (MIAs), 3 of 7 Adelta-fibers and 4 of 10 C-fibers sensitized 45 min after incision. Response threshold was decreased in only 2 of 17 MIAs; receptive field size increased in 7 of 17 MIAs. Abeta-fibers did not sensitize after the incision, and only 8 of 31 (26%) mechanosensitive Adelta- and C-fibers gave evidence of sensitization. In a group of MIA Adelta- and C-fibers, a greater percentage of 17 fibers studied (41%) were sensitized after incision. In this model, the principal effect of an incision, when examined 45 min after the insult, is an increase in receptive field size of the afferents, particularly those characterized as MIAs. To the extent that the mechanical hyperalgesia characterized in the same model is initiated in the periphery, it would appear that spatial summation of modestly increased response magnitude is important to the development of hyperalgesia.

Motion information is spatially localized in a visual working-memory task.

We asked if the information about stimulus motion used in a visual working-memory task is localized in space. Monkeys compared the directions of two moving random-dot stimuli, sample and test, separated by a temporal delay and reported whether the stimuli moved in the same or in different directions. By presenting the two comparison stimuli in separate locations in the visual field, we determined whether information about stimulus direction was spatially localized during the storage and retrieval/comparison components of the task. Two psychophysical measures of direction discrimination provided nearly identical estimates of the critical spatial separation between sample and test stimuli that lead to a loss in threshold. Direction range thresholds measured with dot stimuli consisting of a range of local directional vectors were affected by spatial separation when a random-motion mask was introduced during the delay into the location of the upcoming test. The selective masking at the test location suggests that the information about the remembered direction was localized and available at that location. Direction difference thresholds, measured with coherently moving random dots, were also affected by separation between the two comparison stimuli. The separation at which performance was affected in both tasks increased with retinal eccentricity in parallel with the increase in receptive-field size in neurons in cortical area MT. The loss with transfer of visual information between different spatial locations suggests a contribution of cortical areas with localized receptive fields to the performance of the memory task. The similarity in the spatial scale of the storage mechanism derived psychophysically and the receptive field size of neurons in area MT suggest that MT neurons are central to this task.

Expansion of receptive fields in raccoon somatosensory cortex in vivo by GABA(A) receptor antagonism: implications for cortical reorganization.

The effect of antagonism of GABA(A) receptors on the receptive fields of raccoon primary somatosensory cortical neurons was tested using microiontophoretic administration of bicuculline methiodide (BMI). The size of cutaneous receptive fields was examined using minimal suprathreshold mechanical stimulation before, during, and after BMI administration. In 65 of 102 rapidly adapting neurons, BMI produced a clear expansion of the receptive field. The mean increase in receptive-field size was 286%. The receptive fields on the distal digit, which were initially smaller, showed smaller increases in absolute area than more proximal receptive fields, but the percentage increase did not vary with location. Greater expansion was seen in superficially located neurons than in those below 800 microm. Of particular significance was the finding that the expansion of receptive fields produced by BMI never extended from one digit onto an adjacent digit or onto the palm, even when the original receptive field was at the base of a digit. This finding indicates that intracortical GABAergic inhibition is insufficient to explain cortical reorganization following digit amputation.

Modulation of receptive field properties of thalamic somatosensory neurons by the depth of anesthesia.

Modulation of receptive field properties of thalamic somatosensory neurons by the depth of anesthesia. The dominant frequency of electrocorticographic (ECoG) recordings was used to determine the depth of halothane or urethan anesthesia while recording extracellular single-unit responses from thalamic ventral posterior medial (VPM) neurons. A piezoelectric stimulator was used to deflect individual whiskers to assess the peak onset latency, magnitude, probability of response, and receptive field (RF) size. There was a predictable increase in the dominant ECoG frequency from deep stage IV to light stage III-1 anesthetic levels. There was no detectable frequency at stage IV, a 1- to 2-Hz dominant frequency at stage III-4, 3-4 Hz at stage III-3, 5-7 Hz at stage III-2, and a dual 6- and 10- to 13-Hz pattern at stage III-1. Reflexes and other physical signs showed a correlation with depth of anesthesia but exhibited too much overlap between stages to be used as a criterion for any single stage. RF size and peak onset latency of VPM neurons to whisker stimulations increased between stage III-4 and III-1. A dramatic increase in RF size and response latency occurred at the transition from stage III-3 (RF size approximately 2 whiskers, latency approximately 7 ms) to stage III-2 (RF size approximately 6 whiskers, latency approximately 11 ms). Response probability and magnitude decreased from stage III-4 to stage III-3 and III-2. No responses were ever evoked in VPM cells by vibrissa movement at stage IV. These changes in VPM responses as a function of anesthetic depth were seen only when the nucleus principalis (PrV) and nucleus interpolaris (SpVi) trigeminothalamic pathways were both intact. Eliminating SpVi inputs to VPM, either by cutting the primary trigeminal afferent fibers to SpVi or cutting axons projecting from SpVi to VPM, immediately reduced the RF size to fewer than three whiskers. In addition, the predictable changes in VPM response probability, response magnitude, and peak onset latency at different anesthetic depths were all absent after SpVi pathway interruption. We conclude that 1) the PrV input mediates the near "one-to-one" correspondence between a neuronal response in VPM and a single mystacial whisker, 2) in contrast, the SpVi input to VPM is primarily responsible for the RF properties of VPM neurons at light levels of anesthesia and presumably in the awake animal, and 3) alterations in VPM responses produced by changing the depth of anesthesia are due to its selective influence on the properties mediated by SpVi inputs at the level of the thalamus.

Effects of cholinergic depletion on evoked activity inthe cortex of young and aged rats

Degeneration of cholinergic neurons in the basal forebrain is a neural marker ofAlzheimers disease and is associated with perceptual and cognitive deficits. An idea that hasattracted scientific scutiny is that aging makes the brain more susceptible to neurodegenerativediseases such as Alzheimers. The purpose of this study was to compare the effects of the loss ofcholinergic input from nucleus basalis of Meynert on evoked activity in the posteromedial barrelsubfield of the somatosensory cortex in young (2–2.5 months) and aged (28–30 months) maleFisher hybrid rats. The mean firing rate and receptive fields of single neurons in the posteromedialbarrel subfield of the somatosensory cortex were examined after selective lesions of cholinergicneurons in the nucleus basalis of Meynert with an immunotoxin, IgG 192-saporin.Functional properties of single neurons in young animals were affected much moresignificantly by cholinergic depletion than those in aged animals. In cholinergic-depleted younganimals, the mean firing rate of evoked activity and receptive field of posteromedial barrel subfieldneurons were significantly decreased. Cholinergic depletion caused a 14% decrease in evokedactivity and a 33% increase in receptive field size in young animals. The mean firing rate andreceptive field of single neurons were not affected by cholinergic depletion in aged animals. It isconcluded that functional properties of cortical sensory neurons in young animals are morevulnerable to cholinergic depletion than are those of aged animals and that cholinergic depletiondoes not further impact the properties of neurons exposed to the processes of aging.

Illusions as neuro-signs

One of the reasons visual scientists find illusions fascinating is that their pictorial simplicity belies the complexity of visual processing. Illusions can direct us towards neurophysiological interpretations at many levels, which I have called ‘neuro-signs’. The most useful visual illusions are those that point to the simplest neural level possible, that is, those that provide signs of neural processing at early stages of the visual system, such as in the retina itself. The region of the retina that can change the activity of nerve cells throughout the visual system when light falls on it is called the ‘receptive field’ of those nerve cells. Primate retinal ganglion cells have receptive fields that are concentric and antagonistic — if the centre of a receptive field is excited by light the surround is inhibited (called ‘surround inhibition’), or vice versa. Are there any visual signs of such neural antagonism? There could be. In the black and white grid pattern shown below, a variety of illusory dots can be seen at the intersections of the black and white grid. In the upper half, dark grey dots appear at the white intersections between the black rectangles, although a light meter would not register such effects. This is called a Hermann grid; its reverse in the lower half, where illusory light grey dots are seen in the black intersections, is called a Hering grid. In both cases, the dots at an intersection disappear as soon as it is fixated, but they remain at those nearby. The dots are more difficult to see at the smallest intersections in both grids. Because of this effect, it is thought the illusory dots might be related to the distance from the centre of the retina (or ‘retinal eccentricity’); receptive fields have been found to be much smaller around the centre of the retina than more peripherally. Indeed, the optimal separation for producing the illusory dots increases with retinal eccentricity in a similar manner to the increase in receptive field size. But why do the illusory dots appear at all? One suggestion is that concentric receptive fields of the same dimensions will be stimulated differently when they fall at an intersection between four rectangles than when flanked by two rectangles — there would be more surround inhibition at an intersection than elsewhere. This would make a light intersection darker than its neighbours and a dark intersection lighter. Such an interpretation does not account for the dots that are visible between rectangles that are simply outlines, although these dots are not as compelling. When coloured rectangles are placed on a grey background (see above), the illusory dots at the intersections take on the colour of the rectangles: they appear to be light green in the grey intersections of the upper half, and reddish in the grey intersections of the lower half. This is because some receptive fields at the retinal ganglion cell level display colour opponency — the centre can be excited by, say, red and the surround inhibited by green; others operate on blue–yellow opponency. Hermann–Hering grids provide signs of a link between visual perception and neurophysiology. The link is made at an early stage of visual processing — the differences in the activity of the retinal ganglion cells — with the assumption that the neural signals for these differences are preserved in their transmission to the visual cortex of the brain. N Wade, Department of Psychology, University of Dundee, Dundee DD1 4HN, UK. This is the second in a short series of articles by Nicholas Wade, describing some common visual illusions.

Learning generalisation and localisation: Competition for stimulus type and receptive field

The evidence from neurophysiological recordings from the primate visual system suggests that sensory patterns are processed using units arranged in a hierarchical multi-layered network. Responses of these units show progressively increasing receptive field size combined with selectivity for increasing stimulus complexity at successively higher levels. It is argued that the rate of the increase in receptive field size is less than the maximum possible given the initial spread of neuronal projections that occurs during development. We show here that a competitive learning mechanism using a ‘trace-Hebbian’ learning rule [14] with a larger number of competing output units learns not only positional invariance for a given input feature but can also establish restricted receptive field sizes (i.e. less than the maximum size given the initial connections). Importantly the same stimulus selectivity was maintained throughout the receptive field. It is shown that this is accompanied by a relative increase in the spatial evenness of the representation of each detector type across position within the input array. The network properties were found to be robust and stable over a wide range of learning parameters. We suggest that such a competitive mechanism may help account for the reported properties of cells in the ventral stream of the primate visual system.

Receptive field structure in the visual cortex: does selective stimulation induce plasticity?

Sensory areas of adult cerebral cortex can reorganize in response to long-term alterations in patterns of afferent signals. This long-term plasticity is thought to play a crucial role in recovery from injury and in some forms of learning. However, the degree to which sensory representations in primary cortical areas depend on short-term (i.e., minute to minute) stimulus variations remains unclear. A traditional view is that each neuron in the mature cortex has a fixed receptive field structure. An alternative view, with fundamentally different implications for understanding cortical function, is that each cell's receptive field is highly malleable, changing according to the recent history of the sensory environment. Consistent with the latter view, it has been reported that selective stimulation of regions surrounding the receptive field induces a dramatic short-term increase in receptive field size for neurons in the visual cortex [Pettet, M. W. & Gilbert, C. D. (1992) Proc. Natl. Acad. Sci. USA 89, 8366-8370]. In contrast, we report here that there is no change in either the size or the internal structure of the receptive field following several minutes of surround stimulation. However, for some cells, overall responsiveness increases. These results suggest that dynamic alterations of receptive field structure do not underlie short-term plasticity in the mature primary visual cortex. However, some degree of short-term adaptability could be mediated by changes in responsiveness.

Prostanoid synthesis in the spinal cord enhances excitability of dorsal horn convergent neurones during reperfusion of ischaemic receptive fields on the rat's tail

In 40 rats anaesthetized with enflurane, we identified convergent dorsal horn neurones responding to both noxious (pinch) and innocuous (brush) mechanical stimulation of their receptive fields on the tail. We recorded extracellular activity before and during ischaemia of the receptive fields, as well as during subsequent reperfusion. Two NSAIDs, indomethacin and diclofenac sodium, or saline were applied locally to the spinal cord before the induction of ischaemia. During ischaemia, spontaneous activity of the neurones increased significantly, and the responses to both pinch and brush were reduced significantly; indomethacin and diclofenac sodium had no effect on either spontaneous activity or sensitivity to mechanical stimuli. The neurones became hypersensitive to both pinch and brush during reperfusion of their receptive field, and receptive field size increased. Application of indomethacin and diclofenac sodium to the spinal cord abolished both the hypersensitivity and the increase in receptive field size. Our results indicate that spinal cord prostanoid synthesis facilitates the enhanced excitability of dorsal horn convergent neurones to both noxious and innocuous mechanical stimuli during reperfusion of their receptive fields, but does not affect the neurones' responses to receptive field ischaemia, nor their responses to mechanical stimuli in the absence of a conditioning stimulus.