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PubMedDate not supplied

Cholinergic and noradrenergic afferents influence the functional properties of the postnatal visual cortex in rats.

Based on previous evidence that acetylcholine (ACh) and noradrenaline (NA) play a permissive role in developmental plasticity in the kitten visual cortex, we reinvestigated this topic in the postnatal visual cortex of rats with normal vision. In rats, the functional properties of visual cortical cells develop gradually between the second and the sixth postnatal week (Fagiolini et al., 1994). Cortical cholinergic depletion, by basal forebrain (BF) lesions at postnatal day (PD) 15 (eye opening), leads to a transient disturbance in the distribution of ocular dominance (Siciliano et al., 1997). In the present study, we investigated the development of visual cortical response properties following cytotoxic lesions of the locus coeruleus (LC) alone or in combination with lesions of cholinergic BF. The main result is that early NA depletion impairs the orientation selectivity of cortical neurons, causes a slight increase of their receptive-field size, and reduces the signal-to-noise ratio of cell responses. Similar effects are obtained following NA depletion in adult animals, although the effects of adult noradrenergic deafferentation are significantly more severe than those obtained after early NA depletion. Additional cholinergic depletion causes an additional transient change in ocular-dominance distribution similarly to that obtained after cholinergic deafferentation alone. Comparisons between depletion of NA on the one hand and depletion of both NA and ACh on the other suggest that the effects of combined deafferentation on the functional properties studied result from simple linear addition of the effects of depleting each afferent system alone.

Acetylcholine↗
PubMed1979

Interlaminar connections of tree shrew visual cortex.

The intracortical projections of neurons in layers II and upper III of tree shrew visual cortex were studied after terminal lesions in the supragranular layers of area 17. Examination for terminal degeneration was made using ultrastructural techniques. The majority of degenerating terminals were found in layers V and, to a lesser extent, VI, and were presynaptic to neural profiles in the following distribution: 80.5% on spines of small to medium size dendrites, 19% on dendrite shafts, and less than 1% on neuronal perikarya. Degenerating axons coursed in vertical bundles through layers III, IV, V and VI. These findings are similar to those previously described in rat visual cortex.

Animals↗
PubMed2006

Reduced presynaptic efficiency of excitatory synaptic transmission impairs LTP in the visual cortex of BDNF-heterozygous mice.

The neurotrophin brain-derived neurotrophic factor (BDNF) plays an important role in neuronal survival, axonal and dendritic growth and synapse formation. BDNF has also been reported to mediate visual cortex plasticity. Here we studied the cellular mechanisms of BDNF-mediated changes in synaptic plasticity, excitatory synaptic transmission and long-term potentiation (LTP) in the visual cortex of heterozygous BDNF-knockout mice (BDNF(+/-)). Patch-clamp recordings in slices showed an approximately 50% reduction in the frequency of miniature excitatory postsynaptic currents (mEPSCs) compared to wild-type animals, in the absence of changes in mEPSC amplitudes. A presynaptic impairment of excitatory synapses from BDNF(+/-) mice was further indicated by decreased paired-pulse ratio and faster synaptic fatigue upon prolonged repetitive stimulation at 40 Hz. In accordance, presynaptic theta-burst stimulation (TBS) failed to induce LTP at layer IV to layers II-III synapses during extracellular field-potential recordings in BDNF(+/-) animals. Changes in postsynaptic function could not be detected, as no changes were observed in either the amplitudes of evoked EPSCs, the ratios of AMPA : NMDA currents or the kinetics of evoked AMPA and NMDA EPSCs. In line with this observation, an LTP pairing paradigm that relies on direct postsynaptic depolarization under patch-clamp conditions could be induced successfully in BDNF(+/-) animals. These data suggest that a chronic reduction in the expression of BDNF to nearly 50% attenuates the efficiency of presynaptic glutamate release in response to repetitive stimulation, thereby impairing presynaptically evoked LTP in the visual cortex.

Animals↗
PubMedDate not supplied

Inhibition of labyrinthine nystagmus by visual fixation: effects of ablation of visual cortex and superior colliculi.

A study was conducted to destroy two specific areas of the cat's visual system in order to determine if these lesions would affect the visual inhibition of calorically-induced vestibular nystagmus. The occipital visual cortex was removed in eight cats and the superior colliculi were removed bilaterally in nine cats. Postoperative vestibular testing revealed no significant change in the electronystagmography tracings and response to visual fixation. These findings suggest that, in cats, the visual inhibition of labyrinthine nystagmus is not dependent upon the integrity of the visual cortex or superior colliculi. The hypothesis is brought forward that the visual inhibition of the vestibular nystagmus is merely a reflex of the brain stem to light stimulus, mediated via the cerebellum.

Animals↗
PubMed1999

Involvement of visual cortex in tactile discrimination of orientation.

The primary sense modalities (vision, touch and so on) are generally thought of as distinct. However, visual imagery is implicated in the normal tactile perception of some object properties, such as orientation, shape and size. Furthermore, certain tactile tasks, such as discrimination of grating orientation and object recognition, are associated with activity in areas of visual cortex. Here we show that disrupting function of the occipital cortex using focal transcranial magnetic stimulation (TMS) interferes with the tactile discrimination of grating orientation. The specificity of this effect is illustrated by its time course and spatial restriction over the scalp, and by the failure of occipital TMS to affect either detection of an electrical stimulus applied to the fingerpad or tactile discrimination of grating texture. In contrast, TMS over the somatosensory cortex blocked discrimination of grating texture as well as orientation. We also report that, during tactile discrimination of grating orientation, an evoked potential is recorded over posterior scalp regions with a latency corresponding to the peak of the TMS interference effect (about 180 ms). The findings indicate that visual cortex is closely involved in tactile discrimination of orientation. To our knowledge, this is the first demonstration that visual cortical processing is necessary for normal tactile perception.

Evoked Potentials↗
PubMed1992

Dynamic changes in receptive-field size in cat primary visual cortex.

Immediately after focal retinal lesions, receptive fields (RFs) in primary visual cortex expand considerably, even when the retinal damage is limited to the photoreceptor layer. The time course of these changes suggests that mere lack of stimulation in the vicinity of the RF accompanied by stimulation in the surrounding region causes the RF expansion. While recording from single cells in cat area 17, we simulated this pattern of stimulation with a pattern of moving lines in the visual field, masking out an area covering the RF of the recorded cell, thereby producing an "artificial scotoma." Over approximately 10 min this masking resulted in a 5-fold average expansion in RF area. Stimulating the RF center caused the field to collapse in size, returning to near its original extent; reconditioning with the masked stimulus led to RF reexpansion. Stimulation in the surrounding region was required for the RF expansion to occur--little expansion was seen during exposure to a blank screen. We propose that the expansion may account for visual illusions, such as perceptual fill-in of stabilized images and illusory contours and may constitute the prodrome of altered cortical topography after retinal lesions. These findings support the idea that even in adult animals RFs are dynamic, capable of being altered by the sensory context.

Animals↗
PubMed2003

Long-term depression is not induced by low-frequency stimulation in rat visual cortex in vivo: a possible preventing role of endogenous brain-derived neurotrophic factor.

Low-frequency stimulation (LFS) at 1 Hz for 15 min is an effective protocol to induce homosynaptic long-term depression (LTD) in visual cortical slices. It is reported that LFS becomes ineffective when brain-derived neurotrophic factor (BDNF) is applied to slices. It is not known, however, whether such a protocol induces LTD in visual cortex in vivo, and whether endogenous BDNF has the same or similar action. To address these questions, we recorded field potentials of rat visual cortex evoked by stimulation of lateral geniculate nucleus, white matter, or cortical layer IV. We found that LFS did not induce LTD of cortical responses in vivo. To test the possibility that spontaneous activity from retinas would interfere with the induction of LTD, both eyes were removed or inactivated by tetrodotoxin. LTD was not induced in these conditions either. To test whether the difference in temperature between the two preparations is a factor for the discrepancy, the temperature of slices was increased from 31 to 37 degrees C. LTD was induced in slices at either temperature. Then, we hypothesized that endogenous BNDF and its receptors, TrkB, prevent the induction of LTD. To test this, we infused the cortex with an inhibitor of Trk receptor tyrosine kinases, anti-TrkB IgG1, anti-BDNF, and anti-neurotrophin 4/5 antibodies. LTD was induced when the BDNF-TrkB system was blocked. In slices, the level of phosphorylation of Trks was found to decrease with time. These results indicate that activation of TrkB signal pathway prevents LFS from inducing synaptic depression in visual cortex in vivo.

Animals↗
PubMed1992

Postnatal development of the corticotectal projection from the visual cortex of the mouse.

The postnatal development of the corticotectal projection was investigated by injecting the axon tracer DiI into the visual cortex of mouse pups. It was found that DiI-labeled axons arrive at the ipsilateral superior colliculus and enter the optic nerve layer of this structure on postnatal days 3 and 4 (P3-P4). These corticotectal axons extend into the caudal end of the superior colliculus on P4 and give off small collateral branches that ascend vertically to the superficial gray layer. During the first two postnatal weeks, the collateral branches do not form a demarcated terminal zone, but rather diffusely spread within the superficial gray layer of the superior colliculus. These collateral branches continue to dichotomize and form a bright terminal zone within the superficial gray layer on P11. The terminal zone decreases in size during the second and third postnatal weeks, and appears to be of the same size when compared with the adult counterpart by P19. The terminal zone of the corticotectal axons from the visual cortex is established by P19. In parallel with the maturation of the terminal zone of the corticotectal projection, the distal segment of the corticotectal axons is lost during the second postnatal week. We conclude that the growing tips of the corticotectal axons do not strictly project to their future terminal zone within the superior colliculus, and 'misdirected' axons are eliminated during the early postnatal period.

Animals↗
PubMed1989

Quantitative distribution of GABA-immunoreactive neurons in cetacean visual cortex is similar to that in land mammals.

Sections of the anterior portion of the visual cortex in the lateral gyrus of the Black Sea porpoise were studied to determine the neuronal architecture and numerical density, and the distribution of neurons immunoreactive to gamma-aminobutyric acid (GABA). Cytoarchitecture and neuronal density are similar to those described in another cetacean, the bottlenose dolphin. GABA-positive neurons are distributed through all layers of the visual cortex but are especially dense in layers II and III, and comprise some 20% of the total neuronal population in this part of the cortex. The distribution of GABA-positive neurons is similar to that found in land mammals.

Animals↗
PubMed2002

Visual cortex: suppression by depression?

The response of a neuron in the visual cortex to an oriented light bar is strongly reduced by concurrent presentation of a stimulus with a different orientation. New data suggest this 'cross-orientation suppression' is caused, not by intracortical inhibition, but by rapid depression of thalamocortical synapses.

Animals↗
PubMed1995

Human visual cortex. Progress and puzzles.

A wealth of data is now available on the functional organization of the human visual cortex. Caution is necessary in basing interpretations of such data on information gained from studies of the monkey visual cortex.

Animals↗
PubMedDate not supplied

[A model of the structure of the dipole source of the alpha rhythm in the human visual cortex].

The model of the alpha-rhythm was studied which consisted of a set of elementary dipoles. The dipoles were fixed normally to the surfaces of a cruciform structure which imitated the structure of the visual cortex. The magnitude of dipole moments varied according to the sinusoidal low. Thus, the effect was produced of the waves leaving the epicenters which in one case were located in the lower parts of the cruciform structure and at the ends of the side rays of this structure in the other case. The model enabled imitation of all experimentally found phenomena of the alpha-wave travelling (fronto-occipital travelling, rotatory travelling, diagonal and transverse forms). Additionally, the phenomenon was found which enabled simulation of the flat EEG with remaining cortical alpha activity. The possible velocity of the alpha-wave propagation in the visual cortex was calculated. The model can be applied for testing the hypothesis that the alpha-rhythm is a scanning mechanism in the visual cortex.

Alpha Rhythm↗
PubMed1987

Quantitative analysis of the choline acetyltransferase-immunoreactive axonal network in the cat primary visual cortex: I. Adult cats.

The laminar distribution of cholinergic axons was analyzed quantitatively in the visual cortex of adult cats by using immunocytochemistry with a monoclonal antibody against choline acetyltransferase (ChAT). ChAT(+) fibers and varicosities were counted at different locations within area 17 and the distribution patterns in various animals were compared. Choline acetyltransferase-immunoreactivity was localized in fine, varicose fibers, which were present in all layers of the visual cortex. The density of labeled fibers was highest in layer I, which contained 14% of all fibers and 19.5% of all varicosities, and decreased toward deeper layers. The number of varicosities decreased more markedly toward deeper layers than the frequency of fibers. These distribution patterns were very consistent, showing only slight intra- and interindividual variability.

Animals↗
PubMed2004

Three-dimensional structure and evolution of primate primary visual cortex.

In this study, three-dimensional reconstructions of primate primary visual cortex (V1) were used to address questions about its evolution. The three-dimensional shape of V1 in anthropoids is significantly longer and narrower than in strepsirrhines. This difference is an effect of clade and is not due to differences in activity pattern or V1 size. New measurements of V1 volume were also provided in order to reassess V1 size differences between strepsirrhines and anthropoids. It was found that for a given lateral geniculate nucleus (LGN) volume, anthropoids have a significantly larger V1 than strepsirrhines do. This is important since LGN is the principal source of V1's input. Finally, independent contrasts analysis was used to examine the scaling of V1 relative to LGN, the rest of cortex, and the rest of the brain. It was confirmed that V1 scales with positive allometry relative to LGN. A number of possible explanations for scaling are discussed. V1 scaling may have to do with the tendency of large brains to be more compartmentalized than small brains, or V1 scaling might reflect the geometry of information representation.

Animals↗
PubMed1994

Homosynaptic long-term depression in the visual cortex.

We have investigated the characteristics and mechanism of activity-dependent decreases in synaptic effectiveness in visual cortex. Repetitive, low-frequency stimulation (LFS) of either layer IV or the white matter of visual cortical slices was shown to result in a long-term depression (LTD) of intra- and extracellularly recorded synaptic responses in layer III. In preparations in which responses to stimulation of two independent pathways could be monitored, LFS of one pathway produced LTD of responses to test stimulation of that input only, showing that this form of LTD is homosynaptic. This form of LTD was dependent on the frequency and/or pattern of conditioning stimulation and on activation of NMDA receptors. Okadaic acid, an inhibitor of protein phosphatases 1 and 2a, inhibited LTD, but had no effect on induction of long-term potentiation. In all of these respects, LFS-induced LTD in visual cortex closely resembles what has been recently documented in hippocampus. The combined data support a model in which LTD is triggered by a modest elevation in postsynaptic Ca2+ and activation of protein-serine, threonine phosphatases.

Animals↗
PubMed2005

Development of precise maps in visual cortex requires patterned spontaneous activity in the retina.

The visual cortex is organized into retinotopic maps that preserve an orderly representation of the visual world, achieved by topographically precise inputs from the lateral geniculate nucleus. We show here that geniculocortical mapping is imprecise when the waves of spontaneous activity in the retina during the first postnatal week are disrupted genetically. This anatomical mapping defect is present by postnatal day 8 and has functional consequences, as revealed by optical imaging and microelectrode recording in adults. Pharmacological disruption of these retinal waves during the first week phenocopies the mapping defect, confirming both the site and the timing of the disruption in neural activity responsible for the defect. Analysis shows that the geniculocortical miswiring is not a trivial or necessary consequence of the retinogeniculate defect. Our findings demonstrate that disrupting early spontaneous activity in the eye alters thalamic connections to the cortex.

Animals↗
PubMed2004

Emergence of orientation-selective inhibition in the primary visual cortex: a Bayes-Markov computational model.

The recent consensus is that virtually all aspects of response selectivity exhibited by the primary visual cortex are either created or sharpened by cortical inhibitory interneurons. Experimental studies have shown that there are cortical inhibitory cells that are driven by geniculate cells and that, like their cortical excitatory counterparts, are orientation selective, though less sharply tuned. The main goal of this article is to demonstrate how orientation-selective inhibition might be created by the circuitry of the primary visual cortex (striate cortex, V1) from its nonoriented geniculate inputs. To fulfill this goal, first, a Bayes-Markov computational model is developed for the V1 area dedicated to foveal vision. The developed model consists of three parts: (i) a two-layered hierarchical Markov random field that is assumed to generate the activity patterns of the geniculate and cortical inhibitory cells, (ii) a Bayesian computational goal that is formulated based on the maximum a posteriori (MAP) estimation principle, and (iii) an iterative, deterministic, parallel algorithm that leads the cortical circuitry to achieve its assigned computational goal. The developed model is not fully LGN driven and it is not implementable by the neural machinery of V1. The model, then, is transformed into a fully LGN-driven and physiologically plausible form. Computer simulation is used to demonstrate the performance of the developed models.

Action Potentials↗