Ocular dominance plasticity: Molecular mechanisms revisited.

Ocular dominance plasticity (ODP) is a type of cortical plasticity operating in visual cortex of mammals that are endowed with binocular vision based on the competition-driven disparity. Earlier, a molecular mechanism was proposed that catecholamines play an important role in the maintenance of ODP in kittens. Having survived the initial test, the hypothesis was further advanced to identify noradrenaline (NA) as a key factor that regulates ODP in the immature cortex. Later, the ODP-promoting effect of NA is extended to the adult with age-related limitations. Following the enhanced NA availability, the chain events downstream lead to the ß-adrenoreceptor-induced cAMP accumulation, which in turn activates the protein kinase A. Eventually, the protein kinase translocates to the cell nucleus to activate cAMP responsive element binding protein (CREB). CREB is a cellular transcription factor that controls the transcription of various genes, underpinning neuronal plasticity and long-term memory. In the advent of molecular genetics in that various types of new tools have become available with relative ease, ODP research has lightly adopted in the rodent model the original concepts and methodologies. Here, after briefly tracing the strategic maturation of our quest, the review moves to the later development of the field, with the emphasis placed around the following issues: (a) Are we testing ODP per se? (b) What does monocular deprivation deprive of the immature cortex? (c) The critical importance of binocular competition, (d) What is the adult plasticity? (e) Excitation-Inhibition balance in local circuits, and (f) Species differences in the animal models.

Spike synchronization in cat primary visual cortex depends on similarity of surround-suppression magnitude.

In the primary visual cortex (V1), the spike synchronization seen in neuron pairs with non-overlapping receptive fields can be explained by similarities in their preferred orientation (PO). However, this is not true for pairs with overlapping receptive fields, as they can still exhibit spike synchronization even if their POs are only weakly correlated. Here, we investigated the relationship between spike synchronization and suppressive modulation derived from classical receptive-field surround (surround suppression). We found that layer 4 and layer 2/3 pairs exhibited mainly asymmetric spike synchronization that had non-zero time-lags and was dependent on both the similarity of the PO and the strength of surround suppression. In contrast, layer 2/3 and layer 2/3 pairs showed mainly symmetric spike synchronization that had zero time-lag and was dependent on the similarity of the strength of surround suppression but not on the similarity in POs. From these results, we propose that in cat V1 there exists a functional network that mainly depends on the similarity in surround suppression, and that in layer 2/3 neurons the network maintains surround suppression that is primarily inherited from layer 4 neurons.

Collinear facilitation is independent of receptive-field expansion at low contrast.

Modulation of single-cell responses by compound stimuli (target plus flankers) extending outside the cell's receptive field (RF) may represent an early neural mechanism for encoding objects in visual space, enhancing their perceptual saliency. The spatial extent of contextual modulation is wide. The size of the RF is known to be dynamically variable. It has been suggested that RF expansion when target contrast decreases is the real cause of effects attributed to modulation by flankers. This is not the case. We directly compared, in the same cells, the extent of RF size changes when stimulus contrast decreased with that revealed by systematically changing the target-and-collinear-flankers separation. We found that RF expansion at low contrast was not universal, and that the spatial extent of RF expansion, when it existed, was smaller than that of collinear flanker modulation. We conclude that the two processes in striate cortex work independently from each other.

Contrast-dependent, contextual response modulation in primary visual cortex and lateral geniculate nucleus of the cat.

In the primary visual cortex (V1), the responses of neurons to stimuli presented in their classical receptive fields (CRFs) are modulated by another stimulus concurrently presented in their surround (receptive field surround, SRF). We studied the nature of the modulatory effects of SRF stimulation with respect to stimulus contrast in cat V1. In 51 V1 neurons studied, large SRF stimuli (40 degreesx30 degrees ) induced only the suppression of responses to CRF stimulation and the suppressive effects became stronger as the contrast for SRF stimulation increased. The contrast sensitivity of SRF suppression did not correlate with that of CRF responses. By independently controlling contrast of CRF and SRF stimuli, we studied whether SRF effects vary with CRF response magnitude. Increasing contrast for CRF stimulation caused an upward shift of the range of effective contrasts for SRF stimulation, indicating that a high contrast for SRF stimulation is required for suppressing strong responses to CRF stimulation at high contrasts. To assess the possible origin of the suppressive SRF effect on V1 neurons, we also investigated the contrast dependency of SRF effects in 28 neurons from the lateral geniculate nucleus. Our results suggest that SRF effects obtained at the subcortical level strongly contribute to those in V1. Taken together, we conclude that along the thalamocortical projections, SRF modulation exhibits a gain-control mechanism that scales the suppressive SRF effect depending on the contrast for CRF stimulation. In addition, SRF effects can be facilitatory at low stimulus contrasts potentially due to the enlargement of the summation field.

Muscimol and baclofen differentially suppress retinotopic and nonretinotopic responses in visual cortex.

This study relates to local field potentials and single-unit responses in cat visual cortex elicited by contrast reversal of bar gratings that were presented in single, double, or multiple discrete patch (es) of the visual field. Concurrent stimulation of many patches by means of the pseudorandom, binary m-sequence technique revealed interactions between their respective responses. An analysis identified two distinct components of local field potentials: a fast local component (FLC) and a slow distributed component (SDC). The FLC is thought to be a primarily postsynaptic response, as judged by its relatively short latency. It is directly generated by thalamocortical volleys following retinotopic stimulation of receptive fields of a small cluster of single cells, combined with responses to recurrent excitation and inhibition derived from the cells under study and immediately neighboring cells. In contrast, the SDC is thought to be an aggregate of dendritic potentials related to the long-range lateral connections (i.e. long-range coupling). We compared the suppressive effects of a GABA(A)-receptor agonist, muscimol, on the FLC and SDC with those of a GABA(B)-receptor agonist, baclofen, and found that muscimol more strongly suppressed the FLC than the SDC, and that the reverse was the case for baclofen. The differential suppression of the FLC and SDC found in the present study is consistent with the notion that intracortical electrical signals related to the FLC terminate on the somata and proximal/basal dendrites, while those related to the SDC terminate on distal dendrites.

Artifactual synchrony via capacitance coupling in multi-electrode recording from cat striate cortex.

Elucidation of neural connectivity patterns in the brain are thought to give us a mechanistic understanding of how the brain works. Functional connectivity is best studied by simultaneous recording of single-unit activity from many neurons. Accordingly, various types of multiple-microelectrode systems have been developed. We have studied long-range lateral interactions in cat striate cortex. To physiologically characterize interacting cells recorded simultaneously, we used two microelectrodes whose movements were controlled by two independently-movable microdrives. The tips of the two microelectrodes were separated by approximately 2 mm or more. During preliminary plotting of two receptive fields of cell pairs, we often noted the emergence of perfectly synchronous firing between two spike trains (amplitude ratio, about 20:1) registered with two microelectrodes. Synchronously firing, smaller spikes disappeared when larger spikes of the pair were lost to either substantial advancement of or placing an electrolytic lesion at the electrode registering the latter. The synchrony also disappeared when two microdrive systems were shielded individually. We concluded that the synchrony was attained through capacitance coupling between two microdrive systems. We proposed a few practical recommendations to avoid the contamination of cross correlograms with the false-positive, narrow peak at time zero due to the presence of reflected spike trains.