Electrophysiology of the postreceptoral visual pathway in mice

Pattern VEPs have been recorded locally from the binocular portion of the primary visual cortex of wild type- and different transgenic mice by means of microelectrodes. Local pattern VEPs have been used on the one hand to obtain information on basic cortical layout (topography, laminar analysis) and ocularity (relative contribution of the contralateral and ipsilateral eye), and on the other hand to evaluate several aspects of visual physiology that have a counterpart in visual behavior (visual acuity, contrast sensitivity, motion sensitivity, response latency). As compared to visual behavior, pattern VEPs offer the advantage that several aspects of vision can be evaluated in the same animals, including those with poor behavior due to motor- or cognitive deficits, even during the postnatal development. Pattern VEPs provide a means for characterizing the visual phenotype of mutant mice and for the evaluation of the effects induced by experimental manipulation

Vision in mice with neuronal redundancy due to inhibition of developmental cell death

Transgenic mice overexpressing bcl-2, due to inhibition of naturally occurring cell death, have much larger brains and optic nerves as compared to wild-type mice. Since developmental cell death is believed to exert a crucial role in establishing the mature neural circuitry and function, we asked the question of whether basic aspects of vision were altered in bcl-2 mice. Local visually evoked potentials (VEPs) in response to patterned stimuli were recorded from the primary visual cortex. The representation of the vertical meridian was displaced by about 15% in the bcl-2 mouse, accounting for brain expansion. However, visual acuity, contrast threshold, and response latency were normal, indicating that compensatory mechanisms can ensure normal basic properties of vision in spite of marked neuronal redundancy

The visual physiology of the wild type mouse determined with pattern VEPs

AbstractGenetically manipulated mice are important tools for studies on plasticity and degeneration/regeneration in the visual system. However, a description of the basic properties of the visual performance of the wild type mouse is still lacking. To characterize the visual physiology of the wild type (C57BL/6J) mouse we recorded Visual Evoked Potentials (VEPs) from the primary visual cortex. As compared to behavioral methods, VEPs may have the advantage that different aspects of vision can be screened readily and simultaneously in the same animals, including those with poor visual behavior due to motor or learning deficits. Local VEP responses to patterned visual stimuli have been recorded from the binocular visual cortex of anesthetized mice. Spatial (visual acuity, contrast threshold) and temporal (temporal function, response latency, motion sensitivity) aspects of VEPs were evaluated. The mouse VEP acuity was 0.6 c/deg, which is comparable to the behavioral visual acuity. The VEP peak contrast threshold was 5% (no behavioral data are available). Cortical representation of visual coordinates and cortical magnification factor corresponded to those previously reported using single cell recordings. Laminar analysis of VEPs indicated a dipole source in the supragranular layers of the visual cortex as a major response generator. VEPs showed contribution from both eyes, although biased strongly towards the eye contralateral to the recorded cortex. Results provide a comprehensive framework for characterizing visual phenotypes of a variety of transgenic mice

Temporal Aspects of Contrast Visual Evoked Potentials in the Pigmented Rat: Effect of Dark Rearing

Cortical visual evoked potentials (VEPs) in response to gratings temporally modulated in counterphase were recorded in normal and dark-reared pigmented rats. Temporal modulation was either sinusoidal (0.25–15 Hz, steady state condition) or abrupt (0.5 Hz, transient condition). In normals, the amplitude spectrum of contrast VEPs has two peaks (at about 0.5 and 4 Hz) and a high temporal frequency cut-off of the order of 11 Hz. The VEP phase lags with temporal frequency, showing two different linear slopes for separate frequency ranges (0.25–1 Hz and 1–7 Hz) centred on the peaks of the curve. The different slopes correspond to apparent latencies of 500 and 136 msec, respectively. Dark rearing reduced the cut-off frequency by about 3 Hz and increased apparent latencies by about 42 msec in the low temporal frequency range and 30 msec in the high temporal frequency range. The latency of the first peak of transient VEPs was increased by about 47 msec. Results indicate that the frequency response of rat contrast VEPs is qualitatively similar to that of other mammals (including human), albeit shifted to a lower range of temporal frequencies. Dark rearing significantly alters the VEP temporal characteristics, suggesting that visual experience is necessary for their correct development. Copyright © 1997 Elsevier Science Lt

Role of neurotrophins in the development and plasticity of the visual system: experiments on dark rearing

An extensive series of studies, beginning with the pioneering experiments of Wiesel and Hubel, have shown that correct visual experience is crucial for the development of the visual system. Several years ago, we put forward the hypothesis that neurotrophic factors of the neurotrophin family (NGF, BDNF, NT-3, NT-4) have a role in mediating the effects of visual experience in the developing visual system. This theory is based on the following experimental results: (a) exogenous supply of neurotrophins during the critical period prevents the effects of monocular deprivation; and (b) transplant of cells releasing NGF allows a normal development of the functional properties of visual cortical neurons in dark-reared rats

Requirement of the nicotinic acetylcholine receptor β2 subunit for the anatomical and functional development of the visual system

In the mammalian visual system the formation of eye-specific layers at the thalamic level depends on retinal waves of spontaneous activity, which rely on nicotinic acetylcholine receptor activation. We found that in mutant mice lacking the β2 subunit of the neuronal nicotinic receptor, but not in mice lacking the α4 subunit, retinofugal projections do not segregate into eye-specific areas, both in the dorso-lateral geniculate nucleus and in the superior colliculus. Moreover, β2−/− mice show an expansion of the binocular subfield of the primary visual cortex and a decrease in visual acuity at the cortical level but not in the retina. We conclude that the β2 subunit of the nicotinic acetylcholine receptor is necessary for the anatomical and functional development of the visual system

Heterozygous Knock-Out Mice for Brain-Derived Neurotrophic Factor Show a Pathway-Specific Impairment of Long-Term Potentiation But Normal Critical Period for Monocular Deprivation

Genetic deletion of a single allele of the BDNF gene affects hippocampal LTP and causes several behavioral phenotypes, including deficits in spatial learning. In the developing visual cortex, overexpression of BDNF accelerates the time course of the critical period for monocular deprivation (MD), and exogenous administration of BDNF alters the outcome of MD. We asked whether reduced levels of BDNF could affect visual cortex plasticity by studying long-term potentiation (LTP) induction and the effects of MD in heterozygous BDNF knock-out mice. We found that theta burst stimulation that induced LTP in the layer IV-III pathway of wild-type (wt) mice caused only a transient potentiation in BDNF+/- mice, and that this potentiation vanished in 25 min. In contrast, LTP elicited by stimulation of the white matter (WM), a form of LTP that can be induced only during the critical period, occurred normally in wt and BDNF+/- mice. The effects of MD during the critical period were similar in wt and BDNF+/- mice, indicating that layer IV-evoked, layer III LTP is not required for ocular dominance plasticity. We then asked whether reduction of cortical BDNF levels could prolong the critical period for MD and for the WM-evoked, layer III LTP induction. We found that in adult BDNF+/- mice, WM-evoked, layer III LTP was not inducible, and that the critical period for MD terminated normally. We conclude that deletion of one copy of the BDNF gene selectively impairs LTP of the layer IV-III pathway but does not alter ocular dominance plasticity