The presence of polyribosomes in dendritic spines suggests a potential involvement of local protein synthesis in the modification of synapses. Dendritic spine and synapse ultrastructure were compared after low-frequency control or tetanic stimulation in hippocampal slices from postnatal day (P)15 rats. The percentage of spines containing polyribosomes increased from 12% +/- 4% after control stimulation to 39% +/- 4% after tetanic stimulation, with a commensurate loss of polyribosomes from dendritic shafts at 2 hr posttetanus. Postsynaptic densities on spines containing polyribosomes were larger after tetanic stimulation. Local protein synthesis might therefore serve to stabilize stimulation-induced growth of the postsynaptic density. Furthermore, coincident polyribosomes and synapse enlargement might indicate spines that are expressing long-term potentiation induced by tetanic stimulation.

We describe the effects of a recessive mutation on visual behavior, the electroretinogram (ERG), and photoreceptor structure in zebrafish. At 6 d post-fertilization (dpf), no optokinetic reflex could be elicited in no optokinetic response c (nrc) mutant animals under any test condition. The animals exhibited ERG responses at 5-7 dpf that were markedly abnormal and could be categorized into two groups. The first showed an initial negative a-wave followed by a delayed positive b-wave of small amplitude. Often a second ERG-like response was recorded after the initial b-wave. The second group showed only a large negative a-wave; an initial b-wave was not evident. In most recordings additional oscillatory waves varying in number, amplitude, and time course were observed. Multiple responses at the cessation of long-duration flashes were also observed. Light and electron microscopy revealed that the cone photoreceptor pedicles of nrc fish were highly abnormal. Although the appropriate number of synaptic ribbons formed in these terminals, they "floated" in the terminal, unassociated with postsynaptic processes or arciform densities. The few processes invaginating the nrc pedicles resembled those of horizontal cells. Invaginating bipolar cell processes were rare, but basal contacts were observed on pedicle surfaces. The severity of the mutation did not change between 6 and 8 dpf, showing that there is neither a delay in development nor a degeneration of the terminals; rather, nrc pedicle development appears arrested. Bipolar cell terminals in the inner plexiform layer made normal ribbon synapses; thus, the mutation appears to affect only the outer retina.Key words: retina; photoreceptors; ribbon synapses; electroretinography; electron microscopy; mutations; zebrafish One approach to furthering our understanding of vertebrate visual mechanisms is to analyze animals with visual system mutations. Recessive mutations occur only rarely in nature, but zebrafish can be efficiently mutagenized and readily bred to homozygosity (Mullins et al., 1994;Solnica-Krezel et al., 1994). Furthermore, this vertebrate develops rapidly, has a relatively fast generation time, and possesses other characteristics that make it particularly suitable for mutagenesis screening.Initial screens for recessive mutations in zebrafish focused on early development and searched for morphological abnormalities of the eyes and other organs (Malicki et al., 1996). However, many subtle and interesting recessive mutations lie at the molecular level and are not detectable in such screens; that is, the animals appear normal morphologically. To this end, we have developed a behavioral test to detect visually impaired zebrafish larvae at 5-7 d post-fertilization (dpf) (Brockerhoff et al., 1995). Stripes are passed in front of larvae to elicit the stereotyped visual tracking behavior of the optokinetic reflex (OKR). The eyes follow the stripes with a smooth pursuit movement, followed by a rapid saccade to return the eyes to their original position.As a secondary scre...

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The oligodendrocyte‐myelin glycoprotein (OMgp) is a 110‐kDa glycosylphosphatidylinositol‐linked protein that was initially identified as a myelin‐specific protein but whose precise function remains unknown. In this study, immunohistochemistry, western blots, in situ hybridization, and northern blots were used to determine the distribution of OMgp in the mouse brain. OMgp is present in a concentration detectable on western blots in the brains of newborn mice, and its concentration gradually increases until day 24 of life. OMgp mRNA is also present in amounts detectable on northern blots in the brains of newborn mice, and its concentration gradually increases until day 21 of life, after which the concentration diminishes a little. Most of the OMgp in the mouse brain appears to be expressed in diverse groups of neurons, but it is particularly prominent in large projection neurons such as the pyramidal cells of the hippocampus, the Purkinje cells of the cerebellum, motoneurons in the brainstem, and anterior horn cells of the spinal cord. However, OMgp is not confined to these cells and is expressed in cells in the white matter as well. The OMgp gene is placed within an intron of the neurofibromatosis type I gene and on the opposite strand. This organization raises the possibility that there may be a relationship between the functions of the products of the two genes. In support of this possibility, we show that within the mouse CNS OMgp and neurofibromin are expressed in the same cell types.

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