Four twist genes in zebrafish, four expression patterns.

Twist genes code for regulatory bHLH proteins essential for embryonic development and conserved across the metazoa. There are four genes that constitute the zebrafish twist family: twist1a, twist1b, twist2--orthologs of the mammalian twist1 and twist2 genes; and twist3--a gene from a new clade that does not exist in mammals. Presented here are their embryonic mRNA expression profiles. The study extends the known conservation of twist developmental patterns in tetrapods to the fish, e.g., expression in cephalic neural crest, sclerotome and lateral plate mesoderm. Some other expression domains are unique, like hypochord and dorsal aorta; some, like the notochord, may be ancestral patterns retained from protochordates; and the expression in invaginating/migrating cells may have been retained from the jellyfish. Perhaps this is one of the more ancient functions of twist--conserved from diploblasts to humans--to facilitate cell movement.

Quantitative analysis of synaptic distribution along thalamocortical axons in adult mouse barrels.

Quantitative data on thalamocortical synapses in adult mouse barrels have been obtained largely by using lesion-nduced degeneration to label thalamic afferents. By the time degenerating axons can be identified with the electron microscope, they have broken up into many separate pieces, making it impossible to assess the distribution of synapses along unbroken lengths of afferent. Here, this deficiency is rectified by examining intact lengths of axon labeled by the injection of biotinylated dextran amine into ipsilateral thalamus. Serial thin section reconstructions were analyzed to determine the numbers of synapses per axon length made with dendritic spines vs. shafts and the locations of synapses with respect to axonal varicosities. Results for seven axonal segments from six mice showed an average of 0.2 synapses/microm; 80% were made with spines and 20% with dendritic shafts. Just over two-thirds of axonal varicosities formed one synapse; most of the remainder formed two and rarely three, whereas 8% formed none. Although most synapses occurred at varicosities (88%), more than 12% were made at cylindrically shaped regions of the reconstructed axonal segments. These results serve as a caveat for the use of light microscopy to quantify synapses, wherein the usual approach is to equate one varicosity with one synapse. For thalamocortical afferents to mouse barrels, equating one varicosity with one synapse would prove to be incorrect more than 30% of the time and would exclude the roughly 12% of synaptic connections made at cylindrical regions of thalamocortical afferents.

Changes in mouse barrel synapses consequent to sensory deprivation from birth.

Neonatal sensory deprivation induced by whisker trimming affects significantly the functional organization of receptive fields in adult barrel cortex. In this study, the effects of deprivation on thalamocortical synapses and on asymmetrical and symmetrical synapses not of thalamic origin were examined. Thalamocortical synapses were labeled by lesion-induced degeneration in adult (postnatal day 60) mice subjected to whisker trimming from birth, other synaptic types were unlabeled. Brains were processed for electron microscopy, and numerical densities of synapses were evaluated by using stereologic approaches for whisker trimmed vs. control animals. Results demonstrated no change in nonthalamic, asymmetrical synapses; however, a decrease of 52% in the numerical density of symmetrical synapses (46.3 vs. 88.5 million per mm(3); Z = -2.121; P < 0.05) and a decrease of 43% in the numerical density of thalamocortical synapses (57.5 vs. 102.33 million per mm(3); Z = -2.121; P < 0.05) were observed after deprivation. Thus, experience-dependent plasticity of receptive fields in barrel cortex involves directly axons of both extrinsic and intracortical origin. The proportion of thalamocortical axospinous to axodendritic synapses was the same in control vs. deprived animals: in each instance, 80% of the synapses were axospinous (Z = 0.85; P = 0.2). These results suggest that neither excitatory neurons, whose thalamocortical synapses are primarily axospinous, nor inhibitory neurons, whose thalamocortical synapses are mainly axodendritic (White [1989] Cortical Circuits. Synaptic Organization of the Cerebral Cortex; Structure, Function, and Theory. 1989; Boston: Birkhauser), are affected preferentially by the deprivation-associated decrease in thalamocortical synapses.

Synaptic patterns of thalamocortical afferents in mouse barrels at postnatal day 11.

This study focuses on the synaptic output patterns of thalamocortical axons in mouse barrel cortex at postnatal day (P) 11. Axons were labeled by biotinylated dextran amine transported anterogradely following injection in vivo into the ventrobasal thalamus. Labeled axons in the posteromedial barrel subfield were examined by light and electron microscopy and then reconstructed in three dimensions to assess the spatial distribution of their synapses. Thalamocortical axons form asymmetrical synapses, both at varicosities and along cylindrical portions of the axons; usually, only one synapse occurs per site, contrasting with the case in the adult, in which multiple synapses are typical. At P11, varicosities without synapses are common. As in adult barrels, approximately 80% of synapses formed by thalamocortical axons are with dendritic spines; 20% are with dendritic shafts. The similarity in the distribution of thalamocortical synapses onto spines vs. dendrites in developing and mature barrels indicates that adult synaptic patterns already are specified at a very early stage of thalamocortical synaptogenesis.