The use of retrograde axonal transport of various substances (for example, enzymes, lectins, synthetic fluorescent compounds) has yielded much information on the organization of neuronal pathways. Each type of retrograde tracer has its own set of attributes which define the scope of problems it can address. We describe here a new class of retrograde tracer, rhodamine-labelled fluorescent latex microspheres (0.02-0.2 micron diameter), which have distinct advantages over other available tracers for in vivo and in vitro applications. When injected into brain tissue, these microspheres show little diffusion and consequently produce small, sharply defined injection sites. Once transported back to neuronal somata, the label persists for at least 10 weeks in vivo and 1 yr after fixation. Microspheres have no obvious cytotoxicity or phototoxicity as assessed by intracellular recording and staining of retrogradely labelled cells in a cortical brain slice preparation. This approach was further used to visualize and compare, in cat visual cortex slices, neurones with different projection patterns, and revealed significant differences in patterns of intrinsic axons and dendrites. These properties of microspheres open new avenues for anatomical and physiological studies of identified projection neurones in slices as well as in dissociated cell cultures.

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PubMedDate not supplied

Development of forward and feedback connections between areas V1 and V2 of human visual cortex.

We have determined the sequence in which forward connections between visual cortical areas V1 and V2, and feedback connections between V2 and V1 develop in humans. For this purpose Dil was injected into V1 and V2 of postmortem brains of different pre- and postnatal ages. The laminar distribution of labeled fibers and cell bodies in V1 and V2 indicates that forward and feedback connections emerge shortly before birth. The development of both pathways proceeds over several postnatal months such that the laminar termination pattern of forward connections appears relatively mature before feedback connections reach their mature form. At 37 weeks of gestation both forward and feedback connections originate exclusively from deep-layer neurons, which extend axons in deep layers only. By 9 d postnatal, forward connections from V1 to V2, in addition to layers 5 and 6, also arise from neurons in layer 4B of V1. At this stage for the first time forward fibers enter layer 4 at the topographically appropriate location of V2. At 9 d postnatal most feedback fibers from V2 still occupy deep layers of V1 but many, through interstitial growth, elaborate vertical sprouts at regular intervals along the length of horizontal axons. As feedback connections mature, distal segments of horizontal axons are pruned back to branch points and fibers assume L-shaped configurations. By 7 weeks of age forward fibers from V1 enter V2 through deep and superficial layers and provide input to layers 3 and 4. At this stage feedback fibers from V2 have entered layer 4B of V1. By 4 months of age forward connections have assumed all the laminar characteristics of mature connections; that is, they arise from layers 2/3, 4B, 5, and 6 of V1, and terminate in layers 3 and 4 of V2. In sharp contrast, at 4 months of age feedback connections to V1 are still immature, showing terminations in layers 4B, 5, and 6 but no input to layer 2/3. The protracted postnatal emergence of feedback connections is similar to that of local long-range connections within layer 2/3 of V1 (Burkhalter et al., 1993). Since both of these circuits are thought to provide information about the context in which objects are seen, it is interesting to speculate that the late onset of texture segmentation in infants (Atkinson and Braddick, 1992; Sireteanu and Rieth, 1992) may be related to the postnatal maturation of specific intracortical circuits.

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PubMedDate not supplied

Connectivity of GABAergic calretinin-immunoreactive neurons in rat primary visual cortex.

In rat visual cortex neurons that are immunoreactive for the calcium-binding protein calretinin (CR+) constitute a distinct family which accounts for 17% of gamma-aminobutyric acid (GABA)-expressing cells. It is not clear, however, (i) whether CR is expressed exclusively in GABAergic neurons and (ii) how CR+ neurons are incorporated into neuronal circuits of rat visual cortex. To address these questions we studied synaptic relationships of CR+ neurons with GABA+ and GABA- elements in the neuropil of rat primary visual cortex (area 17). All CR+ neurons are nonpyramidal cells with smooth or sparsely spiny and often beaded dendrites. Of all CR+ neurons, 56% are located in layers 1 and 2/3. In layer 2/3, most CR+ neurons are bipolar-shaped and have vertically oriented dendrites. Many ascending dendritic branches reach layer 1 where they run parallel to pial surface. CR+ axons are thin, highly branched near the cell body and often send descending collaterals to layers 5 and 6. Double immunofluorescence labeling revealed GABA in 94% of CR+ cell bodies in layer 2/3. Electron microscopic analysis shows that all CR+ axon terminals contain elongated vesicles and form symmetric synapses. Postembedding staining shows that 98% of CR+ terminals are GABA+. GABA-immunoreactivity is also present in somata and thick dendrites of CR+ neurons but many thin dendrites are GABA-. CR+ somata, dendrites and axon terminals are enriched in mitochondria. Somata and thick CR+ dendrites are densely innervated. At least 68% of the targets of CR+ terminals in layer 2/3 are GABA+ and > or = 50% of these are other CR+ neurons. The remainder (32%) of targets of CR+ terminals are thin dendrites of GABA- cells. In contrast, in layers 5 and 6, 60% of CR+ terminals form synapses with GABA- somatic profiles. The preferential interactions of layer 2/3 CR+ neurons with GABAergic neurons, and with CR+ neurons in particular, suggests that these cells play a role in the inhibition of inhibitory neurons of the same layer. Through these interactions CR+ cells may reduce inhibition of pyramidal cells in layers 2/3, 5 and 6 and thus disinhibit a column of neurons.

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PubMedDate not supplied

Neuroanatomic abnormalities of primary visual cortex in macaque monkeys with infantile esotropia: preliminary results.

To explore the structural basis for visuomotor deficits in infantile esotropia, we examined binocular connections and metabolic activity in the primary visual cortex of two strabismic macaque monkeys. The animals were documented to have onset of natural esotropia in early infancy. Behavioral testing showed that the animals had normal visual acuity in both eyes and the ocular motor deficits that characterize strabismus with onset in infancy. The neuronal tracer substance biotinylated-dextran-amine was injected into ocular dominance columns (ODC) in area V-1 (striate cortex), revealing a paucity of binocular connections between right-eye and left-eye ODCs. The metabolic label cytochrome-oxidase was used to stain neighboring right-eye and left-eye ODCs, revealing inequalities in metabolic activity compatible with interocular suppression. These results show that infantile esotropes have abnormalities of visual cortex structure that correlate with abnormalities in binocular behaviors.

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PubMedDate not supplied

Histamine and growth.

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