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  • 1
    ISSN: 1432-1106
    Keywords: [3H]GABA accumulation ; GABA immunostaining ; Co-localisation ; Visual cortex ; Inhibitory circuits
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An antiserum to GABA was used in the macaque monkey to determine whether neurons that accumulate exogenously applied [3H]GABA in vivo are also immunoreactive for GABA. Following the injection of [3H]GABA into different laminae of striate cortex in two untreated animals and in one animal treated with amino-oxyacetic acid, selective accumulation of the labelled amino acid was demonstrated in perikarya by autoradiography. Radiographically labelled neurons (n, 519) and their unlabelled neighbours were tested in consecutive 0.5 μm thick sections by immunocytochemistry for GABA immunoreacitivity. Injection of [3H]GABA did not increase the number of neurons showing GABA immunoreactivity. On the contrary many of the cells that accumulated [3H]GABA were immunonegative. These neurons were mostly located in layers IVC and VA following [3H]GABA injection into layers II–III, and in layers upper III and II following injection into layers V and VI. A comparison of the position of these neurons with known local projection patterns in the striate cortex of monkey suggests that GABA-immunonegative neurons may nevertheless become labelled by [3H]GABA if most of their local axon terminals fall within the injection site. The interlaminar projection of GABA-immunopositive neurons, which probably contain endogenous GABA, could be deduced from the position of the [3H]GABA injection site that leads to their autoradiographic labelling. Although the present study confirmed our previous results on the interlaminar connections of neurons that accumulate [3H]GABA, it demonstrated that [3H]GABA labelling alone may not be a sufficient criterion to assess the GABAergic nature of neurons in the striate cortex of monkey.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Visual cortex ; Retina ; Thalamus ; Blindsight ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We removed the striate cortex of one cerebral hemisphere in a macaque monkey, causing almost total retrograde degeneration of the corresponding dorsal lateral geniculate nucleus (dLGN) and extensive transneuronal degeneration of ganglion cells in the corresponding hemi-retina of each eye. The rare surviving geniculate projection neurons were retrogradely labelled by horseradish peroxidase (HRP) from extra-striate cortex and retinogeniculate terminals were labelled by an intraocular injection of HRP. Retinal terminals in the degenerated dLGN made synaptic contact exclusively with the dendrites of interneurons immunopositive for γ-aminobutyric acid (GABA) in both parvocellular and magnocellular regions of dLGN. As well as being postsynaptic to retinal terminals these vescicle-containing dendrites were pre- and postsynaptic to other similar dendrites, and presynaptic to relay cells. Surviving labelled projection neurons received retinal input indirectly, via both the GABA-immunopositive interneurons and GABA-immunonegative terminals characteristic of those from the superior colliculus. In the degenerated, as opposed to the normal dLGN, about 20% of retinal terminals were GABA-immunopositive and GABA-immunoreactivity was prominently elevated in the ganglion and amacrine cell layers of the degenerated half of the retina. The optic nerve also contained numerous GABA-immunopositive axons but very few such axons were found in a normal optic nerve processed in identical manner. The surviving pathways from the retina must underlie the visual abilities that survive striate cortical removal in monkeys and human patients and may involve the degenerated dLGN as well as the mid-brain.
    Type of Medium: Electronic Resource
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