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PubMed1986

The appearance of an L1-like molecule in the chick primary visual pathway.

A monoclonal antibody, 8D9, has been obtained that binds to axons in the chick nervous system. Biochemical and immunological experiments indicate that the 8D9 antigen is related to the mouse L1 cell-adhesion molecule. The results of immunohistochemical experiments using monoclonal antibody 8D9 to study the development of the chick visual system are consistent with the 8D9 antigen functioning in axon fasciculation.

Animals↗
PubMed1988

Axons added to the regenerated visual pathway of goldfish establish a normal fiber topography along the age-axis.

Throughout a goldfish's life, new generations of ganglion cells are added on the retinal margin and their axons extend centrally to occupy predictable positions in the retinotectal pathway, adjacent to their predecessors and subjacent to the pia. The stacking of successive generations of axons defines the age-axis of the pathway. This study examined whether an ordered array of predecessor axons is a prerequisite for the patterned growth of new axons. One optic nerve was crushed intraorbitally and the fish was injected with 3H-thymidine to label the proliferating cells on the retinal margin. The ring of 3H-thymidine-labeled cells separated retina that was present at the time of nerve crush (inside the ring) from new retina added afterward (outside). After a period of 14-16 months postcrush, both tectal lobes received two punctate applications of horseradish peroxidase (HRP), one in the central and the other in peripheral tectum, to retrogradely label contralateral retinal ganglion cell bodies and their axons. The pattern of HRP labeling from the control tectum confirmed earlier work: axons on the central tectum had somata in the central retina, and axons on the peripheral tectum had somata in the peripheral retina. The labeled cells and axons were both in predictable patterns. The somata that were backfilled from applications to the center of the experimental tectum lay inside the radioactive ring and had therefore regenerated their axons. The patterns of their labeled axons in the optic pathway and of their somata in the retina were typical of the regenerated condition as described in earlier studies. The somata backfilled from the periphery of the experimental tectum were outside the radioactive ring and had been added after the optic nerve crush. The patterns of their labeled axons and somata were comparable to the normal pattern. These observations indicate that new axons do not depend on an ordered array of predecessors to reestablish normal order along the age-axis of the pathway.

Aging↗
PubMed1981

Transformation of signals by interneurones in the barnacle's visual pathway.

1. The photoreceptors of the median eye of the giant barnacle drive decrementally-conducting neurones in the supraoesophageal ganglion termed ;inverting cells' (I-cells) which in turn drive impulse-producing neurones termed ;amplifying cells' (A-cells). Using intracellular recording techniques we have studied the role of I-cells in visual processing.2. Horseradish peroxidase injections show that I-cells are interneurones whose processes are confined to the regions of the photoreceptor terminals on both sides of the bilaterally symmetrical ganglion.3. In the dark, I-cell membrane potentials (-45 mV) are considerably less negative than those of other ganglion cells (-60 to -70 mV). At the onset of a maintained light, I-cells undergo a transient peak hyperpolarization which declines to a steady-state response. Both response components are graded with light intensity.4. The reversal potential of the peak of the I-cell light response depends on the external K(+) concentration more strongly than does the dark resting potential (3-30 mm-K(+)). This evidence indicates that the hyperpolarization results from an increase in the cell's permeability to K(+) ions.5. At the offset of light an I-cell undergoes a transient depolarization that overshoots the dark membrane potential. Dimming of a background light can also cause the I-cell membrane potential to overshoot its dark resting value. This overshoot is associated with a large depolarizing synaptic potential in A-cells.6. An overshoot of the dark resting potential can also be elicited by the break of a hyperpolarizing pulse of current injected into an I-cell. The amplitude of this overshoot increases with pulse duration over a time course of seconds.7. In the presence of external tetraethylammonium ion (TEA) and tetrodotoxin, (TTX), the break of a hyperpolarizing pulse or the onset of a depolarizing pulse can evoke in an I-cell an action potential whose rate of rise and amplitude depend on the external Ca concentration. This action potential can be maintained by replacement of external Ca with Ba, or blocked by addition of 15 mm-Co to the saline. These observation's indicate that depolarizing potential changes in this cell activate a voltage-sensitive Ca conductance.8. When hyperpolarizing current pulses are injected into an I-cell, the voltage during the pulse sags back slowly towards the dark resting potential. Thus, during hyperpolarization with light or current an I-cell's membrane properties change over a time course of seconds.9. The onset of a depolarizing pulse or the offset of a hyperpolarizing pulse of current injected into an I-cell leads to a transient depolarization of a simultaneously impaled A-cell. Synaptic transmission occurs when the I-cell is depolarized to the vicinity of the dark resting potential. The amplitude of the response in an A-cell depends on the rate of change of the I-cell voltage.

Animals↗