Nicotinic acetylcholine receptor-like molecules in the retina, retinotectal pathway, and optic tectum of the frog

Abstract

Forty-two monoclonal antibodies (mAbs) generated against nicotinic acetylcholine receptors (AChRs) from electric organ were tested for their ability to cross-react in the optic tectum of the frog Rana pipiens. Twenty-eight of the mAbs tested (67%) bound to the optic neuropil of the tectum as revealed by immunoperoxidase cytochemistry. The pattern of peroxidase stain for cross-reacting mAbs corresponded in position to a subset of the retinotectal projections. Electron microscopic examination revealed that peroxidase reaction product was associated with the surface of vesicle-containing profiles but not with synaptic sites. Removal of one retina resulted in the loss of immunoreactivity in the contralateral tectum. AChR-like immunoreactivity was also associated with the optic tract and optic nerve and with retinal ganglion cells. These results indicate that some classes of retinal ganglion cells bear AChR-like molecules on their surface. The existence of these molecules on ganglion cell axons and terminals seems the most likely explanation for the AChR-like immunoreactivity present in the tectum.

The effects of nicotinic and muscarinic receptor activation on patch-clamped cells in the optic tectum of rana pipiens

“…Nicotinic receptors have been generally regarded as having a presynaptic location in the optic tectum following their immunocytochemical identification on retinal ganglion cell terminals (Sargent et al, 1989). More recent work in Xenopus has provided physiological evidence for this terminal location by showing that activation of nicotinic receptors increases sPSCs recorded in patch-clamped tectal cells (Titmus et al, 1999).…”

“…The optic tectum of the frog contains both nicotinic and muscarinic cholinergic receptors (Sargent et al, 1989;Birdsall et al, 1980;Butt et al, 2000Butt et al, , 2001) but knowledge of the physiological consequences of their activation is incomplete. Assessments of the effects of nicotinic receptor activation have focused on a facilitation of glutamate release from retinal ganglion cell terminals (Titmus et al, 1999;Kuras and Gutmaniene, 2001) while muscarinic receptors have been associated with tectal cell membranes following an enhancement of single unit recordings in response to ACh microiontophoresis (Fite and Wang, 1986).…”

Regulatory mechanisms that govern nicotinic synapse formation in neurons

“…For example, ␣7-nAChR mRNA and protein levels are markedly reduced after deafferentation of the rodent somatosensory cortex by lesioning of the thalamocortical inputs (Broides et al, 1996). Disruption of retinal inputs reduces nAChR ␣5, ␤2, and ␣7 subunit protein levels in the chick optic tectum neuropil (Britto et al, 1994;Torrao et al, 1996), and decreases binding of the nAChR ligands ␣-bgt and cytosine in the frog tectum (Sargent et al, 1989;Butt et al, 2000). These studies are complicated by the fact that nAChRs are expressed on both innervating presynaptic terminals and postsynaptic neurons found in the tectal neuropil, raising the possibility that degeneration of the lesioned nerve contributes to the loss of nAChR expression following denervation (Sargent et al, 1989;Torrao et al, 1996;Butt et al, 2000;Britto et al, 2001).…”

Pharmacology, distribution and development of muscarinic acetylcholine receptor subtypes in the optic tectum of Rana pipiens

“…Optic nerve lesions cause the degeneration of retinal ganglion cell terminals in the tectum and the disappearance of elements associated with them. 49,60,70 Optic nerve lesions had no significant effect on specific [ 3 H]pirenzepine binding in the tectum (Fig. 7A, B).…”

“…Earlier studies have shown that most retinal fibers in the tectum have degenerated after short-term lesions, but long-term lesions allow for the degeneration of all presynaptic retinal fibers. 49,60,70 Behavioral tests were conducted during the survival period to demonstrate that animals responded only to prey seen through the unlesioned left eye. At the end of the survival period, the frogs were anesthetized, the optic nerve lesion was confirmed and the brain was prepared for autoradiography as described above.…”