Glutamate-like Immunoreactivity in the Pigeon Optic Tectum and Effects of Retinal Ablation

The pattern of glutamate-like immunoreactivity was investigated in the pigeon optic tectum. The most impressive aspect of the labelling pattern was an accumulation of immunoreactive terminal-like elements restricted to those superficial tectal layers that correspond to the termination zone of the retinal afferents. These immunoreactive puncta occurred frequently in small clusters. At the level of electron microscopy, many of the labelled nerve endings showed the characteristics of retinal terminals. Moreover, following unilateral retinal ablation a drastic loss of immunoreactive terminal-like puncta was observed in the retinorecipient layers of the tectum contralateral to the lesion. The remaining glutamate-immunoreactive terminal-like elements had the light and electron microscopic features typical of the afferents from the nucleus isthmi, pars parvocellularis (lpc). The relation between the latter result and the transmitter specificity of the afferents from this subtectal nucleus is unclear at present. On the other hand, the light and electron microscopic labelling patterns and the effect of retinal ablation suggest that afferents from retina and from lpc are the only major sources for glutamate-immunoreactive terminals in the pigeon optic tectum. Furthermore, the results are well in line with previous data indicating glutamate as neurotransmitter at least in part of the retinal afferents to the pigeon optic tectum.     

Kainic acid neurotoxicity does not depend on intact retinal input in the goldfish optic tectum

Kainic acid neurotoxicity has been studied in the optic tectum of the goldfish 4 weeks after eye enucleation. The effect of drug treatment has been tested with respect to both neurochemical and morphological parameters. The neurotransmitter-related enzymes, choline acetyltransferase, acetylcholinesterase and glutamate decarboxylase, show about 50% decrease in the deafferented tectum 6 days after kainic acid administration. Relevant morphological alterations of the tectal structure can also be noticed at the same stage. The neurotoxic effects of kainic acid in the deafferented optic tectum are therefore quite similar to the effects of previously noticed for the intact optic tectum of normal fish. Control experiments on the effect of optic nerve degeneration by itself on the levels of the neurotransmitter-related enzymes in the optic tectum, have shown no significant decrease in glutamate decarboxylase, a slight decrease in acetylcholinesterase and a more marked drop in choline acetyltransferase. The findings are discussed with reference to some of the hypotheses advanced in order to explain kainic acid neurotoxicity. It is proposed that the neurotoxic effect of kainic acid after removal of specific excitatory afferents, may vary in different nervous centers depending on differences of the remaining extrinsic connections and of the intrinsic neural circuits.     

Intraocular colchicine inhibits competition between resident and foreign optic axons for functional connections in the doubly innervated goldfish optic tectum

After unilateral optic tectum ablation in the goldfish, regenerating optic axons grow into the optic layers of the remaining ipsilateral tectal lobe and regain visual function. The terminal arbors of the foreign fibers are initially diffusely distributed among the resident optic axons, but within two months the axon terminals from each retina are seen to segregate into irregular ocular dominance patches. Visual recovery is delayed until after segregation. This suggests that the foreign fibers compete with the residents for tectal targets and that the segregation of axon terminations is an anatomical characteristic of the process. Here we investigate whether inhibiting axonal transport in the resident fibers inhibits competition with foreign fibers. The eye contralateral to the intact tectal lobe received a single injection of 0.1 μg colchicine, which does not block vision with the intact eye. We measured visual function using a classical conditioning technique. Segregation of axon terminations was examined shortly following visual recovery by autoradiography. The no-drug control fish showed reappearance of vision with the experimental eye at 9 weeks postoperatively and ocular dominance patches were well developed. Colchicine administered to the intact eye (resident fibers) several weeks postsurgery decreased the time to reappearance of vision with the experimental eye by several weeks. Autoradiography revealed some signs of axonal segregation but the labeled foreign axons were mainly continuously distributed. Administration of colchicine at the time of tectum ablation, or of lumicolchicine at two weeks postoperatively produced normal visual recovery times. Fast axonal transport of³H-labeled protein was inhibited by 1.0 and 0.5 μg but not by 0.1 μg of colchicine or by 1.0 μg of lumicolchicine. Previous studies showed that while 0.1 μg of colchicine does not block vision it is sufficient to inhibit axonal regeneration following optic nerve crush. We conclude that two retinas can functionally innervate one tectum without forming conspicuous ocular dominance columns, and that the ability of residents to compete with the in-growing foreign axons is very sensitive to inhibition of axoplasmic transport or other processes that are inhibited by intraocular colchicine.     

Inhibitory mechanism in zebrafish optic tectum: Visual response properties of tectal cells altered by picrotoxin and bicuculline

In previous work we described 4 tyoes of visu al response among tectal cells of the zebrafish¹⁶. Cells of one class,type I, have no spontaneous activity, but respond phasically at ON and OFF. Their responses to moving edges, to stimuli that grow in size, and to stimuli equal in size and shape to the whole receptive field (RF) suggest that these cells may receive inhibitory input from near neigbor cells of the same type in the tectum, as well as excitatory input from retinal fibers¹⁷. In order to further investigate this hypothesis we have studied the effects of drugs on physiological properties of type I cells recorded in the stratum periventriculare layer of the zebrafish tectum. Small (10–50 nl) injections of drugs were made in the tectum while recording 100–500 μm away with extracellular microelectrodes. Both picrotoxin and bicuculline produce the following effects: (1) onset of spontaneous bursting multiunit activity. This noise can be recorded at all depths within the tectum; (2) abolition of the second postsynaptic wave of the optic nerve shock field potential and the current source responsible for it, which occurs in the upper tectal layers at 8 ms latency. This probably represents the secondary activation of inhibitory synapses in those layers; (3) alteration of visual response properties of individual type I tectal cells. The duration of response to small flashing spots and to stimuli that grow in size both increase significantly. Responses to moving edges, which normally occur mostly as the edge is crossing the RF border, become extended to encompass the entire RF. Finally, the cells show reduced negative spatial summation following drug injection. All of these effects are fully reversible with time after injection as the drugs wash out. Control injections (of teleost Ringer's solution, 100 mM HCl, 165 mM NaCl, and strychnine 2 mM or 5 mM) do not elicit any of these effects. The results reported here are consistent with the hypothesis that tectal type I cells receive a delayed inhibitory input, probably via GABA synapses, which determines major properties of the visual resonse.     

The response of optic tract glia during regeneration of the goldfish visual system. II. Tectal factors stimulate optic tract glia

After transection, retinal ganglion cell axons of the goldfish will regenerate by growing into a primary target tissue, the optic tectum. To determine what role the target tissue may play in regulating glial cell growth, we measured biosynthetic activity of optic tract glia following excision of the optic tectum and compared it to activity of glia found in the regenerating visual system. Ablation of the tectum reduced glial incorporation of both [³H]thymidine and [³⁵S]methionine. Tectal ablation also led to nearly 80% reduction of amino acids incorporated by oligodendroglia as well as a decrease in the amount of newly synthetized protein found within multipotential glia and within cytoplasmic projections of astroglia. Since the tectal influence upon optic tract glia was detected at a time when tract and tectum are physically separated, we sought to determine if the optic tectum contained soluble glia-promoting factors. A soluble fraction recovered from tecta of the regenerating visual system increased amino acid incorporation within optic tract glia at 2–3-fold above preparations incubated with fractions from control, intact tecta. Comparisons of radiolabeled proteins separated by sodium dodecyl polyacrylamide gel electrophoresis from regenerating and factor-stimulated optic tract were similar and indicated that a soluble tectal fraction promoted biosynthesis of specific glial proteins. Our findings suggest that during regeneration of the goldfish visual system glia are influenced by humoral factor(s) released from the synaptic target site.     

Nicotinic depolarization of optic nerve terminals augments synaptic transmission

The role of acetylcholine (ACh) as the neurotransmitter at the vertebrate neuromuscular junction has served as a model in the study of synaptic physiology throughout the nervous system, but its function in the brain has remained obscure. Nicotinic ACh receptors are found on afferent nerve terminals in several regions of vertebrate brain, and nicotinic agonists can cause transmitter release (as measured biochemically). Yet there is no direct evidence that activation of these receptors modulates synaptic function. Here I report that nicotinic agonists directly depolarize optic nerve terminals in goldfish tectum recorded via sucrose gap and simultaneously enhance synaptic transmission recorded via tectal field potentials. I also show that a recurrent cholinergic circuit in tectum, acting on these terminals, initiates antidromic impulses that cause repeated transmission at the retinotectal synapses.     

Pharmacological manipulation of GABA system does not protect the goldfish optic tectum from the neuroexcitatory and neurotoxic action of kainic acid

Inhibition of GABA transaminase which led to a several-fold increase of GABA levels in the goldfish optic tectum or diazepam pre-treatment, were unable to protect tectal neurons from kainic acid neurotoxicity, as judged by light and electron microscopic observations and by the drop of marker enzymes for neurotransmitters. In an in vitro preparation of tectal slices GABA, added to the incubation medium, had no effect on a metabolic parameter (CO₂ production from exogenous glucose) related to the excitatory action of kainic acid. It is concluded that, in the goldfish optic tectum, pharmacological manipulation cannot enhance the activity of GABAergic circuits to the extent necessary to block the neuroexcitatory and neurotoxic action of kainic acid.     

Mass fragmentographic determination of endogenous glycine and glutamic acid released in vivo from the pigeon optic tectum. Effect of electric stimulation of a midbrain nucleus

Various investigations suggests glycine to be an inhibitory transmitter in the pigeon optic lobe in a pathway originating in the nucleus isthmi, pars parvocellularis (Ipc) terminating in the optic tectum. In order to obtain additional evidence for this hypothesis the in vivo release of endogenous glycine in the optic tectum upon electrical stimulation of Ipc was investigated. By perfusing the upper strata of the optic tectum with Ringer solution using a push-pull cannula endogenous amino acids released from the surrounding tissue were collected. Concentration of glycine and glutamic acid in the perfusates were determined by mass fragmentography of their N-pentafluoropropionyl hexafluoroisopropyl esters. Deuterium-labeled glycine and glutamic acid were used as internal standards for quantitative measurements. The resting release of glycine and glutamic acid was 2.9 pmol/min and 1.4 pmol/min, respectively. Electrical stimulation of Ipc was found to induce a 2–40-fold increase of the glycine efflux into the perfusate whereas the efflux of glutamic acid remained at a constant level. These findings strongly support the hypothesis that glycine is a transmitter in Ipc-tectal neurons.     

Responses of the optic tectum to telencephalic stimulation in catfish

In order to test physiologically for cerebrotectal connections in a fish, averaged evoked potentials and unit responses were recorded from the optic tectum following electrical stimulation applied to the telencephalon in the siluroid teleost Ictalurus nebulosus. A single shock applied to the area dorsalis centralis (Dc) of the telencephalon, and only to this area, elicits a sequence of deflections in the ipsilateral optic tectum: an initial negative peak at about 8 ms, (= N8), a larger N25 and a slow P50-N95. The configurations, depth profiles, latencies and susceptibility to repetitive stimulation, together with the known tectal anatomy, suggest that the first wave is due to the afferent fibers from the telencephalon and that N25 is due to deep tectal neurons. Telencephalic input exerts a conditioning effect on the field potentials and unit responses evoked by direct optic nerve shock. Such a shock elicits, in the contralateral tectum, small negative, optic tract axon peaks followed by a large N6, believed to be postsynaptic, and a still later P12. As a first approximation it is argued that the telencephalic input and the retinal input are activating different sets of neuronal elements in the optic tectum, since the configuration and depth profile of the telencephalic and optic nerve shock-elicited potentials are different. A conditioning Dc stimulus has a long-lasting effect on the form of the optic nerve field potential, maximally when the pallial shock precedes the optic by about 90 ms. The effect, observed by subtracting the conditioned from the unconditioned tectal response to optic nerve shock, is a difference wave with N11 and P20. The unit activity from deep tectal laminae is either activated or accelerated following Dc stimulation, while superficially located neurons are not affected. In another group of tectal units, the optic nerve shock-induced response is depressed by a preceding pallial dorsalis centralis stimulus. The evidence is compatible with the assumption of direct projections from Dc to the deep layers of the tectum, but the timing could also permit indirect pathways. In any case, the influence is not simple or identical for different tectal cell classes.     

Pharmacologic evidence for NMDA, APB and kainate/quisqualate retinotectal transmission in the isolated whole tectum of goldfish

The optic tectum of goldfish with intact optic and toral marginal fiber tracts was isolated in a perfusion chamber where the effectiveness of antagonists was tested on synaptic field potential responses to stimulation of each afferent system. There were 3 main conclusions about excitatory synapses. First, monosynaptic activation of retinotectal synapses was not detectably antagonized by D-tubocurarine, implying there is no nicotinic cholinergic component to optic transmission nor strong cholinergic gating of optic terminals. Second, a significant component of retinotectal transmission was shown to be mediated by kainate and quisqualate receptors since 6,7-dinitroquinoxaline-2,3-dione and kynurenate strongly suppressed the optic field potential. In addition, activation of these synapses involves two previously undescribed N-methyl-D-aspartate (NMDA) and APB receptor subtypes since optic field potentials were partially suppressed by 2-amino-5-phosphonovalerate (APV), 2-amino-4-phosphonobutyrate (APB) and MK-801. This is the first evidence that APB receptors exist in the visual system central to the retina. Together, these results are consistent with the possibility that retinal ganglion cells use multiple glutamate receptor subtypes. Third, the optic tectum contains a population of intrinsic glutaminergic synapses activated by a non-optic input, the marginal fibers, which can be suppressed by both APV and kynurenate. The existence of tectal NMDA receptors which are not at primary optic synapses implies that APV used to interfere with rearrangement of optic fibers during development may act not only at afferent synapses but also at a more central component of the circuit.     

Direct connections between dendritic terminals of tectal ganglion cells and glutamate-positive terminals of presumed optic fibres in layers 4-5 of the optic tectum of Gallus domesticus. A light- and electron microscopic study

The principal afferent fibres of the avian optic tectum are the optic fibres of retinal origin. They terminate on the contralateral side, in the external layers (2-7) of the optic tectum (called optic layers) turning into these layers from the external surface. The terminal branchings of the optic fibres develop four densely innervated areas in layers 2, 3, 4-5 and 7. Their terminals are large and of various appearance in the different areas. In the middle third of the optic layer (in layers 4-5), thin dendritic terminal sections of tectal ganglion cells (according to Ramòn y Cajal) of layer 13 terminate into bunches. Phaseolus vulgaris lectin immunotracer corroborates these dendritic endings (further: dendritic terminals) of tectal ganglion cells. The direct connections between these dendritic terminals and the supposed optic fibres were studied under electron microscope and it was found that the large terminals of optic fibres containing round synaptic vesicles establish asymmetrical synapses with several dendritic profiles, among them Phaseolus lectin labelled dendritic terminals of ganglion cells. This result morphologically supports the former physiological observation of a direct synaptic transmission between optic fibres and ganglion cells of layer 13. In addition, on the dendritic terminals of ganglion cells, symmetrical synapses established by GABA-positive terminals were found. The optic terminals, the GABA-immunopositive terminals and the dendritic terminals of ganglion cells form complex synaptic units surrounded with glial sheath, and thus they establish glomerulus-like synaptic units. The size of the dendritic tree and the branching pattern of the dendrites of ganglion cells point to divergence and convergence in visual transmission.     

Intravitreal kainic acid severely reduces the size of the developing optic tectum in newly hatched chickens

Following a single intravitreal injection of 200 nmol of kainic acid (KA) to newly hatched chickens, there are acute and long-term effects on retinal ganglion cells in the chicken retina. Thirty min after injection, most ganglion cells showed cytoplasmic vacuolization. However, 14 days later, most ganglion cell soma appeared normal. Almost 60% of the cells in the ganglion cell layer (GCL) were lost, suggesting that displaced amacrine cells and not more than 40% of the ganglion cells had been eliminated. Following intravitreal injection of wheat germ agglutinin conjugated to horseradish peroxidase 14 days after the KA lesion, the amount of HRP reaction product was reduced in all retinorecipient layers, especially layers IIc and IId, of the tectum contralateral to the KA-treated eye. Fourteen days after the injection of kainic acid, during which the control tecta grow appreciably, all the superficial layers of the tectum contralateral to the kainic acid-lesioned eye, especially layers IIc and IId, were smaller than in controls, and did not differ in size from those seen in tecta contralateral to cut optic nerves. It is not clear whether this is a result of a developmental failure, or a shrinkage, or a combination of these factors. These results suggest that subtypes of ganglion cells may have a disproportionate influence in the maintenance of the cytoarchitectural integrity in the optic tectum. Alternatively the removal of the OFF-bipolar cells and amacrine cells presynaptic to ganglion cells may decrease their metabolism, and restrict the supply of trophic influences to the developing tectal cells.     

Synaptic transmission of excitation from the retina to cells in the pigeon's optic tectum

Intracellular recordings were used to study the synaptic excitation of optic tectum neurons in the pigeon. Electrical stimulation of both contralateral optic nerve and ipsilateral optic tract evoked in the tectal neurons EPSPs which in most cases were followed by an IPSP. An extrapolation procedure based on response latency was used to reveal that the EPSPs were mediated by way of mono-, di- and polysynaptic connections with the retinal endings. The laminar location of the recorded cells was estimated according to the field potential and the recording depth with the exception of the cell which was intracellulary stained with HRP. Monosynaptic EPSPs were recorded from cells in the retinorecipient region (sublayers IIa-f) as well as in the non-retinorecipient region (sublayers IIg-j and layer III) of the tectum, while di- and polysynaptic EPSPs were never recorded from the input layers. Tectofugal projections arise largely from layer III neurons. Thus, these results indicate that retinal excitation is transmitted to the output tectal cells by way of mono-, di- or polysynaptic pathways. The conduction velocities of most retinal fibers mediating the EPSP ranged from 4 to 22 m/s (average 12 m/s). However, in a number of retinal fibers the conduction velocities were in a faster range, up to 36 m/s.     

Picolinic acid modulates kainic acid-evoked glutamate release from the striatum in vitro

Since picolinic acid, a tryptophan metabolite yielded by the kynurenine pathway, selectively attenuates quinolinic and kainic acid excitotoxicity that is dependent on the presence of a glutamatergic afferent input, it was hypothesized that this agent may inhibit the presynaptic release of glutamate. Using superfused rat striatal slices, this study examined the potential of picolinic acid, and related pyridine monocarboxylic acids, to modify kainic acid-induced glutamate release. Kainic acid (0.25, 0.5 and 1.0 mM) stimulated the release of glutamate, an effect which was calcium dependent and was attenuated in the presence of the kainate/AMPA receptor antagonist, 6,7-dinitroquinoxalene-2,3-dione (500 μM). Picolinic acid significantly decreased glutamic acid release evoked by exposure of striatal slices to 1 mM kainate in the presence of calcium. The inhibitory action of picolinic acid on kainate-induced release was also shared by nicotinic and isonicotinic acid. In the absence of external calcium, kainic acid-induced glutamate release was significantly reduced by approximately 65%. Under this condition, picolinic acid (100 μM) failed to influence kainic acid-induced release. Picolinic acid (100 μM) itself increased glutamate release by 35% over basal release. While the ability of picolinic acid to inhibit excitotoxin-induced release supports the notion that it may act presynaptically to modify excitotoxicity, lack of structural specificity in its action tends to cast doubt on this mechanism of action.     

Ultrastructural evidence of the formation of synapses by retinal ganglion cell axons in two nonstandard targets

After unilateral ablation of the optic tectum in the frog (Rana pipiens), retinal ganglion cell axons enter the lateral thalamic neuropil in large numbers. This area is normally a target of the tectal efferent projection but is not innervated directly from the retina in normal frogs nor in frogs undergoing optic nerve regeneration in the presence of an intact tectum. The ability of retinal axons to form synaptic contacts in this nonstandard target, previously suspected only from light microscope studies, has been ultrastructurally verified in the present investigation. Retinal axon terminals were selectively labeled for light and electon microscope study by introducing horseradish peroxidase (HRP) into the optic nerve 73-413 days after unilateral ablation of the contralateral optic tectum. In some of the frogs, the optic nerve had also been crushed to test the ability of retinal axons regenerating over a long distance to form this connection. The HRP-labeled retinal axon terminals had the same untrastructural morphology whether located in the lateral thalamic neuropil or in the correct regions of projection, e.g., the lateral geniculate complex. They contained clear, spherical synaptic vesicles and made Gray type I synapses on the unlabeled postsynaptic dendrites. The magnitude of the projection was disproportionately greater in animals having complete or nearly complete tectal ablation than in a specimen in which the lesion was significantly incomplete. An aberrant projection was also observed in the nucleus isthmi in some of the specimens. These findings have significance for chemoaffinity theories of the specification of synaptic connections in that the ability of retinal axons to synapse in nonstandard targets in this experimental context may be considered evidence for the expression of appropriate cell-surface recognition-molecules by the abnormally targeted postsynaptic neurons. The likelihood that the expression of these postsynaptic labels is normally repressed transynaptically by molecular signals from the intact tectal input is discussed.     

Consequences of misrouting goldfish optic axons

Cut optic axons regenerate into the goldfish tectum by indirect routes. To study the accuracy with which they terminate we made visuotectal maps before and immediately after cutting through the rostral tectum from its medial edge. This severed the normal pathway to medial tectum leaving intact only grossly misrouted axons. In fish mapped in this way, 3 months or more after contralateral optic nerve cuts, each initial map was essentially normal. After a tectal cut the electrical responses were usually weaker; but their receptive field positions proved to match very closely those noted previously for the same recording sites. The mean angular change was only 8.48 degrees and much of this could be accounted for by experimental errors. In fish mapped 6 months or more after attempts to cross-unite the optic tract brachia, initial maps were less regular. Some showed gross rearrangement of groups of terminals; and recognizable irregularities persisted in two fish mapped again after a further 4 or 5 months. However, maps made after tectal cuts in such fish were not noticeably less regular than the initial maps. Field position changes averaged 17.85 degrees. In both groups misrouted axons, filled with horseradish peroxidase after mapping and visualized in whole-mounts, crossed the tectum from lateral regions to reach the medial recording sites. The small field position changes in both groups confirm that axons from detectable terminals only among their retinal neighbours; nevertheless the irregular maps seen after tract cross-union lead us to expect the orderly arrangement of the normal pathway to contribute significantly to the precision of the normal map.     

Localization of α-bungarotoxin binding sites to the goldfish retinotectal projection

The optic tectum of the goldfishCarassius auratus is a rich source of α-bungarotoxin (α-Btx) binding protein. In order to determine whether some fraction of these receptors is present at retinotectal synapses, we have compared the histological distribution of receptors revealed by the use of [¹²⁵Iα-Btx radioautography to the distribution of optic nerve terminals revealed by the use of cobalt and horseradish peroxidase (HRP) techniques. The majority of α-Btx binding is concentrated in those tectal layers containing primary retinotectal synapses. The same layers contain high concentrations of acetylcholinesterase (AChE), revealed histochemically. Following enucleation of one eye, there is a loss of α-Btx binding in the contralateral tectum, observed both by radioautography and by a quantitative binding assay of α-Btx binding. Approximately 40% of the α-Btx binding sites are lost within two weeks following enucleation. By contrast, no significant change in AChE activity could be demonstrated up to 6 months enucleation. These results are discussed in light of recent studies which show that the α-Btx binding protein and the nicotinic acetylcholine receptor are probably identical in goldfish tectum. We conclude that the 3 main classes of retinal ganglion cells projecting to the goldfish tectum are nicotinic cholinergic and that little or no postdenervation hypersensitivity due to receptor proliferation occurs in tectal neurons following denervation of the retinal input.     

Afferents of the lamprey optic tectum with special reference to the GABA input: combined tracing and immunohistochemical study

The optic tectum in the lamprey midbrain, homologue of the superior colliculus in mammals, is important for eye movement control and orienting responses. There is, however, only limited information regarding the afferent input to the optic tectum except for that from the eyes. The objective of this study was to define specifically the gamma-aminobutyric acid (GABA)-ergic projections to the optic tectum in the river lamprey (Lampetra fluviatilis) and also to describe the tectal afferent input in general. The origin of afferents to the optic tectum was studied by using the neuronal tracer neurobiotin. Injection of neurobiotin into the optic tectum resulted in retrograde labelling of cell groups in all major subdivisions of the brain. The main areas shown to project to the optic tectum were the following: the caudoventral part of the medial pallium, the area of the ventral thalamus and dorsal thalamus, the nucleus of the posterior commissure, the torus semicircularis, the mesencephalic M5 nucleus of Schober, the mesencephalic reticular area, the ishtmic area, and the octavolateral nuclei. GABAergic projections to the optic tectum were identified by combining neurobiotin tracing and GABA immunohistochemistry. On the basis of these double-labelling experiments, it was shown that the optic tectum receives a GABAergic input from the caudoventral part of the medial pallium, the dorsal and ventral thalamus, the nucleus of M5, and the torus semicircularis. The afferent input to the optic tectum in the lamprey brain is similar to that described for other vertebrate species, which is of particular interest considering its position in phylogeny.     

An electron microscope study of the retino-receptive layers of the pigeon optic tectum.

The fine structure of the superficial layer of the optic tectum of the pigeon, Columba livia, has been examined both in normal animals and after unilateral eye removal. Optic afferent terminals distributed throughout sublaminae IIa-f, are principally concentrated at three depths in the retinoreceptive zone. At first, degeneration of optic afferent terminals occurs as swelling of synaptic vesicles and accumulation of neurofilaments and later as dense degeneration. There appear to be several classes of optic afferent terminals in the retino-receptive zone, as would be expected from most previous studies of the avian tectum. The non-optic components of the neuropil, which include glomerular and pleomorphic vesicle terminals, and the synaptic interrelationships between optic and non-optic components are described. Optic afferent terminals mainly make synaptic contact with the branches of radial dendrites but also, in sublaminae IIb and IIc, with the dendrites of non-radial cells. In sublamina IIc afferent terminals synapse onto the horizontal presynaptic dendrites of spindle cells and triplet synaptic arrays including optic afferent terminals, horizontal dendrites and radial dendrite profiles and radial dendrite profiles are found. This optic projection to non-radial elements in IIb c, is discussed in relation to light microscope and electrophysiological studies.     

Synaptic interrelationships between the optic tectum and the ipsilateral nucleus isthmi in Rana pipiens

The nucleus isthmi is reciprocally connected to the ipsilateral optic tectum. Ablation of the nucleus isthmi compromises visually guided behavior that is mediated by the tectum. In this paper, horseradish peroxidase (HRP) histochemistry and electron microscopy were used to explore the synaptic interrelationships between the optic tectum and the ipsilateral nucleus isthmi. After localized injections of HRP into the optic tectum, there are retrogradely labeled isthmotectal neurons and orthogradely labeled fibers and terminals in the ipsilateral nucleus isthmi. These terminals contain round. Clear vesicles of medium diameter (40–52 nm). These terminals make synaptic contact with dendrites of nucleus isthmi cells. Almost half of these postsynaptic dendrites are retrogradely labeled, indicating that there are monosynaptic tectoisthmotectal connections. Localized HRP injection into the nucleus isthmi labels terminals primarily in tectal layers B, E, F, and 8. The terminals contain medium-sized clear vesicles and they form synaptic contacts with tectal dendrites. There are no instances of labeled isthmotectal terminals contacting labeled dendrites. Retrogradely labeled tectoisthmal neurons are contacted by unlabeled terminals containing medium-sized and small clear vesicles. Fifty-four percent of the labeled fibers connecting the nucleus isthmi and ipsilateral tectum are myelinated fibers (average diameter approximately 0.6 μm). The remainder are unmyelinated fibers (average diameter approximately 0.4 μm). © 1994 Wiley-Liss, Inc.