Orienting behavior in hamsters with lesions of superior colliculus,pretectum, and visual cortex

Summary We examined cortical and subcortical mediation of visual locomotor orienting function by comparing the behavior of hamsters with discrete bilateral lesions affecting the pretectum, superior colliculus (SC), or visual cortex (VC). Orienting and approach to stationary targets was evaluated by measuring the accuracy of hamsters' approaches to small black apertures, located at eye level along the wall of a circular white arena. Hamsters with bilateral ablation of the visual cortex were slightly impaired for approaches to central field targets, whereas those with ibotenic acid lesions of the pretectum (which spares fibers of passage and thus leaves tectal afferents intact) were totally unimpaired. Hamsters with transection of the brachium of SC (BSC) at the prectectal-SC (PT-SC) border were severely impaired in their ability to approach stationary targets in central and peripheral fields. Thus, we did not detect any of the central field sparing that has been reported by others for rodents with similar lesions. Several possible reasons for the disparity between our results and those of others are discussed. Overall, our results indicate that in hamsters the SC is essential for normal visually guided approach to dark, stationary targets throughout the visual field. Further, our results and qualitative observations indicate that the approach errors are most likely due to deficits of visuomotor integration rather than to a lack of visual scanning.     

Neuronal organization underlying visually elicited prey orienting in the frog--II. Anatomical studies on the laterality of central projections

A complete transverse hemisection of the neuraxis just caudal to the optic tectum in the frog, Rana pipiens, results in a failure to orient toward stimuli in one visual hemifield [Kostyk and Grobstein (1986) Neuroscience 21, 41-55]. The extent of the deficit area implies disturbances in the outputs triggered by both tectal lobes. In this paper we report studies aimed at determining more precisely what damage is involved in producing the hemisection deficit, with the broader objective of identifying particular neural structures which may be important in visually elicited orienting. Small lesions at the level of the hemisection which are restricted to the ventromedial white tracts result in an orienting deficit identical to that produced by a complete hemisection. Large lesions which spare the ventromedial white tracts are without significant effect on orienting turns. The finding is consistent with the hypothesis that the hemisection deficit results from interruption of tectal outflow paths. Interestingly, partial damage of the ventromedial white tracts does not result in disconnection of any local tectal region from premotor circuitry but instead systematically alters the turns triggered from all tectal regions. Ventrolateral lesions at the same level do not produce deficits in orienting but do disturb optokinetic behavior. Introduction of horseradish peroxidase into ventromedial lesions produces retrograde labeling in a large number of structures both rostral and caudal of the lesion. Labeling patterns following introduction of horseradish peroxidase into ventrolateral lesions, which do not affect orienting turns, were qualitatively similar but differed quantitatively. The observed patterns of tectal cell labeling make it unlikely that the hemisection deficit can be accounted for in terms of interruption of direct projections deriving from complementary regions of the two tectal lobes. They also indicate that if there exists an uncrossed tectal outflow adequate to trigger orienting turns, it must be by way of an indirect projection. A more general analysis of the labeling patterns suggests that a crossed tectal projection and uncrossed projections from three midbrain tegmental nuclei (the anterodorsal tegmental nucleus, the nucleus profunds lateralis and the nucleus of the medial longitudinal fasciculus) are likely to be involved in triggering orienting turns. The three midbrain tegmental nuclei are of particular interest in that they provide possible anatomical substrates for an indirect uncrossed descending tectal outflow path.     

The principle of “conservation of total axonal arborizations”: massive compensatory sprouting in the hamster subcortical visual system after early tectal lesions

Summary Unilateral lesions of the right superior colliculus (SC) were made in hamsters on the day after birth. In order to quantify the extent of abnormal innervation by left eye fibers in the diencephalon and midbrain, the left eye was removed on postnatal day 12 or 36, and after an appropriate survival time, the brains were stained for degenerating axons and axon terminals with the Fink-Heimer method. In additional cases, anterograde transport of 3H proline-leucine or horseradish peroxidase was used to assess left eye connectivity. In agreement with previous reports we found abnormal projections in the ventral nucleus of the lateral geniculate body (LGv), in the lateral posterior nucleus (LP) of the thalamus, and in the left SC (the recrossing pathway). We also noted areas of abnormally heavy terminal fields arranged in patches in coronal sections in the dorsal nucleus of the lateral geniculate body (LGd). These patches arise from columns of dense innervation that are oriented along a rostral-to-caudal axis. If the right SC lesion was made large enough to diminish the recrossing pathway, retinofugal axons establish a significantly smaller distal terminal field in the left SC. In these cases, a corresponding increase in the size of terminal fields in all major proximal structures (LGd, LGv, LP, DTN) was observed. The sum of abnormal proximal growth (compensatory sprouting) was found to truly compensate for the distal loss of terminals. The evaluation of hamsters in which left eye connectivity was assessed at the age of 12 days revealed that lesion-induced patches of abnormal growth have already reached their full size by that time. These findings provide evidence for the pruning -effect and demonstrate that retinofugal axons support a fixed number of terminal arborizations (the principle of conservation of total axonal arborizations).     

Cortical and tectal control of visual orientation in the gerbil: Evidence for parallel channels

Summary Two experiments were carried out with Mongolian gerbils to determine the roles of optic tectum and visual cortex in the mediation of visually guided head turns and locomotion elicited and controlled by discrete visual targets. In Experiment 1, the behavior of animals with either a sham operation, a bilateral lesion of optic tectum, or a bilateral ablation of areas 17, 18a, and 18b was recorded on videotape as they ran from the center of a circular arena toward a small visual target projected in different locations around the perimeter of the arena. The amplitude and direction of the head turns and the accuracy of their locomotor responses were reconstructed from a frame by frame analysis of the videotapes.Sham-operate gerbils made a series of head turns before running accurately and efficiently toward the target. The gerbils with lesions of areas 17, 18a, and 18b rarely made more than one head turn before running toward the perimeter of the arena. Although the single head turn they did make was often well-correlated with the position of the target in their visual field, the direction of their locomotor response was largely determined by the direction and amplitude of that head turn. As a consequence, these animals undershot the target more often than did the sham-operate animals, and even ran into the visual half field opposite the target if their head turn had also been made into that half field. Unlike the sham operates, these animals were unable to make further adjustments in their orientation toward the stimulus after their initial head turn.The head turns and locomotor behavior of the gerbils with lesions of optic tectum were even more disorganized and inaccurate than those of the posterior decorticates. Nevertheless, when the target was presented within 45° from their visual midline, their head turns and locomotor responses showed a systematic relationship with the eccentricity of the target. Their behavior to stimuli outside this central wedge of their visual field was completely disorganized and showed no relationship to the location of the target.In Experiment 2, unilateral lesions of area 17 were performed in the gerbils that had already received bilateral tectal lesions to determine whether such lesions would affect the residual ability of these animals to orient toward stimuli located within the central portion of their visual field. During retesting, these animals were able to respond to targets only if they were located in the central portion of the field ipsilateral to the cortical lesion.These results suggest that orientation to discrete visual targets is mediated by both tectal and geniculostriate pathways with the tectofugal system subserving responses to stimuli throughout the entire visual field and the corticofugal system organizing behavior to stimuli within the central portion of the visual field. It is argued that the output from these two parallel sensorimotor systems converges on common motor centers in the pontine reticular formation.Supported by Grant A6313 from the Natural Sciences and Engineering Research Council of Canada to M. A. Goodale     

Ibotenic acid lesions in the pedunculopontine region result in recovery of visual orienting in the hemianopic cat.

Cats rendered hemianopic by a unilateral visual cortical ablation can recover the visual orienting response in the hemianopic visual field following disruption of the caudal non-tectotectal containing half of the commissure of the superior colliculus. Ibotenic acid lesions of a small 'critical zone' in the contralateral substantia nigra result in a similar recovery effect. A conceptual framework developed by Wallace et al. (1990) [J. Comp. Neurol. 296, 222-252] proposed that elimination of contralateral substantia nigra 'critical zone' inhibition on the superior colliculus ipsilateral to a visual cortical lesion is responsible for the recovery. This model is insufficient, however, to explain the observation that hemi-decorticate cats with contralateral substantia nigra 'critical zone' lesions which include but extend beyond the 'critical zone' do not demonstrate the recovery. In these cats, subsequent transection of the commissure of the superior colliculus does lead to the recovery. We hypothesize that another projection through the caudal commissure of the superior colliculus, from the pedunculopontine nucleus, is involved in the recovery effect.Visual orienting behavior was recorded before and after ibotenic acid lesions made in the pedunculopontine nucleus region contralateral to a visual cortical ablation in 16 cats. Four cats with lesions in a small rostral region of the contralateral pedunculopontine nucleus recovered the visual orienting response in the previously hemianopic visual field. Contralateral tectal projections from the pedunculopontine nucleus are thought to be cholinergic and terminate as distinct patches in the intermediate gray layers of the superior colliculus.Since this region of the pedunculopontine nucleus also receives GABA-ergic afferents from the substantia nigra, we propose that a subcortical neural circuit including the substantia nigra, pedunculopontine nucleus, and superior colliculus is involved in the recovery of visual orienting.     

Neuronal organization underlying visually elicited prey orienting in the frog--III. Evidence for the existence of an uncrossed descending tectofugal pathway

A complete transverse hemisection of the neuraxis just caudal to the optic tectum in the frog, Rana pipiens, results in a failure to orient toward stimuli in one visual hemifield [Kostyk and Grobstein (1986) Neuroscience 21, 41-55]. This finding indicates that each tectal lobe gives rise to a crossed descending pathway adequate to cause turns in a direction contralateral to that tectal lobe, and suggests that each may also give rise to an uncrossed descending pathway adequate to cause turns in the ipsilateral direction. To determine whether there is in fact such an uncrossed pathway, we have studied the orienting behavior of frogs after lesions which interrupt crossed pathways. Two groups of animals were studied. In one group we made midline lesions of the ansulate commissure, through which run the major crossed descending projections from both tectal lobes. In the other group, we combined a complete transverse hemisection with removal of the tectal lobe on the same side of the brain, leaving intact only an uncrossed pathway from one tectal lobe. A persistence of orienting turns was observed in both groups of animals. In both, the direction of the turns was that expected on the assumption that an uncrossed pathway would cause ipsilateral turns. We conclude that such a pathway exists. While both groups of animals turned in the expected directions, they did so for stimuli at unexpected locations. Increasingly eccentric stimulus locations to one side of the mid-sagittal plane were associated with increasing amplitude turns to the other. The observation suggests that tectal regions mapping areas of visual space to one side of the mid-sagittal plane are capable of triggering turns not only in that direction but in the opposite direction as well. In the case of ansulate commissure section, mirrored orienting responses were observed for tactile stimuli as well. These and other behavioral anomalies described in the preceding papers [Kostyk and Grobstein (1986) Neuroscience 21, 41-55 and 57-82] suggest that between the topographic retinotectal projection and the premotor circuitry for orienting there may exist an intermediate processing step, one in which stimulus location is represented in a generalized spatial coordinate frame.     

Response suppression induced by afferent stimulation in the superficial and deep layers of the hamster's superior colliculus

Summary Stimulation of the optic chiasm (OX) or visual cortex (VC) elicited a burst of impulses from visual cells in the superficial layers of the hamster's superior colliculus which was followed by a period of response suppression which lasted from 50–200 ms. During this period responses to normally suprathreshold OX and VC shocks, spontaneous activity and even injury discharges were markedly attenuated. For approximately 50% of the visual cells tested VC stimulation also reduced responses to visual stimuli. No correlations between receptive field properties and whether or not VC shocks diminished a given cell's visual responses were noted. Stimulation of either the cervical spinal cord (SC) or somatic sensory cortex (SMCTX) evoked action potentials from somatosensory neurons in the deep tectal laminae. These responses were followed by a period of suppression identical to that seen in the superficial layers after OX or VC shocks. SMCTX stimulation attenuated responses to tactile stimuli for 30% of the cells tested in the deep layers. Again, no correlation was observed between somatosensory response characteristics and whether or not a given cell exhibited response suppression.     

Neuronal organization underlying visually elicited prey orienting in the frog--I. Effects of various unilateral lesions

We have studied the effects on frog orienting behavior of three lesions: unilateral optic nerve section, unilateral tectal lobe ablation, and unilateral transverse hemisection of the neuraxis at a level just caudal to the optic tectum. Unilateral optic nerve section and unilateral tectal lobe ablation produce very similar deficits in visually elicited responses to prey items, an absence of responses for stimuli at locations within the monocular field of one eye. Unilateral hemisection, in contrast, results in abnormalities in visually elicited responses over a wider area, encompassing the entire ipsilateral visual hemifield. The hemisection deficit also differs in character from that following optic nerve section or tectal lesion. Within the affected hemifield, frogs do not fail to respond to stimuli but rather respond with abnormally directed movements. The movements, regardless of stimulus eccentricity on the horizontal, are always forwardly directed. While not varying with horizontal eccentricity, the movements do vary with stimulus elevation and distance. The variation with stimulus distance in the affected hemifield is somewhat different from that in the opposite hemifield. We conclude from the behavior that remains after hemisection lesions that there must exist bilateral descending tectofugal paths capable of triggering movements which vary with stimulus elevation and distance, and a crossed descending tectofugal path capable of triggering turns into one visual hemifield. That the deficit area is larger following a hemisection than following tectal lobe ablation indicates that the hemisection has affected the ability of both tectal lobes to trigger turns in one direction. A possible interpretation of this finding is that the lesion has interrupted not only the crossed descending tectofugal path from one tectal lobe but an uncrossed descending tectofugal path from the other. This hypothetical pathway as well as the others mentioned is incorporated in a model of the organization of the post-tectal circuitry involved in orienting.     

Rearrangements in the retino-geniculate projections of rats following ablation of the superior colliculus in infancy

Summary The superior colliculus was bilaterally or unilaterally ablated at different early postnatal ages in rats. When adult, each rat received a unilateral eye injection of Horesradish peroxidase to reveal the crossed and uncrossed retinal terminal fields within the dorsal lateral geniculate nucleus. Collicular ablation in the first seven days after birth, but not thereafter, produced a small hole or vacancy within the contralateral retinal terminal field which was occupied by an aberrant ipsilateral retinal terminal field. These rearrangements in the retino-geniculate projections occurred in the caudal quarter of the nucleus dorso-laterally just beneath the optic tract, solely ipsilateral to the ablated colliculus. Possible causes of the formation of these rearrangements are discussed, and similarities with other aberrant retinal projections following early damage to the visual system are considered.Abbreviations dLGN Dorsal geniculate nucleus - DTN Dorsal terminal nucleus of the accessory optic tract - HRP Horseradish peroxidase - LP Latero-posterior nucleus - NOT Nucleus of the optic tract - OT Optic tract - PO Olivary pretectal nucleus - PP Posterior pretectal nucleus - SC Superior colliculus - TMB Tetramethyl benzidine     

The organization of descending tectofugal pathways underlying orienting in the frog,Rana pipiens

Summary In the frog, identical orienting deficits, involving a failure to turn toward stimuli in the ipsilateral hemifield, can be produced by small white matter lesions either in the caudal mesencephalon (Kostyk and Grobstein, 1987a) or in the caudal medulla (Masino and Grobstein, 1989). These findings suggest that descending turn signals may run uninterrupted from the midbrain to the spinal cord, and that something other than tectospinal axons may carry such signals. We here report studies to determine whether there is a tecto-recipient structure whose axons pass through the known critical lesion sites in the caudal mesencephalon and medulla, and whether damage to such a structure, sparing tectospinal pathways, produces an orienting deficit. Horseradish peroxidase (HRP) was applied to behaviorally effective lesions in the caudal medulla and the resulting labelling patterns compared with those resulting from application of HRP to nearby but behaviorally ineffective lesions at the same rostrocaudal level. A column of large cells in the ventrolateral midbrain tegmentum (including nMLF as well as parts of AV and PV) was robustly labelled in all effective lesion cases, and less frequently labelled in ineffective cases. A quantitative analysis showed labelling in this region to be more highly correlated with the existence of a behavioral deficit than that in any other brain region. Reconstructions of single retrogradely labelled cells in the rostral part of the column (nMLF) showed that they have dendrites in a position to receive tectal input and axons which pass through the critical lesion sites in both the caudal mesencephalon and the caudal medulla. Tegmental lesions, sparing the tectospinal tracts, produced ipsilateral turning deficits in cases where the large cell column was completely removed but did not when the column was spared. The findings support the hypothesis that tectofugal signals involved in orienting turns descend uninterrupted to the spinal cord on something other than tectospinal axons, and suggest that the critical projections derive from the large cell column of the ventral tegmentum.Abbreviations A Anterior Thalamic nucleus - AD Anterodorsal nucleus - AV Anteroventral nucleus - B Neuropil Bellonci - BO Basal Optic nucleus - CbN Cerebellar nucleus - Cb Cerebellum - CG Central Grey - CPG Corpus Geniculatum Thalamicum - DH Dorsal Horn - Ent Entopeduncular nucleus - Hb Habenular nucleus - IP Interpeduncular nucleus - LA Lateral Anterior Thalamic nucleus - LCC Tegmental Large Cell Column - LP nucleus Lateralis Profundus - LPD Lateral Posterodorsal nucleus - LPV Lateral Posteroventral nucleus - Mg Magnocellular Thalamic nucleus - NB Nucleus Bellonci - nMLF Nu. Medial Longitudinal Fasciculus - NLM Nu. Lentiformis Mesencephalicus - NPC Nucleus of the Posterior Commissure - OT Optic Tectum - PD Posterodorsal Tegmental nucleus - P Posterior Thalamic nucleus - PTG Pretectal Grey - PV Posteroventral Tegmental nucleus - Ris Isthmic Reticular nucleus - Rinf Inferior Reticular nucleus - Rmed Medial Reticular nucleus - Rsup Superior Reticular nucleus - SC Suprachiasmatic nucleus - SF Solitary fasciculus - SO Superior olivary nucleus - SV Secondary visceral nucleus - T6 Tectal layer 6 - T8 Tectal layer 8 - Tel Telencephalon - TP Posterior tubercle - TSL Torus semicircularis laminaris - TSmg Torus semicircularis magnocellular - TSp Torus semicircularis principalis - VH Ventral horn - VLD Ventrolateral dorsal nucleus - VLV Ventrolateral ventral nucleus - VM Ventromedial nucleus - 2V Secondary visceral nucleus - 3 Oculomotor nucleus - 4 Trochlear nucleus - 5me Mesencephalic trigeminal nucleus - 5m Trigeminal motor nucleus - 7m Facial motor nucleus - 8V Ventral vestibular nucleus - 8d Dorsal vestibular nucleus - n8 Vestibular nerve - 9m Glossopharyngeal motor nucleus     

Lack of ingrowth of retinal axons into the visually deafferented superior colliculus in young rats: a horseradish peroxidase study

Suction lesions of the brachium of the left superior colliculus (SC) and pretectal region were made in 6-11-day-old hooded rats. Central retinal projections were examined 15-261 days later by injecting the right eye of each rat with horseradish peroxidase. Retinal fibres were found to have regrown either within glial and connective tissue membranes which formed over the lesion cavity or across the surface of the lesion itself. The axons sometimes grew up the rostral face of the remaining SC to reach the superficial tectal layers; however, there was no significant penetration into the SC neuropil.     

Initial stages of retinofugal axon development in the hamster: evidence for two distinct modes of growth

Summary In order to characterize differences in growth patterns of axons as they elongate toward their targets and during the initial stages of terminal arbor formation within the targets, we examined the primary visual system of fetal and newborn hamsters using three morphological methods: the Cajal-deCastro reduced silver method, the rapid Golgi technique, and anterograde transport of HRP. Axons emerge from the retina between the 10th and 11th embryonic days (E10–E11). The front of retinal axons crosses the chiasm, extends over the primitive dorsal nucleus of the lateral geniculate body (LGBd) by E13, and advances to the back of the superior colliculus (SC) by E13.5–E14. The rate of axon growth during this advance is nearly 2 mm/day. Collateral sprouts appear on axons around E15.5. In the LGBd and SC, these sprouts arise from multiple sites along the parent axons. Only one or a few of the sprouts continue to grow and branch, while others are eliminated. The net rate of axon collateral advance in this second phase is an order of magnitude slower than during the stage of axon elongation. Thus, formation of CNS projections may involve two qualitatively distinct modes of axon growth. The arborization mode contrasts with the elongation mode by the presence of branching, a lack of fasciculation and a slower average rate of extension. The Stereotypic direct advance of axons during elongation also differs from the remodelling which occurs during arborization. The delay between axon arrival at targets and onset of arborization could be a reflection of axons waiting for a maturational change to occur in the retina or in targets. Arborization in the LGBd and SC is initiated around the same time, implicating the former possibility. However, a slower differentiation of retinal arbors in the SC, in addition to morphological differences of arbors in the two structures, suggests that alterations in substrate factors also play a critical role in triggering the early stages of arbor formation.     

Nucleus isthmi: its contribution to tectal acetylcholinesterase and choline acetyltransferase in the frog Rana pipiens

The distribution of acetylcholinesterase and the activity of choline acetyltransferase was studied in the tecta of normal frogs and frogs without retinal and/or nucleus (n.) isthmi inputs. In normal animals acetylcholinesterase activity is found primarily in three bands in the outer layers of the tectum-lamina A, laminae C-F, and lamina G. After retinal and contralateral n. isthmi deafferentation three distinct bands of tectal acetylcholinesterase activity are still present. After bilateral n. isthmi deafferentation there is loss of activity in lamina G and reduced activity in lamina A. With retinal and ipsilateral n. isthmi deafferentation, activity is seen only in lamina A. With retinal and bilateral n. isthmi deafferentation there is virtually no acetylcholinesterase activity in the outer tectal layers. Following unilateral retinal deafferentation there is no statistically significant difference in choline acetyltransferase specific activity between intact and deafferented tectal lobes after two, four and nine weeks. With unilateral nucleus isthmi lesions and survival times of between 10 and 40 days, choline acetyltransferase specific activity in the tectal lobe ipsilateral to the ablation is approximately 38% of the specific activity of the contralateral lobe. With bilateral n. isthmi lesions there is a strong correlation between amount of n. isthmi ablated and reduction of choline acetyltransferase activity. In vitro tectal acetylcholine synthesis was also determined in animals with unilateral n. isthmi ablation. On average, tectal lobes ipsilateral to the ablated n. isthmi synthesize acetylcholine at a rate which is approximately 58% of that of contralateral tecta. Collectively, these results imply that n. isthmi is the sole cholinergic input to the frog optic tectum, with ipsilaterally projecting isthmotectal fibers accounting for the greater share.     

Orienting behavior by rats with visual cortical and subcortical lesions

Summary The effect of visual cortical and subcortical lesions on orienting behavior was assessed by examining the rats' ability to interrupt an ongoing response and perform appropriate head and postural adjustments to repeatedly presented auditory or apparently moving visual stimuli. Large lesions of the entire superior colliculus (SC) or the deep layers of the SC did not result in visual agnosia or the inability to perform the motor responses involved in orienting. Rather, the orienting response simply was not emitted to visual stimuli that the intact rat treated as less salient, but was to those it treated as more salient. Lesions of either the superficial layers of the SC or visual cortex also did not completely prevent orienting to very salient, apparently moving visual stimuli, but did produce changes in the number of responses made to such stimuli and in the occurrence of other components of orienting behavior. It was suggested that the SC and visual cortex play a modulatory role in orienting behavior and that stimulus characteristics must be considered in the development of neuronal models of orienting behavior.This investigation was supported by the Natural Sciences and Engineering Research Council of Canada (Grant AO-179) to R.C. Tees, Canada Council Doctoral Fellowship and Killam Postdoctoral Fellowship to G. C. Midgley     

Effects of eye-enucleation on substance P-immunoreactive fibers of some retinorecipient nuclei of the rat in relation to their origin from the superior colliculus.

We have previously shown that retinal deafferentation causes a decrease in immunoreactive dendrites of substance P-positive neurons of the superficial superior colliculus of the rat. Since some retinorecipient thalamic and pretectal nuclei are putative targets for substance P-containing cells of the superior colliculus, the present study attempted to ascertain whether substance P-immunoreactive fibers in these nuclei are also affected by retinal denervation. We found that unilateral eye removal produced a progressive increase in fibrous substance P immunoreactivity in the nucleus of the optic tract, lateral posterior nucleus, and lateral geniculate nucleus of the side contralateral to the enucleation. On the other hand, unilateral lesions to the superficial layers of the superior colliculus produced a dramatic reduction in substance P immunoreactivity in the ipsilateral nucleus of the optic tract, lateral posterior nucleus, and dorsal and ventral lateral geniculate nuclei. In bilaterally enucleated animals, unilateral lesion to the superior colliculus produced, as expected, loss of immunoreactive fibers only in the lateral posterior nucleus and the retinorecipient nuclei ipsilateral to the lesion. These results suggest that transneuronal changes in the distribution of substance P in collicular neurons observed after enucleation could be reflected in their projections to the other primary visual centers and to the lateral posterior nucleus.     

Cerebellotectal projections studied in cats with horseradish peroxidase or tritiated amino acids axonal transport

Summary After injections of horseradish peroxidase (HRP) into various parts of the superior colliculus (SC) in 14 cats, retrogradely labeled neurons were found in parts of all deep cerebellar nuclei. The present study demonstrated that there are three main origins of the cerebellotectal projections in regard to the locations of the cell bodies: (1) the caudal half approximately of the fastigial nucleus (NM) including the subnucleus medialis parvocellularis (SMP), (2) the ventral and lateral parts of the posterior interpositus nucleus (NIP), and (3) the ventral part of the dentate nucleus (NL) including the subnucleus lateralis parvocellularis (SLP).The pathways and terminations of these projections have also been shown autoradiographically. Thus, fibers from NM crossed within the cerebellum and terminated in the intermediate and deep gray layers of the bilateral SC. Fibers from NIP and NL passed within the superior cerebellar peduncle, which crossed in the tegmentum (decussation of the peduncle) and ended in the two layers of the contralateral SC. In addition, some cerebellofugal fibers were found to terminate in the nuclei interstitialis of Cajal and Darkschewitsch, as well as in parts of pretectum and thalamus.The tecto-ponto- (and olivo-) cerebellotectal loop (cf. Kawamura 1980) has been established morphologically and it is briefly commented on in correlation with the propagation of the teleceptive (optic and acoustic) impulses.Abbreviations AI Stratum album intermedium - AP Stratum album profundum - Cc Crus cerebri - CM Corpus mamillare - EW Nucleus of Edinger-Westphal - f.apm. Ansoparamedian fissure - Flm Fasciculus longitudinalis medialis - f.p.l. Posterolateral fissure - f.ppd. Prepyramidal fissure - f.pr. Fissura prima - f.p.s. Posterior superior fissure - f.sec. Fissura secunda - GI Stratum griseum intermedium - GP Stratum griseum profundum - GS Stratum griseum superficiale - L. Left - MG Medial geniculate body - ND Nucleus of Darkschewitsch - NIA Nucleus interpositus anterior - Nint Nucleus interstitialis of Cajal - NIP Nucleus interpositus posterior - NL Nucleus lateralis (dentatus) - NL-NIA Transition area of nucleus lateralis (dentatus) and nucleus interpositus anterior - NM Nucleus fastigii - Npa Nucleus pretectalis anterior - Npc Nucleus of posterior commissure - Npm Nucleus pretectalis medialis - Npp Nucleus pretectalis posterior - NR Nucleus ruber - Nto Nucleus of optic tract - N.III Oculomotor nerve - O Stratum opticum - PC Posterior commissure - pm. Paramedian lobule - Pg Periaqueductal gray substance - R. Right - Rf Fasciculus retroflexus - SC Superior colliculus - SCC Commissure of SC - Z Stratum zonale - III Nucleus of oculomotor nerve - V, VI, VIIA, VIIB, VIIIA, VIIIB, IX Cerebellar lobules of Larsell Working in the Anatomical Department of Iwate Medical University for six months (several periods during the year 1981)     

Stimulation of the superior colliculus in the alert cat

Summary Electrical stimulation of the cat superior colliculus (SC), in conjunction with the accurate measurement of elicited eye movements and histologically verified electrode positions, has revealed a striking antero-posterior variation in collicular organization. Three zones could be defined in the SC on the basis of eye movement patterns and associated neck muscle EMG activity evoked from the deeper layers. The Anterior zone was coextensive with the central 25 ° of the visual retinotopically coded map contained in the superficial layers. Saccades evoked from this zone were also retinotopically coded, and the latency of EMG activity depended on the position of the eye in the orbit. A similar observation applies to the entire monkey SC. The Intermediate zone was coextensive with the 25 °–70 ° of visual projections. Saccades evoked from this region were goal-directed and were associated with invariant, short latency EMG responses. The Posterior zone was found in the extreme caudo-lateral portion of the SC. Eye movements evoked from this zone were centering saccades associated with constant latency EMG activity. The present results in conjunction with previously demonstrated antero-posterior variations in projections to the SC, suggest that the motor strategies controlling gaze shifts toward visual targets vary depending on the location of the target in the visual field.     

Cross-modal transfer effects on visual discrimination depends on lesion location in the rat visual system

The effects of postoperative visual and auditory training on a brightness discrimination task were examined after lesions of various structures in the visual system. In Experiment 1, rats were trained to avoid shock with visual intensity cues. Twenty-four hours later, each rat received bilateral lesions in one of the following areas of the visual system: (1) sham, (2) visual cortex (VC), (3) pretectal (PT) area, (4) combined PT/VC, (5) superior colliculus (SC), or (6) combined SC/VC. Six days later, each rat received either training with visual or auditory intensity cues, or no training. The next day all rats were retrained on the preoperative visual avoidance task. All lesions except those in the SC condition produced relearning deficits. Auditory training reduced these deficits significantly more than visual training, except in rats with combined SC/VC lesions. In Experiment 2, sham and combined PT/VC lesion rats were given either direct or reversal intensity training using visual or auditory cues before relearning the visual discrimination. Rats given auditory direct training relearned the task faster than rats given reversal training or visual direct training. Postinjury training with an intact sensory system can enhance functional recovery more effectively than training with the damaged system. The differential effects of direct and reversal training suggest that cross-modal training involves both specific and nonspecific transfer that may be mediated through the VC or the SC.     

Tectorecipient zone of cat lateral posterior nucleus: evidence that collicular afferents contain acetylcholinesterase

Summary The superficial layers of the cat's superior colliculus innervate the medial subdivision of the thalamic lateral posterior nucleus (LPm). LPm is set off from adjoining thalamic zones by its denser staining for acetylcholinesterase (AChE). We sought to learn whether the tectal afferents to LPm might themselves be the source of the enzyme staining by examining the effects of collicular lesions on the thalamic staining pattern. Large excitotoxin lesions of the colliculus largely eliminated AChE staining in the ipsilateral LPm. By contrast, fibersparing lesions of LPm itself left AChE staining nearly unchanged. Destruction of collicular neurons by excitotoxins dramatically reduced AChE staining in fibers of the brachium and superficial gray layer of the superior colliculus. The reduction was especially pronounced in the lower part of the superficial gray layer, in which LP-projecting collicular neurons are located. These results are consistent with the view that LP-projecting collicular neurons synthesize AChE and account for much of the histochemically detectable enzyme present both in the lower superficial gray layer and in LPm. In the colliculus, the excitotoxin lesions spared AChE staining in a thin sheet at the upper border of the superficial gray layer and in the enzyme-positive patches in the intermediate layers. This surviving tectal AChE thus is probably presynaptic and could be contained at least partly in cholinergic afferents from the parabigeminal nucleus and pontomesencephalic tegmentum. The collicular lesions had no obvious effect on AChE staining in the parabigeminal nucleus or in the C-laminae or ventral division of the lateral geniculate nucleus.