Abstract:In the primate brain, the primary visual cortex (V1) is a major source of visual information processing in the cerebral cortex, although some patients and monkeys with damage to the V1 show visually guided behaviors in the visual field affected by the damage. Until now, behaviors of the surviving brain regions after damage to V1 and their contribution to the residual visual functions remain unclear. Here, we report that the monkeys with a unilateral lesion of V1 can make not only visually guided saccades but a… Show more
“…Visual input pathways from retina can be classified into two major pathways; one is cortical pathways via LGN and V1, the other is subcortical pathways via the SC. The monkeys with unilateral V1 lesion were used to investigate abilities of the subcortical visual pathways through the SC (Mohler and Wurtz, 1977; Kato et al, 2011; Takaura et al, 2011). In this study, the V1 lesion allowed us to assess contribution of visual information via the SC to support visual classical conditioning and to evoke phasic DA responses following the presentation of conditioned stimuli.10.7554/eLife.24459.003Figure 1.Pavlovian conditioning in V1 lesioned monkeys.( A ) Left: lesion area (depicted in gray) on the whole brain image.…”
Responses of midbrain dopamine (DA) neurons reflecting expected reward from sensory cues are critical for reward-based associative learning. However, critical pathways by which reward-related visual information is relayed to DA neurons remain unclear. To address this question, we investigated Pavlovian conditioning in macaque monkeys with unilateral primary visual cortex (V1) lesions (an animal model of ‘blindsight’). Anticipatory licking responses to obtain juice drops were elicited in response to visual conditioned stimuli (CS) in the affected visual field. Subsequent pharmacological inactivation of the superior colliculus (SC) suppressed the anticipatory licking. Concurrent single unit recordings indicated that DA responses reflecting the reward expectation could be recorded in the absence of V1, and that these responses were also suppressed by SC inactivation. These results indicate that the subcortical visual circuit can relay reward-predicting visual information to DA neurons and integrity of the SC is necessary for visually-elicited classically conditioned responses after V1 lesion.DOI:
http://dx.doi.org/10.7554/eLife.24459.001
“…Visual input pathways from retina can be classified into two major pathways; one is cortical pathways via LGN and V1, the other is subcortical pathways via the SC. The monkeys with unilateral V1 lesion were used to investigate abilities of the subcortical visual pathways through the SC (Mohler and Wurtz, 1977; Kato et al, 2011; Takaura et al, 2011). In this study, the V1 lesion allowed us to assess contribution of visual information via the SC to support visual classical conditioning and to evoke phasic DA responses following the presentation of conditioned stimuli.10.7554/eLife.24459.003Figure 1.Pavlovian conditioning in V1 lesioned monkeys.( A ) Left: lesion area (depicted in gray) on the whole brain image.…”
Responses of midbrain dopamine (DA) neurons reflecting expected reward from sensory cues are critical for reward-based associative learning. However, critical pathways by which reward-related visual information is relayed to DA neurons remain unclear. To address this question, we investigated Pavlovian conditioning in macaque monkeys with unilateral primary visual cortex (V1) lesions (an animal model of ‘blindsight’). Anticipatory licking responses to obtain juice drops were elicited in response to visual conditioned stimuli (CS) in the affected visual field. Subsequent pharmacological inactivation of the superior colliculus (SC) suppressed the anticipatory licking. Concurrent single unit recordings indicated that DA responses reflecting the reward expectation could be recorded in the absence of V1, and that these responses were also suppressed by SC inactivation. These results indicate that the subcortical visual circuit can relay reward-predicting visual information to DA neurons and integrity of the SC is necessary for visually-elicited classically conditioned responses after V1 lesion.DOI:
http://dx.doi.org/10.7554/eLife.24459.001
“…Similarly, we found that inhibition of serum LH in rodents led to increases in brain LH in cognition-associated areas including the cingulate, thalamus, hippocampus, hypothalamus, and superior colliculi: all regions of the brain that have been previously shown to express the CG/LHR (Lei et al 1993;H€ am€ al€ ainen et al 1999;Apaja et al 2004). As a result of the sagittal preparation of our paraffin-embedded tissue, and the precise anatomical localization of LH in the brain, we were only able to systematically quantify LH expression in the superior colliculus, which is relevant given its critical involvement in spatial ability in primates (Klier et al 2003;Takaura et al 2011), and its importance for rodent MWM performance (Jeljeli et al 1999). Importantly, we found that LH increases in the superior colliculus were positively correlated with cognitive performance and negatively correlated with serum LH.…”
Development of Alzheimer’s disease (AD) has been linked to the de-regulation of estrogen and gonadotropins such as luteinizing hormone (LH). In this study, we found increases in AD pathology in the hippocampi of aged female 3xTg AD mice after ovariectomy that were unable to be reduced by estrogen therapy or down-regulation of serum LH levels. Despite the lack of effect of these treatments on AD pathology, down-regulation of serum LH but not estrogen improved factors associated with neuronal plasticity such as spatial memory, inhibition of glycogen synthase kinase-3 beta, expression of beta-catenin, and brain-derived neurotrophic factor transcription. Contrasting previous studies in younger mice, estrogen replacement was not able to rescue behavioral deficits, reduced glycogen synthase kinase-3 beta inhibition and increased hippocampal phosphorylation of tau. Of critical importance, serum LH was negatively correlated with brain LH in regions associated with spatial memory, and increases in brain LH correlated with cognitive improvement. This paralleled changes in human female AD brains which showed a significant reduction in brain LH mRNA compared to healthy age- and PMI-matched controls. Taken together, these findings should promote further research into the LH-dependent mechanisms associated with AD cognitive deficits as well as the effects of estrogen within the aged brain.
“…Taking these findings together, we conclude that the deficits observed in the visually guided saccade task caused by inactivation of the ipsilesional SC in monkeys with previous V1 lesions were primarily caused by inactivation of visual processing, presumably in the superficial layer of the SC, which was carried by the retino‐tectal pathway. Our recent report showed that short‐latency visual responses could be observed after recovery from V1 lesions (Takaura et al. , 2011), which suggested that the retino‐tectal pathway transmits visual inputs to the superficial layer of the SC after V1 lesions.…”
Previous reports on 'blindsight' have shown that some patients with lesions of the primary visual cortex (V1) could localize visual targets in their scotoma with hand and/or eye movements without visual awareness. A role of the retino-tectal pathway on residual vision has been proposed but the direct evidence for this still remains sparse. To examine this possibility, we inactivated the superior colliculus (SC) of unilateral V1-lesioned monkeys using microinjections of muscimol, and analysed the effects on visually guided saccades. Following muscimol injections into the contralesional SC, the monkeys performed the visually guided saccade task with relatively minor deficits. The effects of ipsilesional SC inactivation were more severe. After injections, the monkeys failed to localize the target within the visual field represented at the injection site on the SC map. The effects of ipsilesional SC inactivation may result from sensory deficits, motor deficits or a combination of both. To examine these possibilities, we tested the effects of SC inactivation on the motor system by investigating spontaneous saccades. After inactivation of the ipsilesional SC, spontaneous saccades toward the injection site were not abolished, suggesting that impairment of visually guided saccades following inactivation of the ipsilesional SC could not be explained solely by a motor deficit and was primarily due to a visual deficit, presumably by interfering with processing in the superficial layer. We conclude that the retino-tectal pathway plays an essential role in residual vision after V1 lesion. The results suggest that this pathway may be involved in mediating unconscious vision in blindsight patients.
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