Functional and anatomical consequences of neonatal visual cortical damage in superior colliculus of the golden hamster

1978 ◽  
Vol 41 (6) ◽  
pp. 1466-1494 ◽  
Author(s):  
R. W. Rhoades ◽  
L. M. Chalupa

1. In normal hamsters the visual cortex sends a retinotopically organized projection to the ipsilateral superior colliculus. 2. Acute or chronic unilateral ablations of visual cortex in adult animals decrease the incidence of directionally selective cells encountered in the superficial laminae of the ipsilateral colliculus, but not in the deeper layers (those ventral to the stratum opticum). 3. Unilateral ablations of visual cortex in infant hamsters induce an aberrant crossed projection to the contralateral superior colliculus, confirming the finding of Mustari and Lund (58) in the rat. Horseradish peroxidase (HRP) experiments demonstrated that the cells whose axons comprise the normal as well as the anomalous projection are pyramidal neurons in layer V of cortex. 4. In adult hamsters that underwent early brain damage, about 13% of the cells in the colliculus could be activated by stimulation of the contralateral visual cortex. Only 1 unit (of the 159 cells tested) could be driven by similar stimulation in normal adult hamsters. This indicates that the anomalous crossed projection forms functional synapses in the contralateral tectum. 5. No cells (of the 113 tested) could be activated from the contralateral cortex in hamsters that sustained chronic ablations of visual cortex in adulthood; thus indicating that there is some limited time period during development when unilateral ablations of visual cortex induce an anomalous corticotectal pathway. 6. The visual response properties of superior collicular neurons in the neonatally brain-damaged animals were compared to those of normal hamsters, as well as to those with acute or chronic ablations of visual cortex sustained in adulthood. 7. There was no indication that the anomalous projection contributes to the organization of normal visual response properties in the superior colliculus of the neonatally brain-damaged animals. In fact, the incidence of directionally selective cells in these hamsters was found to be significantly lower than that of normals in both the superficial and deep laminae of the colliculus. 8. We conclude that while unilateral damage of visual cortex in the hamster induces an anomalous corticotectal projection that makes functional synapses, this aberrant input does not compensate for missing, normal corticotectal pathway in the organization of superior collicular response properties.

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Yulia Bereshpolova ◽  
Xiaojuan Hei ◽  
Jose-Manuel Alonso ◽  
Harvey A Swadlow

Some cortical neurons receive highly selective thalamocortical (TC) input, but others do not. Here, we examine connectivity of single thalamic neurons (lateral geniculate nucleus, LGN) onto putative fast-spike inhibitory interneurons in layer 4 of rabbit visual cortex. We show that three ‘rules’ regulate this connectivity. These rules concern: (1) the precision of retinotopic alignment, (2) the amplitude of the postsynaptic local field potential elicited near the interneuron by spikes of the LGN neuron, and (3) the interneuron’s response latency to strong, synchronous LGN input. We found that virtually all first-order fast-spike interneurons receive input from nearly all LGN axons that synapse nearby, regardless of their visual response properties. This was not the case for neighboring regular-spiking neurons. We conclude that profuse and highly promiscuous TC inputs to layer-4 fast-spike inhibitory interneurons generate response properties that are well-suited to mediate a fast, sensitive, and broadly tuned feed-forward inhibition of visual cortical excitatory neurons.


2020 ◽  
Vol 132 (6) ◽  
pp. 2000-2007 ◽  
Author(s):  
Soroush Niketeghad ◽  
Abirami Muralidharan ◽  
Uday Patel ◽  
Jessy D. Dorn ◽  
Laura Bonelli ◽  
...  

Stimulation of primary visual cortices has the potential to restore some degree of vision to blind individuals. Developing safe and reliable visual cortical prostheses requires assessment of the long-term stability, feasibility, and safety of generating stimulation-evoked perceptions.A NeuroPace responsive neurostimulation system was implanted in a blind individual with an 8-year history of bare light perception, and stimulation-evoked phosphenes were evaluated over 19 months (41 test sessions). Electrical stimulation was delivered via two four-contact subdural electrode strips implanted over the right medial occipital cortex. Current and charge thresholds for eliciting visual perception (phosphenes) were measured, as were the shape, size, location, and intensity of the phosphenes. Adverse events were also assessed.Stimulation of all contacts resulted in phosphene perception. Phosphenes appeared completely or partially in the left hemifield. Stimulation of the electrodes below the calcarine sulcus elicited phosphenes in the superior hemifield and vice versa. Changing the stimulation parameters of frequency, pulse width, and burst duration affected current thresholds for eliciting phosphenes, and increasing the amplitude or frequency of stimulation resulted in brighter perceptions. While stimulation thresholds decreased between an average of 5% and 12% after 19 months, spatial mapping of phosphenes remained consistent over time. Although no serious adverse events were observed, the subject experienced mild headaches and dizziness in three instances, symptoms that did not persist for more than a few hours and for which no clinical intervention was required.Using an off-the-shelf neurostimulator, the authors were able to reliably generate phosphenes in different areas of the visual field over 19 months with no serious adverse events, providing preliminary proof of feasibility and safety to proceed with visual epicortical prosthetic clinical trials. Moreover, they systematically explored the relationship between stimulation parameters and phosphene thresholds and discovered the direct relation of perception thresholds based on primary visual cortex (V1) neuronal population excitation thresholds.


2005 ◽  
Vol 94 (5) ◽  
pp. 3357-3367 ◽  
Author(s):  
Elodie Christophe ◽  
Nathalie Doerflinger ◽  
Daniel J. Lavery ◽  
Zoltán Molnár ◽  
Serge Charpak ◽  
...  

Previous studies have shown that layer V pyramidal neurons projecting either to subcortical structures or the contralateral cortex undergo different morphological and electrophysiological patterns of development during the first three postnatal weeks. To isolate the determinants of this differential maturation, we analyzed the gene expression and intrinsic membrane properties of layer V pyramidal neurons projecting either to the superior colliculus (SC cells) or the contralateral cortex (CC cells) by combining whole cell recordings and single-cell RT-PCR in acute slices prepared from postnatal day (P) 5–7 or P21–30 old mice. Among the 24 genes tested, the calcium channel subunits α1B and α1C, the protease Nexin 1, and the calcium-binding protein calbindin were differentially expressed in adult SC and CC cells and the potassium channel subunit Kv4.3 was expressed preferentially in CC cells at both stages of development. Intrinsic membrane properties, including input resistance, amplitude of the hyperpolarization-activated current, and action potential threshold, differed quantitatively between the two populations as early as from the first postnatal week and persisted throughout adulthood. However, the two cell types had similar regular action potential firing behaviors at all developmental stages. Surprisingly, when we increased the duration of anesthesia with ketamine–xylazine or pentobarbital before decapitation, a proportion of mature SC cells, but not CC cells, fired bursts of action potentials. Together these results indicate that the two populations of layer V pyramidal neurons already start to differ during the first postnatal week and exhibit different firing capabilities after anesthesia.


1991 ◽  
Vol 66 (1) ◽  
pp. 293-306 ◽  
Author(s):  
L. J. Larson-Prior ◽  
P. S. Ulinski ◽  
N. T. Slater

1. A preparation of turtle (Chrysemys picta and Pseudemys scripta) brain in which the integrity of the intracortical and geniculocortical pathways in visual cortex are maintained in vitro has been used to differentiate the excitatory amino acid (EAA) receptor subtypes involved in geniculocortical and intracortical synapses. 2. Stimulation of the geniculocortical fibers at subcortical loci produces monosynaptic excitatory postsynaptic potentials (EPSPs) in visual cortical neurons. These EPSPs are blocked by the broad-spectrum EAA receptor antagonist kynurenate (1-2 mM) and the non-N-methyl-D-aspartate (NMDA) antagonist 6, 7-dinitroquinoxaline-2,3-dione (DNQX, 10 microM), but not by the NMDA antagonist D,L-2-amino-5-phosphonovalerate (D,L-AP-5, 100 microM). These results indicate that the geniculocortical EPSP is mediated by EAAs that access principally, if not exclusively, EAA receptors of the non-NMDA subtypes. 3. Stimulation of intracortical fibers evokes compound EPSPs that could be resolved into three components differing in latency to peak. The component with the shortest latency was not affected by any of the EAA-receptor antagonists tested. The second component, of intermediate latency, was blocked by kyurenate and DNQX but not by D,L-AP-5. The component of longest latency was blocked by kynurenate and D,L-AP-5, but not by DNQX. These results indicate that the compound intracortical EPSP is comprised of three pharmacologically distinct components that are mediated by an unknown receptor, by quisqualate/kainate, and by NMDA receptors, respectively. 4. Repetitive stimulation of intracortical pathways at 0.33 Hz produces a dramatic potentiation of the late, D,L-AP-5-sensitive component of the intracortical EPSP. 5. These experiments lead to a hypothesis about the subtypes of EAA receptors that are accessed by the geniculocortical and intracortical pathways within visual cortex.


1995 ◽  
Vol 73 (4) ◽  
pp. 1724-1728 ◽  
Author(s):  
A. A. Kustov ◽  
D. L. Robinson

1. Models of the saccadic system propose that there is an integration of the pulse signal, and there is good evidence that the integrator is reset gradually (Nichols and Sparks 1994, 1995). Other studies of the superior collicular contribution to the saccadic system have proposed a sensory, not motor, nature for its signal. 2. To test experimentally the resetting of the integrator and the nature of the collicular signal, we electrically stimulated the superior colliculus during periods of fixation and during the course of visually guided saccades. Trains of stimuli which were presented during periods of fixation evoked saccades with fixed vectors. Identical stimulation at the beginning of a visually guided saccade evoked saccades whose direction was rotated and amplitude extended from the fixed vector. The direction of the rotation was opposite that of the visually guided saccade, and the magnitude of this rotation could be as large as 80 degrees. 3. Stimulation which was applied at progressively later times during the visually guided saccade, evoked saccades with progressively smaller rotations and progressively less elongations. The time period during which saccades were modified persisted beyond the end of the visually guided saccade, when the eyes were stationary. Thus, we confirm the previous findings (Nichols and Sparks 1994, 1995; Robinson, 1972), that the end of the saccade is not a period of quiescence within the oculomotor pathways. 4. Our results confirm that the resetting of the integration of the saccade signal is gradual rather than abrupt. Furthermore, these data suggest that the superior colliculus signals a motor error.


1992 ◽  
Vol 22 (5) ◽  
pp. 423-429
Author(s):  
N. A. Gadzhieva ◽  
F. B. Kulieva ◽  
L. �. Kul'gavin ◽  
�. I. Kuliev

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