Although it has been known for decades that monocular deprivation shifts ocular dominance in kitten striate cortex, uncertainty persists about the adequate stimulus for deprivation-induced losses of cortical responsiveness. In the current study we compared the effects of 2 days of lid closure and 2 days of monocular blur using an overcorrecting contact lens. Our finding of comparable ocular dominance shifts in visual cortex indicates that deprived-eye response depression is not a result of reduced retinal illumination. The quality rather than the quantity of retinal illumination is the key factor for ocular dominance plasticity. These data have implications for both the mechanism and treatment of amblyopia.
"Thus, prestin loss may induce more subtle or specific changes in auditory cortical function than deafening. It is interesting to note that in the visual system, subtle changes in unilateral vision induce more profound remodeling of cortical circuitry than more extreme protocols, suggesting a complex relationship between synaptic alterations and sensory deprivation . "
[Show abstract][Hide abstract] ABSTRACT: Disturbance of sensory input during development can have disastrous effects on the development of sensory cortical areas. To examine how moderate perturbations of hearing can impact the development of primary auditory cortex, we examined markers of excitatory synapses in mice who lacked prestin, a protein responsible for somatic electromotility of cochlear outer hair cells. While auditory brain stem responses of these mice show an approximately 40 dB increase in threshold, we found that loss of prestin produced no changes in spine density or morphological characteristics on apical dendrites of cortical layer 5 pyramidal neurons. PSD-95 immunostaining also showed no changes in overall excitatory synapse density. Surprisingly, behavioral assessments of auditory function using the acoustic startle response showed only modest changes in prestin KO animals. These results suggest that moderate developmental hearing deficits produce minor changes in the excitatory connectivity of layer 5 neurons of primary auditory cortex and surprisingly mild auditory behavioral deficits in the startle response.
"MD triggers response depression in cortex by degrading images on the retina, not by eliminating retinal activity (Rittenhouse et al. 2006). The adequate stimulus for response depression appears to be the weakly correlated afferent activity arising in the visually deprived retina, and relayed to cortex by the lateral geniculate nucleus (Bear 2003; Blais et al. 2008). "
[Show abstract][Hide abstract] ABSTRACT: As in other mammals with binocular vision, monocular lid suture in mice induces bidirectional plasticity: rapid weakening of responses evoked through the deprived eye followed by delayed strengthening of responses through the open eye. It has been proposed that these bidirectional changes occur through three distinct processes: first, deprived-eye responses rapidly weaken through homosynaptic long-term depression (LTD); second, as the period of deprivation progresses, the modification threshold determining the boundary between synaptic depression and synaptic potentiation becomes lower, favouring potentiation; and third, facilitated by the decreased modification threshold, open-eye responses are strengthened via homosynaptic long-term potentiation (LTP). Of these processes, deprived-eye depression has received the greatest attention, and although several alternative hypotheses are also supported by current research, evidence suggests that alpha-amino-3- hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor endocytosis through LTD is a key mechanism. The change in modification threshold appears to occur partly through changes in N-methyl-D-aspartate (NMDA) receptor subunit composition, with decreases in the ratio of NR2A to NR2B facilitating potentiation. Although limited research has directly addressed the question of open-eye potentiation, several studies suggest that LTP could account for observed changes in vivo. This review will discuss evidence supporting this three-stage model, along with outstanding issues in the field.
Philosophical Transactions of The Royal Society B Biological Sciences 10/2008; 364(1515):357-67. DOI:10.1098/rstb.2008.0198 · 7.06 Impact Factor
"A general observation in many parts of the CNS is that there is a critical period shortly after birth during which plasticity is much greater than in adulthood (Lorenz, 1958; Hensch, 2004). The most studied example is ocular dominance plasticity in the visual cortex, which terminates in rats at around 35 days, in humans at around 5 years (Pizzorusso et al., 2002, 2006; Hensch, 2005; Rittenhouse et al., 2006). After this time, the CNS becomes unable to correct for the loss of visual acuity and impaired visual behaviour associated with amblyopia. "
[Show abstract][Hide abstract] ABSTRACT: Recovery of function following traumatic brain injury (TBI) is partly through neuronal plasticity. However plasticity is limited in the adult CNS compared with young animals. In order to test whether treatments that enhance CNS plasticity might improve functional recovery after TBI, a new rat head injury model was developed, in which a computer-controlled impactor produced full thickness lesions of the forelimb region of the sensorimotor cortex. Behavioural deficits were seen in several sensorimotor tasks, most of which recovered spontaneously by 21 days. However, skilled paw reaching behaviour, a task that requires corticospinal function, was only approximately 40% recovered by 28 days. In order to promote plasticity inosine was infused into the lateral ventricles for 28 days. This treatment produced an almost complete recovery of skilled paw reaching ability, associated with sprouting of the uninjured corticospinal axons across the midline into the territory of the lesioned pathway. In the cervical spinal cord the number of corticospinal axons originating from the uninjured cortex that innervated the contralateral cervical cord was five times that of controls, and in the red nucleus the number of contralaterally projecting axons was four times control values. Inosine treatment did not affect recovery in unskilled behavioural tasks, most of which recovered to normal levels by 28 days without treatment. Animals were placed in an enriched environment as an alternative method to promote plasticity. This resulted in more rapid recovery in several tasks including skilled paw function, but by 28 days normally housed animals had caught up to the same level of improvement.
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