17α Estradiol promotes plasticity of spared inputs in the adult amblyopic visual cortex.

The promotion of structural and functional plasticity by estrogens is a promising approach to enhance central nervous system function in the aged. However, how the sensitivity to estrogens is regulated across brain regions, age and experience is poorly understood. To ask if estradiol treatment impacts structural and functional plasticity in sensory cortices, we examined the acute effect of 17α-Estradiol in adult Long Evans rats following chronic monocular deprivation, a manipulation that reduces the strength and selectivity of deprived eye vision. Chronic monocular deprivation decreased thalamic input from the deprived eye to the binocular visual cortex and accelerated short-term depression of the deprived eye pathway, but did not change the density of excitatory synapses in primary visual cortex. Importantly, we found that the classical estrogen receptors ERα and ERß were robustly expressed in the adult visual cortex, and that a single dose of 17α-Estradiol reduced the expression of the calcium-binding protein parvalbumin, decreased the integrity of the extracellular matrix and increased the size of excitatory postsynaptic densities. Furthermore, 17α-Estradiol enhanced experience-dependent plasticity in the amblyopic visual cortex, by promoting response potentiation of the pathway served by the non-deprived eye. The promotion of plasticity at synapses serving the non-deprived eye may reflect selectivity for synapses with an initially low probability of neurotransmitter release, and may inform strategies to remap spared inputs around a scotoma or a cortical infarct.

Light reintroduction after dark exposure reactivates plasticity in adults via perisynaptic activation of MMP-9.

The sensitivity of ocular dominance to regulation by monocular deprivation is the canonical model of plasticity confined to a critical period. However, we have previously shown that visual deprivation through dark exposure (DE) reactivates critical period plasticity in adults. Previous work assumed that the elimination of visual input was sufficient to enhance plasticity in the adult mouse visual cortex. In contrast, here we show that light reintroduction (LRx) after DE is responsible for the reactivation of plasticity. LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic ablation of matrix metalloproteinase-9 (MMP-9). LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thalamo-cortical synapses. The reactivation of plasticity by LRx is absent in Mmp9-/- mice, and is rescued by hyaluronidase, an enzyme that degrades core ECM components. Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional plasticity in the mature cortex.

Yoga as palliation in women with advanced cancer: a pilot study.

OBJECTIVE: The purpose of this pilot study was to investigate the palliative potential of home-based yoga sessions provided to women with advanced cancer. METHOD: Personalised 45-minute yoga sessions were offered to three women with advanced cancer by an experienced yoga teacher. Each woman took part in a one-to-one interview after the completion of the yoga programme and was asked to describe her experiences of the programme's impact. RESULTS: The personalised nature of the yoga sessions resulted in similar positive physical and psychosocial effects comparable to those demonstrated in other studies with cancer patients. Participants described physical, mental, and emotional benefits as well as the alleviation of illness impacts. The enhancement of mind-body and body-spirit connections were also noted. CONCLUSION: Personalised home-based yoga programmes for people with advanced cancer may produce similar benefits, including palliation, as those institutionally-based programmes for people with non-advanced cancer.

Beyond the body: insights from an Iyengar yoga program for women with disability after breast cancer.

Lymphedema, pain, and range of motion restrictions after breast cancer remain underexplored, and few interventions have been developed for these women. Together with a yoga instructor, our interdisciplinary research team developed a yoga program for women with lymphedema after breast cancer (n = 13). Qualitative interviews and participants' journals show that there were a number of benefits to the yoga program. Themes outlining these are (1) understanding arm morbidity; (2) becoming aware of posture; and (3) countering fatigue. More surprisingly, perhaps, the participants also described the ways in which yoga furthered their understandings of loss associated with disability, the fourth theme, and showed that yoga enhanced their experiences of embodiment, the final theme. Finally, we assert that our research demonstrates the potential for qualitative research connected to the evaluation of interventions and that it demonstrates the blurring of traditional boundaries between interventions and data collection.

Recovery from chronic monocular deprivation following reactivation of thalamocortical plasticity by dark exposure.

Chronic monocular deprivation induces severe amblyopia that is resistant to spontaneous reversal. However, dark exposure initiated in adulthood reactivates synaptic plasticity in the visual cortex and promotes recovery from chronic monocular deprivation in Long Evans rats. Here we show that chronic monocular deprivation induces a significant decrease in the density of dendritic spines on principal neurons throughout the deprived visual cortex. Nevertheless, dark exposure followed by reverse deprivation promotes the recovery of dendritic spine density of neurons in all laminae. Importantly, the ocular dominance of neurons in thalamo-recipient laminae of the cortex, and the amplitude of the thalamocortical visually evoked potential recover following dark exposure and reverse deprivation. Thus, dark exposure reactivates widespread synaptic plasticity in the adult visual cortex, including thalamocortical synapses, during the recovery from chronic monocular deprivation.