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Stroke and Constraint-Induced Movement Therapy

28/12/2013

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Nesin Sibin (PhD Scholar) presented the paper by Zhao etal from the journal Stroke 2013 entitled "Constraint-Induced Movement Therapy Overcomes the Intrinsic Axonal Growth - Inhibitory Signals in Stroke Rats".

ABSTRACT
Background and Purpose —Constraint-induced movement therapy (CIMT) improves functional outcome in patients with stroke possibly through structural plasticity. We hypothesized that CIMT could enhance axonal growth by overcoming the intrinsic growth–inhibitory signals, leading eventually to improved behavioral performance in stroke rats.

Methods—Focal cerebral ischemia was induced by intracerebral injection of endothelin-1. Adult Wistar rats were divided into a sham-operated group, an ischemic group, and an ischemic group treated with CIMT. CIMT started at postoperative day 7 and continued for 3 weeks. Biotinylated dextran amine was injected into the contralateral sensorimotor cortex at postoperative day 14 to trace crossing axons at the cervical spinal cord. The expressions of Nogo-A, Nogo receptor, RhoA, and Rho-associated kinase in the peri-infarct cortex, and the expressions of biotinylated dextran amine, growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated spinal cord were measured by immunohistochemistry and Western blots. Behavioral recovery was analyzed at postoperative days 29 to 32.

Results—Infarct volumes were not different between groups after stroke. CIMT significantly increased the length and the number of midline crossings of contralateral corticospinal axons to the denervated cervical spinal cord. CIMT significantly decreased the expressions of Nogo-A/Nogo receptor and RhoA/Rho-associated kinase in the peri-infarct cortex, and increased the expressions of growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated cervical spinal cord. Behavioral performances assessed by the beam-walking test and the water maze test were improved significantly by CIMT.

Conclusions—CIMT promoted poststroke synaptic plasticity and axonal growth at least partially by overcoming the intrinsic growth–inhibitory signaling, leading to improved behavioral outcome.
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Parkinsons and Microglial activation

21/12/2013

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Abhilash PL (PhD Scholar) presented the paper entitled "NADPH Oxidase and Aging Drive Microglial Activation, Oxidative Stress, and Dopaminergic Neurodegeneration Following Systemic LPS Administration" by Qin etal, from Glia 2013.

ABSTRACT
Parkinson’s disease is characterized by a progressive degeneration of substantia nigra (SN) dopaminergic neurons with age. We previously found that a single systemic lipopolysaccharide (LPS, 5 mg/kg, i.p.) injection caused a slow progressive loss of tyrosine hydroxylase immunoreactive (THþIR) neurons in SN associated with increasing motor dysfunction. In this study, we investigated the role of NADPH oxidase (NOX) in inflammation-mediated SN neurotoxicity. A comparison of control (NOX2þ/þ) mice with NOX subunit gp91phox-deficient (NOX2/) mice 10 months after LPS administration (5 mg/kg, i.p.) resulted in a 39% (P < 0.01) loss of THþIR neurons in NOX2þ/þ mice, whereas NOX2/ mice did not show a significant decrease. Microglia (Iba1þIR) showed morphological activation in NOX2þ/þ mice, but not in NOX2/ mice at 1 hr. 

Treatment of NOX2þ/þ mice with LPS resulted in a 12-fold increase in NOX2 mRNA in midbrain and 5.5–6.5-fold increases in NOX2 protein (þIR) in SN compared with the saline controls. Brain reactive oxygen species (ROS), determined using diphenyliodonium histochemistry, was increased by LPS in SN between 1 hr and 20 months. Diphenyliodonium (DPI), an NOX inhibitor, blocked LPS-induced activation of microglia and production of ROS, TNFa, IL-1b, and MCP-1. Although LPS increased microglial activation and ROS at all ages studied, saline control NOX2þ/þ mice showed age-related increases in microglial activation, NOX, and ROS levels at 12 and 22 months of
age. 

Together, these results suggest that NOX contributes to persistent microglial activation, ROS production, and dopaminergic neurodegeneration that persist and continue to increase with age.
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Neurobiology of Attention

20/12/2013

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Rukmani MR ( MPhil Scholar) presented her seminar on "Neurobiology of Attention"

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APPICON 2013

7/12/2013

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The 59th Annual National Conference of Association of Physiologists and Pharmacologists of India was held from 26th - 30th November, 2013 at the Convention Centre, NIMHANS Bangalore.

Chief Patron: Prof. P. Satish Chandra                             Patron: Prof. T R Raju
Chair Person: Prof. Bindu M Kutty                                  Joint Organizing Secretary: Dr. B.S. Shankaranarayana Rao
Scientific Committee-Chair: Laxmi T. Rao                     Treasurer: Dr. H. Nagarathna
Registration Committee: Dr. Phalguni A Alladi                Reception Committee: Dr. Veena Kumari

The photo collection can be seen on our Flickr page.

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