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Statins Promote Long-Term Recovery after Ischemic Stroke by Reconnecting Noradrenergic Neuronal Circuitry.

Cho KJ, Cheon SY, Kim GW - Neural Plast. (2015)

Bottom Line: Inhibitors of HMG-CoA reductase (statins), widely used to lower cholesterol in coronary heart and vascular disease, are effective drugs in reducing the risk of stroke and improving its outcome in the long term.This study investigated the effects of statins on the recovery of NA neuron circuitry and its function after transient focal cerebral ischemia (tFCI).Statins may be implicated to play facilitating roles in the recovery of the NA neuron and its function.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, College of Medicine, Yonsei University, Seoul 120-752, Republic of Korea.

ABSTRACT
Inhibitors of HMG-CoA reductase (statins), widely used to lower cholesterol in coronary heart and vascular disease, are effective drugs in reducing the risk of stroke and improving its outcome in the long term. After ischemic stroke, cardiac autonomic dysfunction and psychological problems are common complications related to deficits in the noradrenergic (NA) system. This study investigated the effects of statins on the recovery of NA neuron circuitry and its function after transient focal cerebral ischemia (tFCI). Using the wheat germ agglutinin (WGA) transgene technique combined with the recombinant adenoviral vector system, NA-specific neuronal pathways were labeled, and were identified in the locus coeruleus (LC), where NA neurons originate. NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group. The damaged NA circuitry was partly reorganized with the gradual recovery of autonomic dysfunction and neurobehavioral deficit. Newly proliferated cells might contribute to reorganizing NA neurons and lead anatomic and functional recovery of NA neurons. Statins may be implicated to play facilitating roles in the recovery of the NA neuron and its function.

No MeSH data available.


Related in: MedlinePlus

Immunoreactivity of WGA in the tFCI mouse brain. WGA immunoreactivity at 30, 180, and 240 days after tFCI in the vehicle- and atorvastatin-treated groups showed that NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group at 180 days. aci: anterior commissure, intrabulbar part; hf DG: hippocampal fissure and dentate gyrus; LHb: lateral habenular nucleus; Op: optic nerve layer of the superior colliculus; InWh: intermediate gray layer of the superior colliculus. Scale bar = 500 μm.
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fig2: Immunoreactivity of WGA in the tFCI mouse brain. WGA immunoreactivity at 30, 180, and 240 days after tFCI in the vehicle- and atorvastatin-treated groups showed that NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group at 180 days. aci: anterior commissure, intrabulbar part; hf DG: hippocampal fissure and dentate gyrus; LHb: lateral habenular nucleus; Op: optic nerve layer of the superior colliculus; InWh: intermediate gray layer of the superior colliculus. Scale bar = 500 μm.

Mentions: After transient focal cerebral ischemia (tFCI), WGA immunoreactivity showed the transsynaptic pattern of NA neurons according to day in each vehicle-treated or statin-treated mouse (Figure 2). NA circuits containing thalamic area, lateral hypothalamic area, cortex, and hippocampus were destroyed with severe infarction (data not shown). Although a large infarction was formed in the MCA territory, mice that survived slowly and gradually recovered the damaged area in the long-term stage (Figure 2(a)). When statin was given for a long period, the convalescence periods were faster than the vehicle-treated mice (Figure 2(b)). Whereas WGA immunoreactivity was not detected in some region such as superior colliculus from 1 month to 8 months in vehicle-treated mice after tFCI, a very strong WGA immunoreactivity was observed in the statin-treated mice in the intrabulbar part of the anterior commissure (aci) and lateral habenular nucleus (LHb). These features indicated that damaged NA circuits were partly reorganized over time in the area of previous lesion.


Statins Promote Long-Term Recovery after Ischemic Stroke by Reconnecting Noradrenergic Neuronal Circuitry.

Cho KJ, Cheon SY, Kim GW - Neural Plast. (2015)

Immunoreactivity of WGA in the tFCI mouse brain. WGA immunoreactivity at 30, 180, and 240 days after tFCI in the vehicle- and atorvastatin-treated groups showed that NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group at 180 days. aci: anterior commissure, intrabulbar part; hf DG: hippocampal fissure and dentate gyrus; LHb: lateral habenular nucleus; Op: optic nerve layer of the superior colliculus; InWh: intermediate gray layer of the superior colliculus. Scale bar = 500 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4581556&req=5

fig2: Immunoreactivity of WGA in the tFCI mouse brain. WGA immunoreactivity at 30, 180, and 240 days after tFCI in the vehicle- and atorvastatin-treated groups showed that NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group at 180 days. aci: anterior commissure, intrabulbar part; hf DG: hippocampal fissure and dentate gyrus; LHb: lateral habenular nucleus; Op: optic nerve layer of the superior colliculus; InWh: intermediate gray layer of the superior colliculus. Scale bar = 500 μm.
Mentions: After transient focal cerebral ischemia (tFCI), WGA immunoreactivity showed the transsynaptic pattern of NA neurons according to day in each vehicle-treated or statin-treated mouse (Figure 2). NA circuits containing thalamic area, lateral hypothalamic area, cortex, and hippocampus were destroyed with severe infarction (data not shown). Although a large infarction was formed in the MCA territory, mice that survived slowly and gradually recovered the damaged area in the long-term stage (Figure 2(a)). When statin was given for a long period, the convalescence periods were faster than the vehicle-treated mice (Figure 2(b)). Whereas WGA immunoreactivity was not detected in some region such as superior colliculus from 1 month to 8 months in vehicle-treated mice after tFCI, a very strong WGA immunoreactivity was observed in the statin-treated mice in the intrabulbar part of the anterior commissure (aci) and lateral habenular nucleus (LHb). These features indicated that damaged NA circuits were partly reorganized over time in the area of previous lesion.

Bottom Line: Inhibitors of HMG-CoA reductase (statins), widely used to lower cholesterol in coronary heart and vascular disease, are effective drugs in reducing the risk of stroke and improving its outcome in the long term.This study investigated the effects of statins on the recovery of NA neuron circuitry and its function after transient focal cerebral ischemia (tFCI).Statins may be implicated to play facilitating roles in the recovery of the NA neuron and its function.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, College of Medicine, Yonsei University, Seoul 120-752, Republic of Korea.

ABSTRACT
Inhibitors of HMG-CoA reductase (statins), widely used to lower cholesterol in coronary heart and vascular disease, are effective drugs in reducing the risk of stroke and improving its outcome in the long term. After ischemic stroke, cardiac autonomic dysfunction and psychological problems are common complications related to deficits in the noradrenergic (NA) system. This study investigated the effects of statins on the recovery of NA neuron circuitry and its function after transient focal cerebral ischemia (tFCI). Using the wheat germ agglutinin (WGA) transgene technique combined with the recombinant adenoviral vector system, NA-specific neuronal pathways were labeled, and were identified in the locus coeruleus (LC), where NA neurons originate. NA circuitry in the atorvastatin-treated group recovered faster than in the vehicle-treated group. The damaged NA circuitry was partly reorganized with the gradual recovery of autonomic dysfunction and neurobehavioral deficit. Newly proliferated cells might contribute to reorganizing NA neurons and lead anatomic and functional recovery of NA neurons. Statins may be implicated to play facilitating roles in the recovery of the NA neuron and its function.

No MeSH data available.


Related in: MedlinePlus