Action potentials generated in the sinoatrial node （SAN） dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormali...Action potentials generated in the sinoatrial node （SAN） dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.展开更多
Although intrathecal administration of adenosine analogues or A_1 adenosine receptor agonists is known to result in antinociception, this has not been examined yet at the cellular level. In the present study, we exami...Although intrathecal administration of adenosine analogues or A_1 adenosine receptor agonists is known to result in antinociception, this has not been examined yet at the cellular level. In the present study, we examined pharmacologically the actions of adenosine on spontaneous sensory transmission in substantia gelatinosa (SG) neurons of an adult rat spinal cord slice under the condition where a postsynaptic action of adenosine展开更多
Objective.To study the speciality of orbicularis oculi muscles, nerves and oris muscles, nerves and mechanism of difference of faclal muscular injury in facial paralysis deeply.Methods. The conductive velocity of the ...Objective.To study the speciality of orbicularis oculi muscles, nerves and oris muscles, nerves and mechanism of difference of faclal muscular injury in facial paralysis deeply.Methods. The conductive velocity of the efferent nerves of orbicularis oculi and oris muscles of the health human beings and guinea pigs is measured with electromyogram (EMG) apparatus.Results. The conductive velocity of orbicularis oculi nerve is quicker and oris muscles are controlled by facial nerves on both sides. Measuring the threshold of Strength-Duration (S-D) curves of the motor point of orbicularis oculi and oris muscles shows the threshold of the former is lower. Measuring the diameter of orbicularis oculi and oris nerve fibers on the guinea pigs and rabbits shows the diameter of orbicularis oculi nerve fiber is bigger. The area of secondary synapse space of orbicularis oculi motor end plate is larger than that of oris under scanning electromicroscope.Conclusions. Orbicularis oculi muscles,orbicularis oculi nerves and oris muscles,oris nerves all have their own characteristic on physiology and anatomy. It elucidated the mechanism that orbicularis oculi muscle is easy to be injuried.展开更多
Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruptio...Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruption resulting from trauma and biochemical reaction is a common pathological event in spinal cord injury and chronic neurodegenerative diseases.Myelin damage-induced axonal conduction block is considered to be a significant contributor to the devastating neurological deficits resulting from trauma and illness.Potassium channels are believed to play an important role in axonal conduction failure in spinal cord injury and multiple sclerosis.Myelin damage has been shown to unmask potassium channels,creating aberrant potassium currents that inhibit conduction.Potassium channel blockade reduces this ionic leakage and improves conduction.The present review was mainly focused on the development of this technique of restoring axonal conduction and neurological function of demyelinated axons.The drug 4-aminopyridine has recently shown clinical success in treating multiple sclerosis symptoms.Further translational research has also identified several novel potassium channel blockers that may prove effective in restoring axonal conduction.展开更多
During the past three decades, the Wingless-type MMTV integration site （Wnt） signaling cascade has emerged as an essential system regulating multiple processes in developing and adult brain. Accumulating evidence po...During the past three decades, the Wingless-type MMTV integration site （Wnt） signaling cascade has emerged as an essential system regulating multiple processes in developing and adult brain. Accumulating evidence points to a dysregulation of Wnt signaling in major neurodegenerative pathologies including Parkinson＇s disease （PD）, a common neurodegenerative disorder characterized by the pro- gressive loss of midbrain dopaminergic （mDA） neurons and deregulated activation of astrocytes and microglia. This review highlights the emerging link between Wnt signaling and key inflammatory pathways during mDA neuron damage/repair in PD progression. In particular, we summarize recent evidence documenting that aging and neurotoxicant exposure strongly antagonize Wnt/β-catenin signaling in mDA neurons and subventricular zone （SVZ） neuroprogenitors via astrocyte-microglial interactions. Dysregulation of the crosstalk between Wnt/β-catenin signaling and anti-oxidant/anti-inflammatory pathways delineate novel mechanisms driving the decline of SVZ plasticity with age and the limited nigrostriatal dopaminergic self-repair in PD. These findings hold a promise in devetoping therapies that target Wnt/β-catenin signaling to enhance endogenous restoration and neuronal outcome in age-dependent diseases, such as PD.展开更多
文摘Action potentials generated in the sinoatrial node （SAN） dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.
文摘Although intrathecal administration of adenosine analogues or A_1 adenosine receptor agonists is known to result in antinociception, this has not been examined yet at the cellular level. In the present study, we examined pharmacologically the actions of adenosine on spontaneous sensory transmission in substantia gelatinosa (SG) neurons of an adult rat spinal cord slice under the condition where a postsynaptic action of adenosine
文摘Objective.To study the speciality of orbicularis oculi muscles, nerves and oris muscles, nerves and mechanism of difference of faclal muscular injury in facial paralysis deeply.Methods. The conductive velocity of the efferent nerves of orbicularis oculi and oris muscles of the health human beings and guinea pigs is measured with electromyogram (EMG) apparatus.Results. The conductive velocity of orbicularis oculi nerve is quicker and oris muscles are controlled by facial nerves on both sides. Measuring the threshold of Strength-Duration (S-D) curves of the motor point of orbicularis oculi and oris muscles shows the threshold of the former is lower. Measuring the diameter of orbicularis oculi and oris nerve fibers on the guinea pigs and rabbits shows the diameter of orbicularis oculi nerve fiber is bigger. The area of secondary synapse space of orbicularis oculi motor end plate is larger than that of oris under scanning electromicroscope.Conclusions. Orbicularis oculi muscles,orbicularis oculi nerves and oris muscles,oris nerves all have their own characteristic on physiology and anatomy. It elucidated the mechanism that orbicularis oculi muscle is easy to be injuried.
基金supported by the Purdue Research Foundation(No. 61133)National Institute of Health,USA(No.1R21 NS050174-01A1)
文摘Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruption resulting from trauma and biochemical reaction is a common pathological event in spinal cord injury and chronic neurodegenerative diseases.Myelin damage-induced axonal conduction block is considered to be a significant contributor to the devastating neurological deficits resulting from trauma and illness.Potassium channels are believed to play an important role in axonal conduction failure in spinal cord injury and multiple sclerosis.Myelin damage has been shown to unmask potassium channels,creating aberrant potassium currents that inhibit conduction.Potassium channel blockade reduces this ionic leakage and improves conduction.The present review was mainly focused on the development of this technique of restoring axonal conduction and neurological function of demyelinated axons.The drug 4-aminopyridine has recently shown clinical success in treating multiple sclerosis symptoms.Further translational research has also identified several novel potassium channel blockers that may prove effective in restoring axonal conduction.
文摘During the past three decades, the Wingless-type MMTV integration site （Wnt） signaling cascade has emerged as an essential system regulating multiple processes in developing and adult brain. Accumulating evidence points to a dysregulation of Wnt signaling in major neurodegenerative pathologies including Parkinson＇s disease （PD）, a common neurodegenerative disorder characterized by the pro- gressive loss of midbrain dopaminergic （mDA） neurons and deregulated activation of astrocytes and microglia. This review highlights the emerging link between Wnt signaling and key inflammatory pathways during mDA neuron damage/repair in PD progression. In particular, we summarize recent evidence documenting that aging and neurotoxicant exposure strongly antagonize Wnt/β-catenin signaling in mDA neurons and subventricular zone （SVZ） neuroprogenitors via astrocyte-microglial interactions. Dysregulation of the crosstalk between Wnt/β-catenin signaling and anti-oxidant/anti-inflammatory pathways delineate novel mechanisms driving the decline of SVZ plasticity with age and the limited nigrostriatal dopaminergic self-repair in PD. These findings hold a promise in devetoping therapies that target Wnt/β-catenin signaling to enhance endogenous restoration and neuronal outcome in age-dependent diseases, such as PD.
