ABSTRACT
@#Objective To investigate the neural mechanisms of speech motor control in individuals with Parkinson's disease (PD) under different strategies of motor execution control.MethodsThe techniques of the psychoacoustic and event-related potentials (ERPs) based on the altered auditory feedback paradigm were used in the present study. Two groups, including 17 PD patients and 17 healthy controls, were instructed to produce sustained vowels under the internal and external cueing tasks while hearing their voice randomly pitch-shifted downwards. The vocal responses and associated ERPs were recorded and compared across the groups and tasks.ResultsBehavioral results showed that the amplitude of acoustic compensation response was larger in PD patients than in the healthy controls (F=5.415, P=0.027), however, the main effect was not significant in the tasks (F=0.039, P=0.840). At the cortical level, PD patients produced significantly larger N1 responses to pitch perturbations in the internal cueing task related to the external cueing task (F=8.634, P=0.006), while such task effect was not observed in the healthy controls (F=1.550, P=0.231). Also, PD patients produced significantly larger N1 responses than the healthy controls in the internal cueing condition (F=5.476, P=0.026), but not in the external cueing condition (F=0.249, P=0.621). Conclusion Speech motor control in PD can be influenced by the strategies of motor execution control. Compared to the internal cueing task, the external cueing task can increase neural efficiency in the encoding of speech auditory feedback PD patients that improve auditory-motor integration for speech production.
ABSTRACT
Objective To observe the impact of ningxinjieyu capsule on contents of monoamine neurotransmitters and their metabolites in cerebral cortex of chronic depression model rats.Methods The chronic stressed depression model rats were established by chronic unpredictable stress and separation.the model rats randomly divided into model group,ningxinjieyu high-dose group(10.8 mg/(kg · d)),mid-dose group(3.6 mg/(kg · d)),low-dose group(1.2 mg/(kg · d)) and Fluoxetine group(3.6 mg/(kg · d)) and the normal rats as the control group.Finally the changes of Noradrenaline (NE),Dopamine (DA),5-hydroxy tryptamine (5-HT),3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) would be observed using HPLC-ECD technique.Results Compared with the control group,the contents of NE,DA and 5-HT were significantly lower in the model group (P＜0.01).Compared with the model group,the contents of DA were increased in the different concentrations of ningxinjieyue capsule groups,and the contents of 5-HT were higher in the low-dose and high-dose groups ((272.15± 129.89) ng/g,(445.08± 127.56) ng/g,(375.33±52.38) ng/g) ; the contents of NE were increased in the low-dose and mid-dose groups ((408.08 ± 89.55) ng/g,(530.12± 149.87) ng/g,(542.53 ± 96.10) ng/g) ; the contents of HVA were increased in the mid-dose and high-dose groups; the contents of DOPAC were increased in the low-dose group; the contents of 5-HT,DA and NE were increased in the fluoxetine group(P＜0.01 or P＜0.05).Conclusion Ningxinjieyu capsule has antidepressant effect,the mechanisms might be regulated to the contents of monoamine neurotransmitters and their metabolites in cerebral cortex.
ABSTRACT
Objective To investigate the role and neuroinflammatory mechanism of iron on dopamine ( DA) neurons in multiple primary midbrain cultures that mimic human substantia nigra pars compacta.Methods Ferrous chloride ( Fe2+ ) with the desired concentrations of 5,25 and 100 μmol/L was used to ( 1 ) treat primary midbrain neuron-microglia-astroglia cultures for 7 days and the numbers of DA neurons and total neurons were counted after tyrosine hydroxylase (TH) and neuron-specific neuclear protein neurons in 5,25 and 100 μmol/L Fe2 + -treated groups were 89%,70% and 55% of control group,and 25,100 μmol/L Fe2+ significantly decreased DA neuronal numbers compared with control group ( F = 12.047,P ＜0.01);DA neuronal bodies were shrunk and smaller,cytoplasmic stainings were reduced,neuronal dendrites were decreased;(2) The numbers of Neu-N ( + ) total neurons in 5,25 and 100 μmol/L Fe2+-treated groups were 100%,104% and 101% of control group and Fe2+ did not decrease DA neuronal numbers compared with control group (t =4.458,P ＞ 0.05 );5,25 and 100 μmol/L Fe2+-induced difference between total neurons and DA neurons were 11%,34% and 46%,and 25 and 100 (Amol/L Fe2+ produced significant difference(t =8.098,P ＜0.05;t = 11.218,P＜0.05);(3) In primary midbrain neuron-microglia-astroglia and neuron-astroglia cultures,the numbers of DA neurons in 25 μmol/L Fe+-treated group were 70% and 98% of control group,respectively.The difference between two groups was 28%,which was statistically significant (t =8.061,P＜0.05);The numbers of DA neurons in 100 μmol/L groups were 183%,190 % and 240% of control group,and 25 and 100 μmol/L Fe2 + significantly increased microglial numbers compared with control group ( F = 6.101,P ＜ 0.01 );dramatic changes of microglial morphology were indicated by the enlarged cell bodies and irregular shape.Conclusions Fe2 + provokes selective DA neuronal damage and microglia are the mediators of the neurotoxic effect,which may be due to microglial over-activation featured by the significant production of neurotoxic factors and morphological changes of microglia.This investigation cast a new light for PD therapy by inhibiting Fe2+ -induced neuroinflammation characterized by the microglial over-activation.