The startle reflex is considered a primitive physiological reflex, a defense response that occurs in the organism when the body feels sudden danger and uneasiness, characterized by habituation and sensitization effects, and studies on the startle reflex often deal with pre-pulse inhibition (PPI) and sensorimotor gating. Under physiological conditions, the startle reflex is stable at a certain level, and when the organism is in a pathological state, such as stroke, spinal cord injury, schizophrenia, and other diseases, the reflex undergoes a series of changes, making it closely related to the progress of disease. This paper summarizes the startle reflex in physiological and pathological states by reviewing the databases of PubMed, Web of Science, Cochrane Library, EMBASE, China Biology Medicine, China National Knowledge Infrastructure, VIP Database for Chinese Technical Periodical, Wanfang Data, and identifies and analyzes the startle reflex and excessive startle reaction disorder.
Purpose: Establishing an ideal animal model is essential for studying the pathogenesis, prevention and treatment of vascular dementia (VD). The present study was designed to compare the differences of behavior, cerebral blood flow (CBF), cardiac output and the levels of myocardial enzyme of three different VD rat models. Methods: The rats were randomly divided into sham-operated group (SHAM), permanent bilateral common carotid artery occlusion group (BCCAO), BCCAO combined with sodium nitroprusside (2.0mg•kg −1 ) group (BCCAO+2.0SNP) and BCCAO combined with sodium nitroprusside (2.5mg•kg −1 ) group (BCCAO+2.5SNP). After operation, Morris water maze test, echocardiographic evaluation and the measurement of CBF were performed, then the levels of myocardial enzymes in serum were assessed during euthanasia. Results: Compared with SHAM rats, the three VD model rats showed different degrees of cognitive impairment, lower cardiac output and CBF, and BCCAO rats showed higher levels of myocardial enzymes. Compared with BCCAO rats, the spatial learning ability of BCCAO+2.0SNP rats and BCCAO+2.5SNP rats was more severely impaired, while the levels of myocardial enzymes of BCCAO+2.0SNP rats were lower. Compared with BCCAO+2.0SNP rats, BCCAO +2.5SNP rats showed no significant difference in cognitive function and cardiac function.
Conclusion:Our present study demonstrated that all of the three different VD rat models exhibited cognitive and cardiac function impairment. The BCCAO+2.0SNP model and BCCAO +2.5SNP model damaged the spatial learning ability more seriously. The BCCAO+2.5SNP model caused more comprehensive cognitive impairment. In addition, the BCCAO+2.0SNP model and BCCAO+2.5SNP model might cause more serious damage to cardiac function.
Vascular dementia (VaD), a cognitive disorder caused by cerebrovascular pathologies, is the most common cause of dementia in the elderly, being second only to Alzheimer's disease. Researches have shown that adequate cerebral blood flow (CBF) is the first condition for maintaining the structural integrity and normal function of the brain, and VaD is generally considered to be resulted from neuronal loss due to reduced CBF. Collateral circulation, a compensation mechanism for CBF, provides an alternative vascular pathway for blood to reach ischemic tissues, which has been confirmed to be associated with better clinical outcomes of ischemic diseases. At present, considerable effort has been devoted to enhancing the functional prognosis of acute ischemic stroke by improving collateral circulation. Since ischemic stroke is the primary contributor to VaD, it is necessary to explore whether improving collateral circulation is beneficial to prevent or slow the progression of VaD. This article reviews the compensatory characteristics of different levels of cerebral collateral circulation, addresses the relationship between collateral circulation and VaD, and highlights that improving collateral circulation may be a potential adjunctive strategy in preventing and slowing the progression of VaD.
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