下丘脑弓状核注射神经降压素的镇痛效应及机制探讨

采用微量注射法,对37只大鼠进行了实验观察.结果如下:①下丘脑弓状核(ARC)注射神经降压素(NT)可使甩尾反应潜伏期(TFL)或痛阈显著升高.对照组注射生理盐水,TFL无明显变化.②ARC先注射纳洛酮,再注射NT,TFL变化值与单纯注射NT组相比明显下降.③ARC注射β-内啡肽(β-End)抗血清,再注射NT,TFL显著下降.④ARC注射生理盐水不影响注射NT的镇痛效应.上述结果表明,大鼠ARC注射NT可产生明显的镇痛效应,该效应可被ARC预先注射纳洛酮或β-内啡肽抗血清翻转,提示NT在ARC的镇痛作用,部分是由β-End介导的.     

Elevated hypothalamic neuropeptide Y levels in rats with dorsomedial hindbrain lesions

Lesions centered on the area postrema (AP) and adjacent nucleus of the solitary tract (AP/mNTS-lesions) are reported to result in increased consumption of highly palatable diets. Recent studies suggest that neuropeptide Y (NPY) may cause a preference for carbohydrate-rich diets. Thus, it is possible that NPY may play a role in the enhanced intake of highly palatable diets by AP/mNTS-lesioned rats. In the studies reported here, we found that lesions centered on the AP result in increased levels of NPY-immunoreactivity in the paraventricular nucleus of the hypothalamus. Additionally, steady-state NPY mRNA in the basomedial hypothalamus including the arcuate nucleus was elevated. Enhanced NPY was not found throughout the hypothalamus however, as NPY-immunoreactivity was not elevated in the lateral hypothalamus or the tissue bordering the anteroventral third ventricle. These data suggest the possibility that elevated hypothalamic NPY, particularly in the arcuate and paraventricular nuclei, may contribute to the altered food intake and energy balance observed in rats with lesions centered on the AP.     

Sparing of the flexor carpi ulnaris in ulnar neuropathy at the elbow

A common misconception attributes sparing of the flexor carpi ulnaris (FCU) in ulnar neuropathy at the elbow (UNE) to its innervating branch arising "at or above the elbow." We examined the relationship of FCU branches to the medial epicondyle (ME) and humeroulnar aponeurotic arcade (HUA) in 30 cadaver elbows. In only three did the first FCU branch arise at or proximal to the ME. In 36 UNE cases with fibrillations in the first dorsal interosseous, the FCU was normal in 10, mildly abnormal in 11, and severely abnormal in 15. FCU involvement correlated with the severity of the neuropathy and with whether compression was retroepicondylar or at the HUA. We conclude that sparing of the FCU in UNE is unrelated to the level of origin of its innervating branch, but rather is related to the internal neural topography and to the severity and level of compression.     

Effect of food deprivation and leptin repletion on the plasma levels of estrogen (E2) and NADPH-d reactivity in the ventromedial and arcuate nuclei of the hypothalamus in the female rats

The exact role of leptin in fasting has not been completely elucidated. To determine whether leptin can act in fasting to influence plasma estrogen levels and nitric oxide synthase reactivity in food regulating centers of the brain, we fasted female rats for 4 days and treated them i.p. with vehicle or 100 microg of recombinant mouse leptin as 1 ml on the 3rd and 4th day twice daily (10.00 and 17.00 h). Proestrus blood was collected at 10.00, 14.00, 18.00 and at 22.00 h, plasma obtained and assayed for estrogen (E2) and leptin levels. Verification of ovulation occurrence was by examining the oviduct for extruded ovum. The rat brains were removed and processed for nitric oxide synthase reactivity in the ventromedial hypothalamus (VMH) and arcuate nucleus (ARC) using NADPH-diaphorase histochemistry, a marker for neurons expressing NOS enzyme. Leptin effect on dependable variables such as food intake, water intake and body weight gain was also investigated. Four days fasting significantly decreased body weight, estrogen and postfast leptin levels, nitric oxide reactivity in the VMH and ARC nucleus and stopped ovulation in many (4 out of 5) rats fasted and given vehicle. Leptin treatment significantly increased plasma estrogen and postfast leptin levels, restored ovulation in many (4 out of 5) rats and increased nitric oxide reactivity in the VMH and ARC. Leptin significantly inhibited food intake, water intake and gain in body weight during recommenced feeding. These observations suggest that leptin could act in the pituitary-ovarian axis during fasting to improve reproductive function by partly stimulating estrogen secretion.     

Network dynamics in dyslexia: Review and implications for remediation

Extant neurobiological theories of dyslexia appear fractional in focusing on isolated brain regions, mechanisms, and functional pathways. A synthesis of current research shows support for an Interactive Specialization (IS) model of dyslexia involving the dysfunctional orchestration of a widely-distributed, attentionally-controlled, hierarchical, and interhemispheric circuit of intercommunicating neuronal networks. This circuitry is comprised principally of the frontostriatal-parietal cognitive control system of networks, the posterior corpus callosum, and the left arcuate fasciculus. During development, the coalescence of these functionally specialized regions, acting together, may be essential to preventing the core phonemic and phonological processing deficits defining the dyslexic phenotype. Research demonstrating an association of each with processing phonology presents the foundational outline for a comprehensive, integrative theory of dyslexia and suggests the importance of inclusive remedial efforts aimed at promoting interactions among all three networking territories.     

Demonstration of the reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia: direct evidence for macroreentry as the underlying mechanism

The exact reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) remains unclear. This case report demonstrates the reentrant circuit of ILVT. A 20-pole electrode catheter was placed along the left posterior fascicle during electrophysiologic study. ILVT was reproducibly induced by programmed ventricular stimulation. During the tachycardia, sequential diastolic potentials bridging the entire diastolic period were observed in the recordings from the electrodes positioned from left ventricular mid-septum to inferoapical septum. The slow conduction zone appeared to be composed of a false tendon in this patient. Entrainment of the ILVT from the right ventricular outflow tract at a different pacing cycle length revealed that a dominant conduction delay occurred at the proximal site of the slow conduction zone. Entrainment studies from several sites on the left ventricular septum confirmed that these sites where sequential electrical activity was recorded were included within the reentrant circuit. However, the left posterior fascicle itself seemed to be a bystander. This report provides the direct evidence of macroreentry as the underlying mechanism of this ILVT, adjacent to the left posterior fascicle.     

High resolution muscle measurements provide insights into equinus contractures in patients with cerebral palsy

Muscle contractures that occur after upper motor neuron lesion are often surgically released or lengthened. However, surgical manipulation of muscle length changes a muscle's sarcomere length (L_s), which can affect force production. To predict effects of surgery, both macro‐ (fascicle length (L_f)) and micro‐ (L_s) level structural measurements are needed. Therefore, the purpose of this study was to quantify both L_s and L_f in patients with cerebral palsy (CP) as well as typically developing (TD) children. Soleus ultrasound images were obtained from children with CP and TD children. L_f was determined and, with the joint in the same position, CP biopsies were obtained and formalin fixed, and L_s was measured by laser diffraction. Since soleus L_s values were not measurable in TD children, TD L_s values were obtained using three independent methods. While average L_f did not differ between groups (CP = 3.6 ± 1.2 cm, TD = 3.5 ± 0.9 cm; p > 0.6), L_s was dramatically longer in children with CP (4.07 ± 0.45 µm vs. TD = 2.17 ± 0.24 µm; p < 0.0001). While L_f values were similar between children with CP and TD children, this was due to highly stretched sarcomeres within the soleus muscle. Surgical manipulation of muscle‐tendon unit length will thus alter muscle sarcomere length and change force generating capacity of the muscle. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:33–39, 2015.     

TIDAL WAVES: Network mechanisms in the neuroendocrine control of prolactin release

Neuroendocrine tuberoinfundibular dopamine (TIDA) neurons tonically inhibit pituitary release of the hormone, prolactin. Through the powerful actions of prolactin in promoting lactation and maternal behaviour while suppressing sexual drive and fertility, TIDA neurons play a key role in reproduction. We summarize insights from recent in vitro studies into the membrane properties and network behaviour of TIDA neurons including the observations that TIDA neurons exhibit a robust oscillation that is synchronized between cells and depends on intact gap junction communication. Comparisons are made with phasic firing patterns in other neuronal populations. Modulators involved in the control of lactation – including serotonin, thyrotropin-releasing hormone and prolactin itself – have been shown to change the electrical behaviour of TIDA cells. We propose that TIDA discharge mode may play a central role in tuning the amount of dopamine delivered to the pituitary and hence circulating prolactin concentrations in different reproductive states and pathological conditions.