“WHAT'S BUGGING THE GUT IN OCD?” A REVIEW OF THE GUT MICROBIOME IN OBSESSIVE–COMPULSIVE DISORDER

The gut microbiome has become a topic of major interest as of late, with a new focus specifically on psychiatric disorders. Recent studies have revealed that variations in the composition of the gut microbiota may influence anxiety and mood and vice versa. Keeping the concept of this bidirectional “microbiota-gut-brain” axis in mind, this review aims to shed light on how these findings may also be implicated in obsessive–compulsive disorder (OCD); potentially outlining a novel etiological pathway of interest for future research in the field.     

THE RESEARCH ON MECHANISMS OF AMYLOID- β PROTEIN INDUCING ALZHEIMER'S DISEASE IN RAT AND EFFECTS OF NIMODIPINE TREATMENT

0bjective In order to clarify the mechanism of the neurotoxics of Aβ, we studied the effects on the rCBF, extra-cellular amino acid (EAA), apoptosis and Bcl-2 protein expression, and their relationship with learning and memory deficiency. Methods Aβ was injected into NBM in rats to establish the AD model, learning and memory abilities were observed by Y-maze. The rCBF was measured by hydrogen clearance method. The EAA was detected by microdialysis in vivo with HPLC. The apoptosis and Bc1-2 protein expression was examined by flow cytometry. The male SD rats were divided into three groups: the model group was injected Aβ (10 μ g) into NBM of the rat. The control group was injected NaC1 (0.9%) in the same way. The treatment group was made with intraperitoneal injections of Nimodipine for 2 weeks after A β injections. Results The administration of Aβ into rat′s NBM could lead to the loss of learning and memory abilities. It was found that in frontal cortex and hippocampus, the rCBF decrease, however, with no trend of progressive decline. On the other hand, the levels of EAA increased, especially glutamate. Furthermore, A β significantly induced neurons apoptosis of frontal cortex and hippocampi cell, and upregulated the expression of the bcl-2. The Nimodipine might entirely improve rCBF of AD rats nearly to normal level, lessen the release of EAA and augment restrain neurotransmission. It might reduce the apoptosis partly, but it couldn't improve the learning and memory disorders completely. Conclusion The results implied that the neurotoxic effect of Aβ exists multi-mechanism.     

NEURAL CONTROL OF THE SOLEUS H –REFLEX IS RELATED TO THE LATERALITY PATTERN IN LIMBS

Background: Results from performance studies suggested the relationship of lower limb dominance with handedness in right and left – handers, what brings support to some other findings suggesting the role of peripheral factors in the neural control of movements Objective: The aim of the study was toinvestigate the effect of laterality pattern on the neural mechanisms of motor control on peripheral level. Design.The laterality evaluation and the motor evoked potentials of dominant and non dominant limbs were provided, by the use of the H-reflex circuitry. Setting: Experiment was performed in the motor diagnostics laboratory of the Academy of Physical education in Katowice, Poland in June 2009. Participants: 20 young male adults aged 21-23 presenting two laterality patterns in hand-foot combination (right handed-right footed and left handed-left footed groups) took part in the experiment. All of them were carefully screened to eliminate any neurological or muscle diseases or trauma and gave informed consent . Methods: A comparison of the soleus H-reflex parameters elicited at rest in lower extremities. The soleus H-reflex and the direct motor response (M-wave) were elicited in lower extremities of each participant in the same laboratory session. Main outcome measures: Onset latencies as well as min-max amplitudes of the M-wave and the H-reflex were taken into an analysis. Additionally, the motor and sensory conduction velocities were calculated as well as symmetry coefficients of response parameters. Results: The analysis of symmetry coefficients (SC) of direct and late motor responses confirmed differences between two laterality patterns in amplitude and latency of the H-reflex as well as in a sensory conduction velocity (p< 0,05), but not in M-wave parameters. The amplitude of the H-reflex and the calculated sensory Ia afferent conduction velocity in the dominant lower extremity were significantly depressed in the right-sided group in comparison to the left-sided group (p=0.001). The right- sided group presented significantly faster motor fibers conduction velocity in the dominant leg (p=0.006), with no similar effect in the left-sided group. Conclusion: The neural control of the H-reflex elicited at rest is related to the laterality pattern in Hand-foot combination in healthy adults. It strongly suggests the possible existence of intrinsic control mechanisms of the afferent feedback related to functional dominance in human limbs.     

DO NERVE GROWTH FACTOR‐RELATED MECHANISMS CONTRIBUTE TO LOSS OF CUTANEOUS NOCICEPTION IN LEPROSY?

While sensory loss in leprosy skin is the consequence of invasion by M. leprae of Schwann cells related to unmyelinated fibres, early loss of cutaneous pain sensation, even in the presence of nerve fibres and inflammation is a hallmark of leprosy, and requires explanation. In normal skin, nerve growth factor (NGF) is produced by basal keratinocytes, and acts via its high affinity receptor (trk A) on nociceptor nerve fibres to increase their sensitivity, particularly in inflammation. We have therefore studied NGF‐ and trk A‐like immunoreactivity in affected skin and mirror‐site clinically‐unaffected skin from patients with leprosy, and compared these with non‐leprosy, control skin, following quantitative sensory testing at each site. Sensory tests were within normal limits in clinically‐unaffected leprosy skin, but markedly abnormal in affected skin. Sub‐epidermal PGP 9.5‐ and trk A‐positive nerve fibres were reduced only in affected leprosy skin, with fewer fibres contacting keratinocytes. However, NGF‐immunoreactivity in basal keratinocytes, and intra‐epidermal PGP 9.5‐positive nerve fibres, were reduced in both sites compared to non‐leprosy controls, as were nerve fibres positive for the sensory neurone specific sodium channel SNS/PN3, which is regulated by NGF, and may mediate inflammation‐induced hypersensitivity. Keratinocyte trk A expression (which mediates an autocrine role for NGF) was increased in clinically affected and unaffected skin, suggesting a compensatory mechanism secondary to reduced NGF secretion at both sites. We conclude that decreased NGF‐ and SNS/PN3‐immunoreactivity, and loss of intra‐epidermal innervation, may be found without sensory loss on quantitative testing in clinically‐unaffected skin in leprosy; this appears to be a sub‐clinical change, and may explain the lack of cutaneous pain with inflammation. Sensory loss occurred with reduced sub‐epidermal nerve fibres in affected skin, but these still showed trk A‐staining, suggesting NGF treatment may restore pain sensation.     

CORRELATIVE STUDY OF THE COGNITIVE IMPAIRMENT,REGIONAL CEREBRAL BLOOD FLOW,AND ELECTROENCEPHALOGRAM ABNORMALITIES IN CHILDREN WITH DOWN’S SYNDROME

The aim of this study was to investigate possible correlations of the cognitive impairment with abnormalities of regional cerebral blood flow and electroencephalogram in children with (Down's Syndrome) DS. Nine patients with DS were evaluated by single photon emission computed tomography (SPECT) in combination with clinical findings, electroencephalography (EEG), and magnetic resonance imaging (MRI). In cases with IQs below 40, there were one or more findings of abnormal EEG/MRI and brain perfusion SPECT. In 6 cases (66.7%) EEG findings were normal, but 3 (33.3%) had abnormal EEG findings. Perfusion abnormalities were most pronounced in the fronto-parieto-temporal region in the form of hypoperfusion (n = 5) and in the right hemisphere (n = 5) than the left hemisphere (n = 1). These findings suggest that the children with DS had varying levels of structural, perfusion, and electrophysiological abnormalities in the brain and these abnormalities were reflected by measurable alterations of the cognitive functions.     

TRIORTHOCRESYL PHOSPHATE–INDUCED NEURONAL LOSSES IN LUMBAR SPINAL CORD OF HENS—AN IMMUNOHISTOCHEMISTRY AND ULTRASTRUCTURE STUDY

To investigate the neuronal losses of hens’ spinal cords in the model of organophosphate-induced delayed neuropathy (OPIDN) and to analyze the impact of apoptosis on the pathogenesis of OPIDN. Adult hens were challenged with triorthocresyl phosphate (TOCP) at a single dose (750 mg/kg). Neuronal losses in the 3rd lumbar spinal cord (L3) were assessed by light-microscopy and electron-microscopy methods at different days post exposure, respectively. The typical OPIDN signs were seen in the TOCP-exposed hens at about 9th day. The number of large nerve cells declined gradually. And these cells were verified as neurons by immunostained with neuronal marker NeuN. The expression of FasL reached proximal at about 9th day, decreased from 14th day. Neurons in TOCP exposed groups displayed degenerative morphologies in electronic microscopy. Some neurons showed apoptotic-like ultrastructure profiles at 5th day. The nuclear membrane was complete with chromatin condensed to the margins of nuclear membrane like a crescent-shaped body. Mitochondria morphologic changes appeared early (5 d) following exposure to TOCP, and developed in a time-dependent fashion. Apoptosis might be involved in the development of OPIDN, and play a role in the pathogenesis of OPIDN.