Neuron cell are built from a myriad of axon and dendrite structures. It transmits electrochemical signals between the brain and the nervous system. Three-dimensional visualization of neuron structure could help to facilitate deeper understanding of neuron and its models. An accurate neuron model could aid understanding of brain's functionalities, diagnosis and knowledge of entire nervous system. Existing neuron models have been found to be defective in the aspect of realism. Whereas in the actual biological neuron, there is continuous growth as the soma extending to the axon and the dendrite; but, the current neuron visualization models present it as disjointed segments that has greatly mediated effective realism. In this research, a new reconstruction model comprising of the Bounding Cylinder, Curve Interpolation and Gouraud Shading is proposed to visualize neuron model in order to improve realism. The reconstructed model is used to design algorithms for generating neuron branching from neuron SWC data. The Bounding Cylinder and Curve Interpolation methods are used to improve the connected segments of the neuron model using a series of cascaded cylinders along the neuron's connection path. Three control points are proposed between two adjacent neuron segments. Finally, the model is rendered with Gouraud Shading for smoothening of the model surface. This produce a near-perfection model of the natural neurons with attended realism. The model is validated by a group of bioinformatics analysts' responses to a predefined survey. The result shows about 82% acceptance and satisfaction rate.
The fundamental pattern of chewing induced by the network of neurons called central pattern generator has been reported
to be modified by the information arising from the various oro-facial sensory receptors including muscle spindles of jaw
closing muscles. The cell bodies of primary afferent neurons from these muscle spindles lie in mesencephalic trigeminal
nucleus (MTN) in the brainstem. The aim of the study was to understand whether muscle spindles from jaw-closing
muscles play any role in hard food chewing. Single neuronal discharge of muscle spindle afferents was recorded from the
MTN simultaneous with jaw-movement and electromyograpic (EMG) activities of the left masseter (jaw-closing) muscle
during chewing soft and hard foods (apple and pellet) in awake rabbits. Ten consecutive chewing cycles were taken for
analysis. Discharge of nineteen muscle spindles from seven rabbits was successfully recorded. Muscle-spindle discharge
was significantly higher during the closing phase of jaw-movement for the hard food chewing than for the soft food. The
jaw-closing muscle EMG activity was significantly higher during hard food chewing compared to soft food. The spindle
discharge was higher when the masseter muscle activity was greater for chewing hard food. Significant positive (r=0.822,
p=<0.001) correlation was found between the difference of muscle activity between apple and pellet and the difference
of spindle discharge between apple and pellet. Above findings suggest that the increase of spindle discharge during
hard food chewing may play a role for facilitating jaw-closing muscle activities and thereby provides servo-assistance
to jaw-closing muscles to compensate the hardness of food.
Kisspeptin is a hypothalamic neuropeptide, which acts directly on gonadotropin-releasing hormone (GnRH)-secreting neurons via its cognate receptor (GPR54 or Kiss-R) to stimulate GnRH secretion in mammals. In non-mammalian vertebrates, there are multiple kisspeptins (Kiss1 and Kiss2) and Kiss-R types. Recent gene knockout studies have demonstrated that fish kisspeptin systems are not essential in the regulation of reproduction. Studying the detailed distribution of kisspeptin receptor in the brain and pituitary is important for understanding the multiple action sites and potential functions of the kisspeptin system. In the present study, we generated a specific antibody against zebrafish Kiss2-R (=Kiss1Ra/GPR54-1/Kiss-R2/KissR3) and examined its distribution in the brain and pituitary. Kiss2-R-immunoreactive cell bodies are widely distributed in the brain including in the dorsal telencephalon, preoptic area, hypothalamus, optic tectum, and in the hindbrain regions. Double-labeling showed that not all but a subset of preoptic GnRH3 neurons expresses Kiss2-R, while Kiss2-R is expressed in most of the olfactory GnRH3 neurons. In the posterior preoptic region, Kiss2-R immunoreactivity was seen in vasotocin cells. In the pituitary, Kiss2-R immunoreactivity was seen in corticotropes, but not in gonadotropes. The results in this study suggest that Kiss2 and Kiss2-R signaling directly serve non-reproductive functions and indirectly subserve reproductive functions in teleosts.
Selective serotonin reuptake inhibitors (SSRIs) are widely used antidepressants for the treatment of depression. However, SSRIs cause sexual side effects such as anorgasmia, erectile dysfunction, and diminished libido that are thought to be mediated through the serotonin (5-hydroxytryptamine, 5-HT) system. In vertebrates, gonadotropin-releasing hormone (GnRH) neurons play an important role in the control of reproduction. To elucidate the neuroendocrine mechanisms of SSRI-induced reproductive failure, we examined the neuronal association between 5-HT and GnRH (GnRH2 and GnRH3) systems in the male zebrafish. Double-label immunofluorescence and confocal laser microscopy followed by three-dimensional construction analysis showed close associations between 5-HT fibers with GnRH3 fibers and preoptic-GnRH3 cell bodies, but there was no association with GnRH2 cell bodies and fibers. Quantitative real-time PCR showed that short-term treatment (2 wk) with low to medium doses (4 and 40 μg/L, respectively) of citalopram significantly decreased mRNA levels of gnrh3, gonadotropins (lhb and fshb) and 5-HT-related genes (tph2 and sert) in the male zebrafish. In addition, short-term citalopram treatment significantly decreased the fluorescence density of 5-HT and GnRH3 fibers compared with controls. Short-term treatment with low, medium, and high (100 μg/L) citalopram doses had no effects on the profiles of different stages of spermatogenesis, while long-term (1 mo) citalopram treatment with medium and high doses significantly inhibited the different stages of spermatogenesis. These results show morphological and functional associations between the 5-HT and the hypophysiotropic GnHR3 system, which involve SSRI-induced reproductive failures.
This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing
oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is
increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source
of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell
stress response, which is a common trigger leading to embryonic cell death. Having more
profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst
implantation, foetal growth, pregnancy outcome and survival of the neonates affected by
nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances
PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-
cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the
number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria.
TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy,
resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented
oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably
minimizing vesicular apoptosis during oocyte maturation. Further extensive research is
required to develop TCTs as a tool in specific therapeutic approaches to overcome the
detrimental effects of OS.
This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell stress response, which is a common trigger leading to embryonic cell death. Having more profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst implantation, foetal growth, pregnancy outcome and survival of the neonates affected by nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria. TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy, resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably minimizing vesicular apoptosis during oocyte maturation. Further extensive research is required to develop TCTs as a tool in specific therapeutic approaches to overcome the detrimental effects of OS.