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Shahriar Gharibzadeh

Publications and source records attributed to Shahriar Gharibzadeh.

16 recordsLinked to original sources
PubMed2006

Adjustable primitive pattern generator: a novel cerebellar model for reaching movements.

Cerebellum has been assumed as an array of adjustable pattern generators (APGs). In recent years, electrophysiological researches have suggested the existence of modular structures in spinal cord called motor primitives. In our proposed model, each "adjustable primitive pattern generator" (APPG) module in the cerebellum is consisted of a large number of parallel APGs, the output of each module being the weighted sum of the outputs of these APGs. Each spinal field is tuned by a coefficient, representing a descending supraspinal command, which is modulated by ith APPG correspondingly. According to this model, motor control can be interpreted in terms of the modification of these coefficients. Vector summation of force fields implies that the complex nonlinearities in neuronal behavior are eliminated, causing our model to be simple and linear. The force field vectors, derived from motor primitives, depend on the state of movement and its derivative and the time that causes different repertoire of movement. This is physiologically plausible. Our model agrees with virtual trajectory hypothesis, stating that dynamics are not computed explicitly in central nervous system, but the desired trajectory, is fed into the spinal cord. We think that the dysmetria and the ataxia seen in some cerebellar diseases may be the result of local disruption of some APPGs. Accordingly, determining the exact location of related motor primitives in human spinal cord and stimulating them by functional neurostimulation may provide a good management for these clinical signs. Surely, experimental researches and clinical trials are needed to validate our hypothesis.

Animals↗
PubMed2006

The chaotic nature of temper in humans: a long short-term memory recurrent neural network model.

In mathematics and physics, chaos theory deals with the behavior of certain nonlinear dynamical systems that under certain conditions exhibit a phenomenon known as chaos, which is characterised by a sensitivity to initial conditions. Mathematicians paradoxically call such states of order chaos and distinguish them from randomness. New models for describing and predicting different aspects of behavior are being created which once seemed unpredictable. This is done by focusing on the overall patterns of behavior, showing how stable or unstable they are and identifying the circumstances that make them change. In this paper, we indicate why human temper and mood changes have a chaotic nature. Then, we develop a chaotic model based on a long short-term memory recurrent neural network with irregular embeddings derived by the gamma test to model temper tantrum. We finally use a feedback delay controller to stabilize its chaotic behavior, because it is a plausible method for stabilizing biological neural systems. A lot of aspects of this model are analogous to the human counterpart. The model might suggest, for example, that if a particular person had stronger ego defenses, and attended a little less vigilantly to the external world, he or she might find a stable attractor amidst of a broader landscape of chaotic attractors. A therapist or self-control would be analogous to the delayed feedback controller, by specifically encouraging those changes, he might help the person reach a stable behavior. Finally, some comments are proposed to facilitate the normal behavior.

Computer Simulation↗
PubMed2006

A cybernetic view on wind-up.

Wind-up is described traditionally as a frequency dependent increase in the excitability of spinal cord neurons, evoked by electrical stimulation of afferent C-fibers. Different kinds of wind-up have been reported, but wind-up of Abeta fibers in hyperalgesic states has gained little attention. In this paper, we present a cybernetic view on Abeta fiber wind-up and consider the involved molecular mechanisms as feedback and feedforward processes. Furthermore, our previous hypothesis, the sprouting phenomenon, is included in this view. Considering the proposed model, wind-up in hyperalgesic states might leave out in three different ways: (1) blocking the NMDA receptors by increasing extracellular Mg2+, 2) blocking the receptors and channels that contribute to Ca2+ inward current, and 3) blocking the Abeta fibers by local anesthetics. It seems that wind-up may be inhibited more effectively by using these three blocking mechanisms simultaneously, because in this case, the feedback process (main controller), the feedforward process (trigger), and Abeta stimulation (trigger) would be inhibited concurrently. Wind up may aggravate the pain in clinical hyperalgesic situations such as post-surgical states, some neuropathic pains, fibromyalgia syndrome, and post-herpetic neuralgia. Surely, clinical studies are needed to validate the effectiveness of our abovementioned suggestions in relieving such clinical pains.

Anesthetics, Local↗
PubMed2006

Dynamic behavior of gap junctions in each cardiac cycle: a novel view on the electrical coupling of normal cardiocytes.

Two main mechanisms have been suggested for the propagation of action potentials in cardiac muscle cells: (1) the free flow of local circuit current through gap junctions and (2) the effect of electrical field. Different evidences confirm each of two mechanisms. We think that gap junctions are not continuously open in a normal heart cycle; instead, they open and close intermittently. In other words, gap junction has a dynamic behavior in each cardiac cycle, managing different routes of propagation in the diverse moments of normal cycle. Gap junctions could be open in phases 0, 1, 3, 4 and close in phase 2 (plateau) of action potential. Whenever gap junction is open, conduction can be fulfilled rapidly by current flow and whenever it is closed, the electrical field will be the main route of propagation. When the prejunctional cell is in the peak of action potential(AP), gap junction is closed and the postjunctional cell should use the electrical field to be stimulated. Then, when the prejunctional cell comes to the end of AP, the gap junction opens and current will potentiate the rising phase of AP in the postjunctional cell. Moreover, this process causes accumulation of calcium in the postjunctional cell near phase 2. We believe that our hypothesis on the mechanism of cardiac action potential propagation may have exciting advantages. This novel view on gap junction dynamic behavior may be useful for better exploitation of drugs or designing new remedies in arrhythmias. We also hypothesize that in conditions as cardiac failure, in which cardiac contractility is diminished and increasing intracellular calcium concentration is needed, gap junction closing drugs may be effective. It is worth noting that future clinical studies are needed to validate these predictions.

Action Potentials↗
PubMed2005

Sprouting phenomenon, a new model for the role of A-beta fibers in wind up.

Wind up is a progressive frequency-dependent facilitation of the responses of nociceptive neurons observed on the application of repetitive (usually electrical) stimuli of constant intensity. The NMDA and NK1 receptors are essentially involved in wind up. After induction of wind up, stimulation of C-fibers show the characteristics of wind up, but stimulation of Abeta fibers for induction of wind up is controversial. In this study, we have proposed a new model for the role of Abeta fibers in wind up, through sprouting of nerve fibers in the dorsal horn of spinal cord. We named it "sprouting phenomenon". It has been reported that in some clinical hyperalgesic states induced by peripheral injury or inflammation, wind up may aggravate the pain. For example, studies have indicated the presence of wind up in post-surgical states, some neuropathic pains, fibromyalgia syndrome, and post-herpetic neuralgia. According to sprouting phenomenon, it seems that some clinical interventions can be assessed to alleviate post-inflammatory pains: (1) Immediate and complete relief of inflammation by anti-inflammatory agents to prevent repetitive excitation of C-fibers and subsequent morphological changes of dorsal horn laminae; (2) using local anesthetics in order to prevent pain signal transmission; (3) prevention of sprouting by intrathecal injection of some anti-proliferation agents; (4) using NMDA or NK1 receptor antagonists to prevent central mechanism of wind up. Some clinical trials have indicated the effectiveness of these antagonists. It is worth noting that future clinical studies are needed to validate these predictions.

Animals↗
PubMed2005

Modeling the Parkinson's tremor and its treatments.

In this paper, we discuss modeling issues of the Parkinson's tremor. Through the work we have employed physiological structure as well as functioning of the parts in brain that are involved in the disease. To obtain more practical similarity, random behaviors of the connection paths are also considered. Medication or treatment of the disease both by drug prescription and electrical signal stimulation are modeled based on the same model introduced for the disease itself. Two new medication strategies are proposed based on the model to reduce the side effects caused by the present drug prescription.

Antiparkinson Agents↗