By X. Marius. Empire State College.
However motilium 10 mg cheap, RSU tuning curves did not show a velocity bias buy motilium 10mg free shipping, as their average tuning curve was symmetric with a peak centered on the peak of vibrissa resonance. This symmetry may be explained as the result of intracortical sharpening by FSU activity – FSUs respond strongly and at a shorter latency to high frequency stimuli, and are, therefore, well positioned to inhibit RSU responses26 (see Figure 2. Whatever the mechanism, excitatory neuron activity in an SI barrel reﬂects the frequency tuning of vibrissa motion amplitude, and not velocity tuning, potentially providing relatively precise frequency coding that reﬂects vibrissa ampliﬁcation. Velocity Sensitivity: Impact on the Representation of Speciﬁc Frequency Bands Diamond and colleagues recently presented a subset of high-frequency stimuli to multiple vibrissae simultaneously while recording MUA activity in SI. We similarly observed that, for a given amplitude of vibrissa stimulation, many single neuron and MUA responses demonstrated high-pass sensitivity in addition to vibrissa resonance tuning (Figure 2. High-pass frequency/velocity sensitivity has several potential impli- cations for the neural representation of vibrissa resonance. First, it suggests that those vibrissae that have a resonance tuning peak closer to the velocity threshold for the neuron being recorded will be more likely to evoke neural activity (Figure 2. Second, those vibrissae with lower fun- damental resonance frequencies will require greater ampliﬁcation to reach the veloc- ity threshold (Figure 2. Third, those * While it remains an open question whether neurons in the vibrissa sensory system are sensitive to “velocity” or to some other factor that co-varies with velocity, we will follow the trend in the literature and will use the term velocity as shorthand for this class of features. This is because of a ceiling effect as these motions are already effective in driving robust neural activity and there is little dynamic range in the mean ﬁring rate remaining to allow the expression of resonance-related tuning (Figure 2. An important implication of this framework is that, for any given amplitude of stimulation, vibrissae with intermediate resonance tuning frequencies may be in the proper range to evoke neural resonance tuning. In our previous experiments, pre- liminary data suggested that the 1 to 3 arcs demonstrated the highest incidence of observable resonance-related neural tuning and that MUA responses showed the greatest sensitivity to these velocity interactions, i. A second implication of the apparent saturation of mean ﬁring rate at high velocities of stimulation is that a secondary coding mechanism, beyond resonance or velocity sensitivity — e. HIGHER HARMONICS: IMPLICATIONS FOR THE VIBRISSA RESONANCE HYPOTHESIS Higher harmonics of vibrissa motion may also generate high frequency/high velocity input to the vibrissa sensory system. In our previous studies,26,28 we did not system- atically characterize higher harmonics for a variety of study-design and methodolog- ical reasons.
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In the and one parent with a single defective NEU1 gene will United States discount motilium 10 mg fast delivery, it is estimated to occur in one out of every inherit at least one defective NEU1 gene purchase motilium 10 mg with mastercard. In Australia, the estimate is one out a 50% chance of inheriting two defective genes and, of 4. Since neuraminidase deficiency is an auto- therefore, developing neuraminidase deficiency. The off- somal rather than a sex-linked disorder, it occurs equally spring of one parent with neuraminidase deficiency and in males and females. The offspring of parents who deficiency requires two copies of the defective gene, one both carry one defective NEU1 gene have a 50% chance inherited from each parent. Thus, neuraminidase defi- of inheriting one defective NEU1 gene and a 25% chance ciency is much more common in the offspring of couples of inheriting two genes and developing neuraminidase who are related to each other (consanguineous mar- deficiency. Finally, the children of one parent with a sin- riages), such as first or second cousins. Type 2 sialidosis seems to occur more frequently defective gene, but will not develop neuraminidase defi- among Japanese. Signs and symptoms Mutations in the NEU1 gene The clinical symptoms of neuraminidase deficiency A number of different mutations that can cause neu- are similar to the symptoms of the mucolipidoses, includ- raminidase deficiency have been identified in the NEU1 ing I-cell disease (mucolipidosis II) and pseudoHurler gene. The type of neuraminidase deficiency, sialidoses polydystrophy (mucolipidosis III). Furthermore, the clin- types I or II, as well as the severity of the symptoms, ical distinctions between sialidoses types I and II may not depends on the specific mutation(s) that are present. Some mutations change one amino acid out of the 415 amino acids that compose a single neuraminidase mole- Sialidosis type I cule. Many of the identified mutations are clustered in The symptoms of sialidosis type I do not appear until one region on the surface of the protein. Infants and children with this result in a sharp reduction in the activity of the enzyme form of neuraminidase deficiency may have a normal 804 GALE ENCYCLOPEDIA OF GENETIC DISORDERS appearance and grow normally until adolescence. At that time, the appearance of red spots in both eyes, known as KEY TERMS cherry-red macules or cherry-red macular spots, may be one of the first symptoms of neuraminidase deficiency. Dysostosis multiplex—A variety of bone and Eventually, color and/or night blindness may develop.