Journal of Integrative Neuroscience

Exogenous catalase influences neural control of cardiovascular system; however, we do not know yet if its inhibition into the fourth cerebral ventricle (4^th V) influences baroreflex regulation. We evaluated the effects of central catalase inhibition on baroreflex in conscious Wistar rats. We used males Wistar rats (320–370 g), which were implanted with a stainless steel guide cannula into 4^th V. The femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. After basal MAP and HR recordings, the baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Baroreflex was evaluated before 5, 15, 30 and 60 minutes after 3-amino-1, 2, 4-triazole (ATZ, 0.001 g/100 μL) injection into the 4^th V. Vehicle treatment did not change baroreflex responses. ATZ attenuated bradycardic peak and reduced HR range at 30 minutes. ATZ into the 4^th V reduced bradycardic and tachycardic reflex responses to increase and decrease MAP, respectively (p < 0.05) 30 minutes after its microinjection without significantly changing the basal MAP and HR. In conclusion, central catalase inhibition influenced the highest parasympathetic response to MAP increase in conscious Wistar rats without change baroreflex gain.

It has been proposed, particularly in connection with dyslexia and schizophrenia, that motion perception can be used to assess magnocellular integrity. This suggestion is examined in this paper. The following observations are made: (1) motion information, i.e., information about direction and speed, is extracted at the cortical level, (2) the magnocellular system provides input to the motion selective cortical entities, and (3) so do the parvo- and koniocellular systems. Therefore, although the magnocellular system clearly has the ability to influence motion perception so do other parts of the visual system, e.g., cortical mechanisms. It is concluded that motion perception by itself is not a reliable test of magnocellular integrity.

Schizophrenia, it has been hypothesized, is linked to a deficiency in the magnocellular portion of the visual system. Abnormal backward masking has been invoked as support for this hypothesis. The rationale for linking backward masking to the magnocellular system is the hypothesis that fast responses in the magnocellular systems catches up with, and then inhibits slower responses in the parvocellular system. However, the latency difference between the magno- and parvocellular systems is at most 20 ms. Magnocellular abnormalities as a result would be expected to manifest themselves only at relatively short stimulus onset asynchronies (SOAs) or interstimulus intervals (ISIs). The present study examines this implication. It is found that a substantial number of investigations have uncovered abnormal masking at SOAs or ISIs of 300 ms or larger, and some even at ISIs as large as 700 ms. It is difficult to reconcile abnormalities at these SOAs and ISIs with magno-parvocellular latency differences of 20 ms or less. It is concluded that the abnormal masking does not support the existence of a magnocellular deficiency in schizophrenia.

Recently, we put forward a redox molecular hypothesis involving the natural biophysical substrate of visual perception and imagery. Here, we explicitly propose that the feedback and feedforward iterative operation processes can be interpreted in terms of a homunculus looking at the biophysical picture in our brain during visual imagery. We further propose that the brain can use both picture-like and language-like representation processes. In our interpretation, visualization (imagery) is a special kind of representation i.e., visual imagery requires a peculiar inherent biophysical (picture-like) mechanism. We also conjecture that the evolution of higher levels of complexity made the biophysical picture representation of the external visual world possible by controlled redox and bioluminescent nonlinear (iterative) biochemical reactions in the V1 and V2 areas during visual imagery. Our proposal deals only with the primary level of visual representation (i.e. perceived "scene").

In this paper we argue that, in addition to electrical and chemical signals propagating in the neurons of the brain, signal propagation takes place in the form of biophoton production. This statement is supported by recent experimental confirmation of photon guiding properties of a single neuron. We have investigated the interaction of mitochondrial biophotons with microtubules from a quantum mechanical point of view. Our theoretical analysis indicates that the interaction of biophotons and microtubules causes transitions/fluctuations of microtubules between coherent and incoherent states. A significant relationship between the fluctuation function of microtubules and alpha-EEG diagrams is elaborated on in this paper. We argue that the role of biophotons in the brain merits special attention.

To expand our studies on the mechanisms underlying the clinical decline of the nerve excitability properties in patients with hereditary demyelinating neuropathies, the contribution of myelin sheath aqueous layers on multiple membrane properties of simulated fiber demyelinations is investigated. Three progressively greater degrees of internodal systematic demyelinations (two mild and one severe termed as ISD1, ISD2 and ISD3, respectively) without/with aqueous layers are simulated using our previous multi-layered model of human motor nerve fiber. The calculated multiple membrane excitability properties are as follows: potentials (intracellular action, electrotonic), strength-duration time constants, rheobasic currents and recovery cycles. They reflect the propagating, accommodative and adaptive processes in the fibers. The results show that all membrane properties, except for the strength-duration time constants and refractoriness, worsen when the myelin lamellae and their corresponding aqueous layers are uniformly reduced along the fiber length. The effect of the aqueous layers is significantly higher on the accommodative and adaptive processes than on the propagating processes in the fibers. Our multi-layered model better approximated some of the functional deficits documented for axons of patients with Charcot-Marie-Tooth disease type 1A. The study provides new and important information on the mechanisms underlying the pathophysiology of hereditary demyelinating neuropathies.

Recently, patients with chronic demyelinating neuropathies have demonstrated significant abnormalities in their multiple nerve excitability properties measured by a non-invasive threshold tracking technique. In order to expand our studies on the possible mechanisms underlying these abnormalities, which are not yet well understood, we investigate the contributions of the aqueous layers within the myelin sheath on multiple membrane properties of simulated fibre demyelinations. Four degrees of systematic paranodal demyelinations (two mild demyelinations termed PSD1 and PSD2, without/with aqueous layers respectively, and two severe demyelinations termed PSD3 and PSD4, with/without aqueous layers, respectively) are simulated using our previous multi-layered model of human motor nerve fibre. We studied the following parameters of myelinated axonal function: potentials (intracellular action, electrotonic — reflecting the propagating and accommodative fibre processes, respectively) and strength-duration time constants, rheobases, recovery cycles (reflecting the adaptive fibre processes). The results show that each excitability parameter is markedly potentiated when the aqueous layers within their paranodally demyelinated sheaths are taken into account. The effect of the aqueous layers is significantly higher on the propagating processes than on the accommodative and adaptive processes in the fibres. The aqueous layers restore the action potential propagation, which is initially blocked when they are not taken into account. The study provides new and important information on the mechanisms of chronic demyelinating neuropathies, such as chronic inflammatory demyelinating polyneuropathy (CIDP).

One of the problems in imaging from brain tissues is light-scattering. Thus, multiphoton laser scanning microscopy is widely used to optically access fluorescent signals located deeply in tissues. Here we report that Nipkow-type spinning-disk one-photon confocal microscopy, which embodies high temporal resolution and slow photobleaching, is also capable of imaging tissues to a depth of up to 150 μm. Using a Nipkow-disk microscope, we conducted functional multi-cell calcium imaging of CA3 neurons from in toto intact hippocampal preparations and astrocytes from in vivo neocortical layer 1. This novel application of Nipkow-disk microscopy expands the potential usefulness of this type of microscopy and will contribute to our understanding of natural neuronal microcircuitry.