Acta Neurobiologiae Experimentalis 

About: Acta Neurobiologiae Experimentalis is an academic journal published by Nencki Institute of Experimental Biology. The journal publishes majorly in the area(s): Hippocampal formation & Hippocampus. It has an ISSN identifier of 0065-1400. It is also open access. Over the lifetime, 2582 publications have been published receiving 38575 citations.

Secondary injury mechanisms in traumatic spinal cord injury: a nugget of this multiply cascade

Abstract: The pathophysiology of acute spinal cord injury (SCI) involves primary and secondary mechanisms of injury. Though both mechanisms are involved in the neurological dysfunction in SCI most research however has focused on understanding the pathophysiology of the secondary damage and reducing the amount of delayed cell loss following SCI. Research has revealed extensive therapeutic windows in secondary injury mechanisms that could be manipulated by appropriate exogenous interventions. In contrast, primary injury to the cord happens unexpectedly, and it is associated with inevitable delays; ranging from several hours to days before care intervention is administered. Therefore, apart from achieving patient's stabilization, the therapeutic window in the primary phase of injury is essentially obliterated, and consequently inaccessible for specialized. Coupled to this, the exacerbating effect of secondary injury mechanisms has generally commenced before the specialist intervention. Hence, knowledge of secondary injury mechanisms and their intricacies are invaluable requisite for any tailored therapeutic strategy in the persistent search for a cure of SCI. There are about 25 well-established secondary injury mechanisms in SCI, and are found in bits or clusters in literature. A vast number of these articles are not open access. Besides, articles with a comprehensive catalog of these mechanisms are not readily available. This article has cataloged over twenty five identified secondary mechanisms of injury in the spinal cord in an open access portal, and is particularly versatile for starters in spinal cord injury research.

In vitro models of the blood-brain barrier.

Abstract: The blood-brain barrier (BBB) is an active interface between the circulation and the central nervous system (CNS) with a dual function: the barrier function restricts the transport from the blood to the brain of potentially toxic or harmful substances; the carrier function is responsible for the transport of nutrients to the brain and removal of metabolites. The BBB plays a crucial role in the clinical practice as well. On the one side there is a large number of neurological disorders including cerebral ischemia, brain trauma and tumors, neurodegenerative disorders, in which the permeability of the BBB is increased. On the other hand due to the relative impermeability of the barrier many drugs are unable to reach the CNS in therapeutically relevant concentration, making the BBB one of the major impediments in the treatment of CNS disorders. The significant scientific and industrial interest in the physiology and pathology of the BBB led to the development of several in vitro models of the BBB. These models are mainly based on the culture of cerebral endothelial cells. The best in vitro models which mimic the best way the in vivo anatomical conditions are the co-culture models in which brain endothelial cells are co-cultured with astrocytes and/or pericytes. Our in vitro BBB model is characterized by high transendothelial electrical resistance (TEER regularily above 200 Ohm x cm(2)), low permeability and expression of several transporters. Our experiments have proven that the model is suitable for basic research and for testing the interaction between the BBB and potential drug candidates (toxicity, permeability, interaction with efflux transporters) as well.

Neuroplasticity and cellular resilence in mood disorder

Abstract: Although mood disorders have traditionally been regarded as good prognosis diseases, a growing body of data suggests that the long-term outcome for many patients is often much less favorable than previously thought. Recent morphometric studies have been investigating potential structural brain changes in mood disorders, and there is now evidence from a variety of sources demonstrating significant reductions in regional CNS volume, as well as regional reductions in the numbers and/or sizes of glia and neurons. Furthermore, results from recent clinical and preclinical studies investigating the molecular and cellular targets of mood stabilizers and antidepressants suggest that a reconceptualization about the pathophysiology and optimal long-term treatment of recurrent mood disorders may be warranted. It is proposed that impairments of neuroplasticity and cellular resilience may underlie the pathophysiology of mood disorders, and further that optimal long-term treatment for these severe illnesses may only be achieved by the early and aggressive use of agents with neurotrophic/ neuroprotective effects. It is noteworthy that lithium, valproate and antidepressants indirectly regulate a number of factors involved in cell survival pathways including CREB, BDNF, bcl-2 and MAP kinases, and may thus bring about some of their delayed long-term beneficial effects via underappreciated neurotrophic effects. The development of novel treatments which more directly target molecules involved in critical CNS cell survival and cell death pathways have the potential to enhance neuroplasticity and cellular resilience, and thereby modulate the long-term course and trajectory of these devastating illnesses.

A re-evaluation of the effects of lesions of the pontine tegmentum and locus coeruleus on phenomena of paradoxical sleep in the cat.

Abstract: Bilateral lesions placed in the pontiene tegmentum resulted in episodes of paradoxical sleep in which the characteristic atonia of that sleep stage was absent in six cats Following each period of synchronized sleep, in which the degree of muscle tone of the dorsal cervical muscles gradually diminished, cats with such lesions would slowly raise their heads, move their limbs at all joints, make several attempts to rise and eventually leap violently During such episodes they were unresponsive to strong lights, touching and mild pinching Only sound would arouse them This behavior appeared as early as the 2nd postoperative day, the 1st day of recording Such episodes supplanted normal paradoxical sleep with atonia and lasted unchanged for as long as 6 months in one cat until it was killed while still in good health Complete recovery of atonia was observed in one cat after 3 weeks Either no recovery or else eventual recovery to excessively active periods of paradoxical sleep while remaining recumbent characterized the sleep of the other four The conclusion drawn from these experiments and from a review of the literature is that the hypotheses stating that the locus coeruleus or other isolated nuclei of the pons are specifically concerned with the initiation of paradoxical sleep are not clearly supported by available evidence