Critical Reviews in Neurobiology (Crit Rev Neurobiol )

Publisher: Begell House

Description

Critical Reviews in Neurobiology presents up-to-date information from pertinent neurobiological disciplines with relevance to basic neuroscience, clinical neurobiology, and psychiatric considerations. Developmental neurobiology and the neurobiology of the aging are included. The journal integrates wide-ranging, often contradictory literature in a focused manner. Articles satisfy the needs of basic neuroscience researchers, as well as allowing clinicians to keep abreast of the scientific basis of neurology and allied medical areas. The Journal provides a means of placing basic science information into clinical perspective, speaking directly to the issues that have become prominent during the past decade. Critical Reviews in Neurobiology provides focus by reviewing significant contributions from a wide range of disciplines in the context of their impact on important clinical problems.

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  • Website
    Critical Reviews in Neurobiology website
  • Other titles
    Critical reviews in neurobiology, Chemical Rubber Company critical reviews in neurobiology, CRC critical reviews in neurobiology
  • ISSN
    0892-0915
  • OCLC
    15076105
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Begell House

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    • Archiving status unclear
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    • Author cannot archive a post-print version
  • Conditions
    • Deposit in institutional repositories is not allowed
    • NIH Authors can deposit in PubMed Central for public release after 12 month embargo
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    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: This article attempts to show why classical conceptual views of the brain that can be found in any neuroscience textbook are not capable of providing an adequate explanation of brain-initiated normal and pathological behaviors and why the classical view should therefore be replaced with a new concept of the brain. The major reason for the inadequacy of the classical model is its explanation of the relationship between structure and function in the brain. This article introduces a new brain concept based on two discoveries: the discovery of the neural network computational principle and the discovery of the generic functional organization of hierarchical neural optimal control systems. A neural optimal control system is a learning system that possesses a model of the behavior of its controlled object. A hierarchy of neural optimal control systems is functionally organized in such a way that a higher level neural optimal control system treats a lower one as its controlled object and creates a model of its behavior. The ability of the new conceptual brain model to explain brain mechanisms of normal and pathological behaviors is demonstrated through the examples of spinal reflexes and central pattern generators, the cerebellum, skeletomotor cortico-basal ganglia-thalamocortical loop, and Parkinson's disease and some other brain disorders. In this article, a new understanding of the relationship between structure and function in the brain is introduced. This article also discusses organizational and educational changes in the neurosciences that may be necessary to accelerate a broad acceptance of this new concept of the brain.
    Critical Reviews in Neurobiology 02/2009; 19(2-3):119-202.
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    ABSTRACT: Specific effects of the dopamine synaptic transmission modulator on the activity of sensomotor cortical neurons in a wakeful animal, performing a conditioned reflex are discussed. First, specific responses in the neocortical neurons after application of glutamate agonists and antagonists and gamma aminobutyric acid are described and then the effect of dopamine, its agonists and antagonists and amantadine, a dopamine releaser, on the background and induced pulse activities in the cortical neurons, as well as on specific characteristics of conditioned reflex motor responses, such as latency and intensity are analyzed in detail.
    Critical Reviews in Neurobiology 01/2008; 20(1-3):1-141.
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    ABSTRACT: Intermediate filaments (IFs), along with microfilaments and microtubules, comprise the three intracellular filaments identified in eukaryotic cells to date. Together, these three distinct filamentous networks act in a dynamic and tightly interconnected fashion to comprise the eukaryotic cytoskeleton. As such, they are involved in a number of essential and diverse cellular processes, including division, molecular transport, and the maintenance of structural integrity in the face of mechanical stress. Underscoring the ubiquitous importance of IF proteins to the normal function of cellular systems, mutations in IF-encoding genes that affect the structure, function, or regulation of these proteins are commonly found in association with a range of heritable genetic diseases. The diversity of IF-related disease is indeed as wide as the distribution of IF proteins themselves, effecting the development of a broad range of disease phenotypes. Here we review, with specific reference to recent developments in the correlation of genotype with phenotype, how the perturbation of IF networks can elicit the development of human neurological disease.
    Critical Reviews in Neurobiology 02/2007; 19(1):1-27.
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    ABSTRACT: Delta-9-tetrahydrocannabinol (THC) is the primary psycho-active ingredient in Cannabis spp., the most widely used illicit drug in the United States. THC is an exogenous agonist of the central cannabinoid receptor (CB1), one of the most abundant G-coupled receptors in the mammalian brain. Although CB1 receptors are distributed throughout the brain, they are found at very high levels in the cerebellum. Despite the variety of disturbances associated with acute cannabis intoxication, including altered short-term memory, dissociation of thoughts, motor impairments, and paranoia, among others, a reliable index of cannabinoid system function has in large part eluded scientists. Thus, there is a demand in contemporary clinical neuroscience for methods sensitive to cannabinoid system function, not only for assessing how cannabis use influences human information processing, but also to assess the involvement of the endocannabinoid system (ECS) in clinical disease and evaluate the effects of CB1-based drug therapies. The purpose of the present article, therefore, is to address this current need by integrating two separate literatures. The first literature demonstrates that the ECS mediates synaptic plasticity, specifically, long-term depression (LTD) of parallel fibers at the parallel fiber-Purkinje junction in the cerebellar cortex. The second literature suggests that LTD at this junction is necessary for the acquisition of the primary dependent variable in delay eyeblink conditioning (EBC)--the exhibition of temporally measured conditioned responses. These two literatures are integrated by proposing an updated EBC circuit that incorporates the CB1 receptor and the endogenous cannabinoids. Finally, the implications of the model is discussed in consideration of recent evidence from CB1 knockout mice, human cannabis users, and schizophrenia patients, with the expectation that translational research on the cannabinoid system will be advanced.
    Critical Reviews in Neurobiology 02/2007; 19(1):29-57.
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    ABSTRACT: Methylphenidate is the drug most often used to treat attention deficit/hyperactivity disorder (ADHD), a common behavioral disorder of children and young adults. The objectives of this study are (1) to use two different experimental assays of measuring animal activity--the wheel-running activity and the computerized open field--to establish which is more sensitive to acute and repetitive methylphenidate (MPD) administration and (2) to determine whether repetitive MPD treatment elicits adverse effects such as tolerance and behavioral sensitization. The dose-response protocol of MPD (0.6, 2.5, and 10.0 mg/kg) administration was performed in three groups of animals, with an additional saline control group as follows: single saline injection as the control/baseline followed by 6 consecutive days of MPD injections (0.6, 2.5, or 10.0 mg/kg MPD), 3 days of washout, and a day of MPD rechallenge. In general, the two different activity assays showed similar observations for the acute effect of MPD by eliciting increases in activity in a dose-dependent manner. The groups receiving repetitive 0.6 and 2.5 mg/kg MPD tested in the open-field assay exhibited further increase in activity that can be interpreted as behavioral sensitization, whereas the groups receiving 10 mg/kg MPD exhibited a reduction in activity, suggesting that tolerance was developed to the drug. All the groups (0.6, 2.5, and 10.0 mg/kg MPD) tested following repetitive MPD in the wheel-running assay exhibited a further increase in their activity, for example, all the groups exhibited behavioral sensitization. These different observations were interpreted as potentially measuring different kinds of locomotor activity.
    Critical Reviews in Neurobiology 02/2007; 19(1):59-77.
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    ABSTRACT: Inflammation is a defense reaction against diverse insults that serves to remove noxious agents and to limit their detrimental effects. There is increasing evidence that post-ischemic inflammation plays an important role in brain ischemia. However, whether inflammatory processes are deleterious or beneficial to recovery is presently a matter of debate and controversy. Experimentally and clinically, stroke is followed by an acute and a prolonged inflammatory response characterized by the production of inflammatory cytokines, leukocyte and monocyte infiltration in the brain, and the activation of resident glial cells. These events may contribute to ischemic brain injury. Several groups report conflicting results regarding the role of inflammation and effects of anti-inflammatory treatments in cerebral ischemia. Experimental studies employing knockout mice for different cytokines and chemokines provide only partial answers. This highlights the importance of clarifying the role of the immune response in pathological changes at the site of ischemic lesions in the brain. Here, we describe dual effects of the brain's inflammatory response and new evidence for a neuroprotective role of proliferating microglial cells in ischemia. In addition, we discuss a potential role of post-ischemic inflammation in brain regeneration and modulation of synaptic plasticity.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):145-57.
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    ABSTRACT: Thin acute slices and dissociated cell cultures taken from different parts of the brain have been widely used to examine the function of the nervous system, neuron-specific interactions, and neuronal development (specifically, neurobiology, neuropharmacology, and neurotoxicology studies). Here, we focus on an alternative in vitro model: brain-slice cultures in roller tubes, initially introduced by Beat Gähwiler for studies with rats, that we have recently adapted for studies of mouse cerebellum. Cultured cerebellar slices afford many of the advantages of dissociated cultures of neurons and thin acute slices. Organotypic slice cultures were established from newborn or 10-15-day-old mice. After 3-4 weeks in culture, the slices flattened to form a cell monolayer. The main types of cerebellar neurons could be identified with immunostaining techniques, while their electrophysiological properties could be easily characterized with the patch-clamp recording technique. When slices were taken from newborn mice and cultured for 3 weeks, aspects of the cerebellar development were displayed. A functional neuronal network was established despite the absence of mossy and climbing fibers, which are the two excitatory afferent projections to the cerebellum. When slices were made from 10-15-day-old mice, which are at a developmental stage when cerebellum organization is almost established, the structure and neuronal pathways were intact after 3-4 weeks in culture. These unique characteristics make organotypic slice cultures of mouse cerebellar cortex a valuable model for analyzing the consequences of gene mutations that profoundly alter neuronal function and compromise postnatal survival.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):179-86.
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    ABSTRACT: Acute cocaine toxicity is frequently associated with seizures. The mechanisms underlying the convulsant effect of cocaine are not well understood. Previously, we have shown that cocaine depresses whole-cell current evoked by gamma-aminobutyric acid (GABA) in hippocampal neurons freshly isolated from rats. Cocaine's effect was voltage-independent and concentration-dependent. In the present study, using whole-cell patch-clamp recording on rat neurons freshly isolated from hippocampus, we examined the intracellular mechanisms involved in cocaine's action. Increasing intracellular Ca(2+) concentration ([Ca]i) from 0.01 to 5 microM strongly increased the depressant effect of cocaine. By contrast, 1-[N, O-bis (5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62), a specific antagonist of Ca/calmodulin-dependent protein kinase (CaMKII), attenuated or enhanced cocaine's action in different neurons: in three out of nine neurons dialysed with 5 microM KN-62,1 mM cocaine depressed GABA current by only 33%, but in another three out of nine neurons, cocaine depressed GABA current by as much as 83%. Chelerythrine (a specific CaCa(2+)/phospholipid-dependent protein kinase C [PKC] antagonist) had minimal effect on cocaine's action. We suggest that cocaine induces an increase in [Ca]i, which stimulates phosphatase activity and thus leads to dephosphorylation of GABA receptors. This dephosphorylation-mediated disinhibitory action may play a role in cocaine-induced convulsant states.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):85-94.
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    ABSTRACT: Once the tools for controlling calcium gradients became available to electrophysiologists, they began the quest for understanding the role of Ca2+ in the control of neuronal activity. In the early 1970s Paul Feltz and I spent a rich period in K. Krnjevic's laboratory in Montreal, and I was already involved in a research, which showed that an increase in intracellular Ca2+ concentration can lead to hyperpolarization of motoneurones. At about the same time, a potassium conductance activated by intracellular calcium injection was identified in mammals and snails. Since then, most of my work has dealt with the study of Ca2+ entry in neurons. Here I review the progress that led fi rst to the biophysical characterization and, later, to the molecular identification of T-type calcium channels. With the advent of new optical methods, in particular two-photon microscopy, we may be on the brink of a step forward in our understanding of how T channels play a role in the integrative processes that take place in a large cortical neuron such as the Purkinje cell.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):169-78.
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    ABSTRACT: During neuronal development, gamma-aminobutyric acid (GABA), which is the principal inhibitory neurotransmitter in the mature brain, exerts a paradoxical depolarizing action that plays an important role in the generation of neuronal synaptic activities in the immature cortical structures and in the formation of the neuronal network. The depolarizing action of GABA is due to a differential organization of the chloride homeostasis system; in immature neurons it maintains an elevated intracellular chloride concentration ([Cl-]i), whereas in mature neurons it keeps [Cl-]i at relatively low levels. Several recent studies have shown that the function of chloride transporters during neuronal development extends beyond the simple maintenance of chloride homeostasis and might play an active role in neuronal growth and formation of synaptic connections. In the present manuscript, we summarize such evidence and discuss the perspectives in the study of the functional role of ion transporters in determining the mode of GABA actions.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):105-12.
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    ABSTRACT: The mammalian thoracolumbar spinal cord contains all the necessary elements to generate a rhythmic oscillatory activity that is transformed into locomotor commands to agonist and antagonist limb muscles to produce gait at various speed. This motor program is produced by interneurons in the ventral horn and can be readily recorded even with in vitro spinal cord preparations isolated from rats or mice (once dorsal afferents are stimulated or excitatory neuronchemicals applied). The locomotor program is continuously modulated and refined by afferent sensory inputs and by signals descending from brain centers. Nevertheless, this program is not the only type of rhythmic discharge produced by spinal networks. In fact, activation of metabotropic group I glutamate receptors or block of certain K+ currents by 4-aminopyridine generates non-locomotor discharges, and, at the same time, facilitates evoked locomotor activity, which then suppresses any other interfering rhythmicity. These findings suggest that accessory networks, activated by suitable stimuli, might be exploited to restore locomotor activity damaged by a lesion, an obvious goal for neuro-rehabilitation purposes. The structure of the locomotor networks appears to include a rhythm-generating circuit that drives a pattern formation circuit, commanding motoneurons to discharge appropriate signals to skeletal muscles. Studies with the K+-channel blocker tetraethylammonium have indicated that this hierarchical arrangement is preserved in vitro. Hence, isolated spinal cord preparations represent an interesting experimental tool to investigate new mechanisms to upregulate various components of locomotor networks, especially after the induction of experimental lesions.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):25-36.
  • Critical Reviews in Neurobiology 02/2006; 18(1-2):1-4.
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    ABSTRACT: Both long-lasting changes in synaptic function and long-term memory require gene expression. However, the molecular mechanisms by which gene expression is turned on are not fully understood. In this review, we highlight the role of the eukaryotic initiation factor 2 alpha (eIF2alpha) signalling pathway in long-term synaptic plasticity and memory.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):187-95.
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    ABSTRACT: The direction of plasticity at CA3-CA1 hippocampal synapses is determined by the strength of afferent stimulation. Weak stimuli lead to long-term depression (LTD) and strong stimuli to long-term potentiation (LTP), but both require activation of synaptic N-methyl-D-aspartate receptors (NMDARs). These receptors are therefore necessary and required for the induction of plasticity at CA3-CA1 synapses even though they carry little of the current responsible for the basal excitatory post-synaptic potential (EPSP). The influx of Ca(2+) via NMDARs triggers the subsequent and persistent changes in the expression of alpha-amino-3-hydroxy-5 methylisoxazole-4-proprionic acid receptors (AMPARs) and these receptors are responsible for the major part of the basal EPSP. The degree of activity of NMDARs is determined in part by extracellular Mg(2+) and by the co-agonists for this receptor, glycine and D-serine. During strong stimulation, a relief of the voltage-dependent block of NMDARs by Mg(2+) provides a positive feedback for NMDAR Ca(2+) influx into postsynaptic CA1 spines. In this review, we discuss how the induction of LTP at CA3-CA1 synapses requires further signal amplification of NMDAR activity. We discuss how the regulation of NMDARs by protein kinases and phosphatases is brought into play. Evidence is presented that Src family kinases (SFKs) play a "core" role in the induction of LTP by enhancing the function and expression of NMDARs. At CA3-CA1 synapses, NMDARs are largely composed of NR1 (NMDA receptor subunit 1)-NR2A or NR1-NR2B containing subunits. Recent, but controversial, evidence has correlated NR1-NR2A receptors with the induction of LTP and NR1-NR2B receptors with LTD. However, LTP can be induced by activation of either subtype of NMDAR and the ratio of NR2A:NR2B receptors has been proposed as an alternative determinant of the direction of synaptic plasticity. Many transmitters and signal pathways can modify NMDAR function and expression and, for a given stimulus strength, they can potentially lead to a change in the balance between LTP and LTD. As opposed to the "core" mechanisms of LTP and LTD, the resulting alterations in this balance underlie "meta-plasticity." Thus, in addition to their contribution to core mechanisms, we will also discuss how Src-family kinases could preferentially target NR1-NR2A or NR1-NR2B receptors to alter the relative contribution of these receptor subtypes to synaptic plasticity.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):71-84.
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    ABSTRACT: We have previously described a new endogenous phosphorylation mechanism that maintains ionotropic gamma-aminobutyric acid receptor (GABAAR) function and have shown that the kinase involved is the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). This enzyme is closely associated with the receptor and phosphorylates the alpha1 subunit of the receptor. In a wealth of studies, a reduction in GABAergic neurotransmission has been suggested as a pathophysiological mechanism for human epilepsy. In this paper, we present evidence showing both reduced efficacy of this glycolysis-dependent GABAAR phosphorylation mechanism and of GABAergic inhibition in epileptogenic cortical tissue samples obtained during curative surgery of patients with partial seizures, as compared to non-epileptogenic human cortical tissue. This feature is not due to a reduction in the density of GABAAR alpha1 subunits in the epileptogenic tissue as evidenced by photoaffinity labeling. Maintaining the receptor in a phosphorylated state either by favoring the endogenous phosphorylation or by inhibiting a membrane-bound phosphatase sustains the GABAAR responses in the human epileptogenic cortex. The deficiency in endogenous phosphorylation and the associated decreased GABAAR function can account for transient failures of GABAergic inhibition and may favor seizure initiation and propagation. These findings suggest a functional link between epileptic pathology and the regional cerebral glucose hypometabolism observed in patients with partial epilepsies, since the dysfunction of the GABAergic mechanism is dependent on locally produced glycolytic ATP. They also point to new targets for developing molecules active in drug-resistant epilepsies.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):197-203.
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    ABSTRACT: Homeostatic plasticity is an important physiological process in the mammalian nervous system. In this review, we discuss methodological and mechanistic similarities and differences in cortical and hippocampal studies of homeostatic plasticity. Although there are many similarities, there are also region-specific differences in the effects and/or mechanisms that regulate homeostatic plasticity in these two regions. In this review, we propose a new experimental paradigm to study homeostatic plasticity that may address some unanswered questions in the field.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):125-34.
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    ABSTRACT: Synapses mediated by gamma-aminobutyric acid (GABA) A receptors are notoriously altered during periods of enhanced activity. Since a loss of inhibitory tone is a basic cause of seizures and epilepsies, it is important to determine the underlying mechanisms and the way this could be alleviated or at least reduced. Alterations of the intracellular content of chloride are thought to be a major player in the sequence of events that follow episodes of hyperactivity. In this review, I discuss these mechanisms both in the adult and developing brain, relying on studies in which chloride and GABAergic currents were measured by electrophysiological and imaging techniques. The main conclusion is that in adult systems, status epilepticus induces a complete re-organization of the networks, with cell death, axonal growth, and glutamatergic neosynapse formation leading to an increased glutamatergic drive. This, in turn, will decrease the threshold of seizure generation and thus contribute to seizure generation. In contrast, GABAergic synapses are not readily "plastic" as the lost interneurones and synapses are not replaced. Somatostatin-positive 0-LM Interneurons that innervate the dendrites of the principal cells in the hippocampus degenerate selectively, leading to a loss of the inhibitory drive in the dendrites, whereas somatic projecting basket cells and somatic inhibitory drives are relatively spared. This imbalance leads to a reduction of the inhibitory strength that is necessary but not sufficient to generate ongoing seizures. An additional important factor is the persistent increase of the intracellular chloride concentration that leads to a long-lasting shift in the depolarizing direction of the actions of GABA that will also contribute to seizure generation. In the developing brain, a major source of seizure generation is the depolarizing and often excitatory actions of GABA due to a higher intracellular chloride concentration ([Cl-]I) in immature neurons, a property that has been confirmed in all developing systems and animal species studied. As a consequence, immature GABAergic synapses will excite targets and facilitate the emergence of seizures, in keeping with the well-known higher incidence of seizures in the developing brain. Using a unique preparation with two intact hippocampi placed in a three-compartment chamber in vitro, we have provided direct evidence that seizures beget seizures and that GABA signaling plays a central role in this phenomenon. Indeed, recurrent seizures triggered in one hippocampus by a convulsive agent propagate to the other hippocampus and transform the naive hippocampus into one that generates seizures once disconnected from the other hippocampus. This transformation is conditioned by the occurrence during the seizures of high-frequency oscillations (40 Hz and above). Interestingly, these oscillations are only produced when N-methyl-D-aspartate (NMDA-) and GABA receptors are operative and not blocked in the naïve hippocampus. Therefore, GABA-receptor antagonists are pro-convulsive in the developing brain but, in fact, anti-epileptic. This paradoxical conclusion has quite a few clinical implications that are discussed.
    Critical Reviews in Neurobiology 02/2006; 18(1-2):135-44.