Chronic restraint stress impairs endocannabinoid mediated suppression of GABAergic signaling in the hippocampus of adult male rats

Chronic stress, a risk factor for the development of psychiatric disorders, is known to induce alterations in neuronal networks in many brain areas. Previous studies have shown that chronic stress changes the expression of the cannabinoid receptor 1 (CB1) in the brains of adult rats, but neurophysiological consequences of these changes remained unclear. Here we demonstrate that chronic restraint stress causes a dysfunction in CB1 mediated modulation of GABAergic transmission in the hippocampus. Using an established protocol, adult male Sprague Dawley rats were daily restrained for 21 days and whole-cell voltage clamp was performed at CA1 pyramidal neurons. When recording carbachol-evoked inhibitory postsynaptic currents (IPSCs) which presumably originate from CB1 expressing cholecystokinin (CCK) interneurons, we found that depolarization-induced suppression of inhibition (DSI) was impaired by the stress. DSI is a form of short-term plasticity at GABAergic synapses that is known to be CB1 mediated and has been suggested to be involved in hippocampal information encoding. Chronic stress attenuated the depolarization-induced suppression of the frequency of carbachol-evoked IPSCs. Incubation with a CB1 receptor antagonist prevented this DSI effect in control but not in chronically stressed animals. The stress-induced impairment of CB1-mediated short-term plasticity at GABAergic synapses may underlie cognitive deficits which are commonly observed in animal models of stress as well as in patients with stress-related psychiatric disorders.     

Diffusion MRI abnormalities in pediatric neurological disorders

Diffusion-weighted imaging (DWI) makes it possible to measure early changes in cellular function in the central nervous system. The purpose of this article is to discuss the diagnostic value of diffusion-weighted and diffusion tensor imaging (DTI) in different pediatric cerebral disorders. First, the principles of DWI and DTI are briefly reviewed. The clinical usefulness of these imaging techniques is then discussed using cases with pediatric neurological disorders, such as hypoxic-ischemic encephalopathy in neonates, trauma (shaken baby syndrome), encephalopathy or encephalitis in infants, posterior reversible encephalopathy syndrome and congenital brain anomaly (callosal dysgenesis). In addition, using DTI, we evaluate normal brain development, particularly in the corpus callosum and cortico-spinal tract, and discuss the application of DTI to the study of white matter in the developing brain.     

Movement therapy induced neural reorganization and motor recovery in stroke: a review

This paper is a review conducted to provide an overview of accumulated evidence on contemporary rehabilitation methods for stroke survivors. Loss of functional movement is a common consequence of stroke for which a wide range of interventions has been developed. Traditional therapeutic approaches have shown limited results for motor deficits as well as lack evidence for their effectiveness. Stroke rehabilitation is now based on the evidence of neuroplasticity, which is responsible for recovery following stroke. The neuroplastic changes in the structure and function of relevant brain areas are induced primarily by specific rehabilitation methods. The therapeutic method which induces neuroplastic changes, leads to greater motor and functional recovery than traditional methods. Further, the recovery is permanent in nature. During the last decade various novel stroke rehabilitative methods for motor recovery have been developed. This review focuses on the methods that have evidence of associated cortical level reorganization, namely task-specific training, constraint-induced movement therapy, robotic training, mental imaging, and virtual training. All of these methods utilize principles of motor learning. The findings from this review demonstrated convincing evidence both at the neural and functional level in response to such therapies. The main aim of the review was to determine the evidence for these methods and their application into clinical practice.     

Smoking experience modulates the cortical integration of vision and haptics

Human neuroplasticity of multisensory integration has been studied mainly in the context of natural or artificial training situations in healthy subjects. However, regular smokers also offer the opportunity to assess the impact of intensive daily multisensory interactions with smoking-related objects on the neural correlates of crossmodal object processing. The present functional magnetic resonance imaging study revealed that smokers show a comparable visuo-haptic integration pattern for both smoking paraphernalia and control objects in the left lateral occipital complex, a region playing a crucial role in crossmodal object recognition. Moreover, the degree of nicotine dependence correlated positively with the magnitude of visuo-haptic integration in the left lateral occipital complex (LOC) for smoking-associated but not for control objects. In contrast, in the left LOC non-smokers displayed a visuo-haptic integration pattern for control objects, but not for smoking paraphernalia. This suggests that prolonged smoking-related multisensory experiences in smokers facilitate the merging of visual and haptic inputs in the lateral occipital complex for the respective stimuli. Studying clinical populations who engage in compulsive activities may represent an ecologically valid approach to investigating the neuroplasticity of multisensory integration.     

Tuning the gain of somato-sympathetic reflexes by stimulation of the thoracic spine in humans

An outbred rat model of novelty-seeking phenotype can differentiate between rats that show high rates (high responders; HRs) versus low rates (low responders; LRs) of locomotor reactivity to a novel environment. In the present study, LR and HR rats were exposed to a regimen of environmental and social stimuli (ESS) consisting of 14 random exposures of isolation, crowding or novel environment, once per day during the peripubertal-juvenile period (postnatal days 28-41) or handled as controls. Twenty-four hours after the last ESS exposure or control handling, all animals were tested on the forced swim and social interaction tests for depressive-like and social anxiety-like behaviors respectively. The ESS exposure during the peripubertal-juvenile period led to antidepressive-like effects on the forced swim test associated with increase in acetylation of histones 3 and 4 at the promoter regions P2 and P4 of the brain-derived neurotrophic factor (BDNF) gene in the dorsal hippocampus of HRs. Moreover, epigenetic activation of the hippocampal BDNF in the HRs following ESS exposure was accompanied by increase in the supra-pyramidal mossy fibre (SP-MF) and total mossy fibre terminal field volumes compared to handled controls. These findings suggest that the ESS exposure in the peripubertal-juvenile period may constitute an example of environmental induction of the hippocampal BDNF, and may mimic behavioral effects of exogenous antidepressants in the HR phenotype.     

A dynamic network perspective of chronic pain

We briefly summarize recent advances regarding brain functional representation of chronic pain, reorganization of resting state brain activity, and of brain anatomy with chronic pain. Based on these observations and recent theoretical advances regarding network architecture properties, we develop a general concept of the dynamic interplay between anatomy and function as the brain progresses into persistent pain, and outline the role of mesolimbic learning mechanisms that are likely involved in maintenance of chronic pain.     

Neuroplasticity and major depression,the role of modern antidepressant drugs

The pathophysiology of depression has been traditionally attributed to a chemical imbalance and critical interactions between genetic and environmental risk factors, and antidepressant drugs suggested to act predominantly amplifying monoaminergic neurotransmission. This conceptualization may be currently considered reductive. The current literature about the pathophysiological mechanisms underlying depression, stress-related disorders and antidepressant treatment was examined. In order to provide a critical overview about neuroplasticity, depression and antidepressant drugs, a detailed Pubmed/Medline, Scopus, PsycLit, and PsycInfo search to identify all papers and book chapters during the period between 1980 and 2011 was performed. Pathological stress and depression determine relevant brain changes such as loss of dendritic spines and synapses, dendritic atrophy as well as reduction of glial cells (both in number and size) in specific areas such as the hippocampus and prefrontal cortex. An increased dendritic arborisation and synaptogenesis may instead be observed in the amygdala as a consequence of depression and stress-related disorders. While hippocampal and prefrontal functioning was impaired, amygdala functioning was abnormally amplified. Most of molecular abnormalities and biological changes of aberrant neuroplasticity may be explained by the action of glutamate. Antidepressant treatment is associated with neurogenesis, gliogenesis, dendritic arborisation, new synapse formation and cell survival both in the hippocampus and prefrontal cortex. Antidepressants (ADs) induce neuroplasticity mechanisms reversing the pathological effects of depression and stress-related disorders. The neuroplasticity hypothesis may explain the therapeutic and prophylactic action of ADs representing a new innovative approach to the pathophysiology of depression and stress-related disorders.     

Short- and long-term efficacy of electroconvulsive stimulation in animal models of depression: The essential role of neuronal survival

Background

Severe and medication-resistant psychiatric diseases, such as major depressive disorder, bipolar disorder or schizophrenia, can be effectively and rapidly treated by electroconvulsive therapy (ECT). Despite extensive long-standing clinical use, the neurobiological mechanisms underlying the curative action of ECT remain incompletely understood.

Cortical changes in complex regional pain syndrome (CRPS)

Recent research suggests that changes in cortical structures can contribute to the pathophysiology of Complex Regional Pain Syndrome (CRPS). This review provides an overview of studies showing cortical involvement in CRPS, including mislocalizations of tactile stimuli, changes in size and organization of the somatosensory map, changes in motor cortex representation and body perception disturbances. In addition, we review experimental treatment approaches, such as mirror therapy and motor imagery programs, aimed at restoring the integrity of neural processing in the sensory-motor cortex in individuals with CRPS. The intervention effects are promising and can be theoretically motivated on the basis of established principles of neural organization, although important questions concerning the precise neural mechanisms of action remain unanswered.