The neurobiology of focus and distraction: The case for incorporating mindfulness into leadership.

Increasingly health leaders are experiencing greater demands and pressures, which require the need for better focus while limiting unwarranted distractions. This article offers a neurobiological explanation of how the brain focuses and becomes distracted, in order to help health leaders gain insight into their own effectiveness. Two main neural circuits are contrasted: the mind-wandering default mode circuit and the attentional central executive system.

Calpain activation is involved in early caspase-independent neurodegeneration in the hippocampus following status epilepticus.

Evidence for increased calpain activity has been described in the hippocampus of rodent models of temporal lobe epilepsy. However, it is not known whether calpains are involved in the cell death that accompanies seizures. In this work, we characterized calpain activation by examining the proteolysis of calpain substrates and in parallel we followed cell death in the hippocampus of epileptic rats.

Endothelial proliferation and increased blood-brain barrier permeability in the basal ganglia in a rat model of 3,4-dihydroxyphenyl-L-alanine-induced dyskinesia.

3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia is associated with molecular and synaptic plasticity in the basal ganglia, but the occurrence of structural remodeling through cell genesis has not been explored. In this study, rats with 6-hydroxydopamine lesions received injections of the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) concomitantly with L-DOPA for 2 weeks. A large number of BrdU-positive cells were found in the striatum and its output structures (globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata) in L-DOPA-treated rats that had developed dyskinesia.

Reduced hippocampal neurogenesis in R6/2 transgenic Huntington's disease mice.

We investigated whether cell proliferation and neurogenesis are altered in R6/2 transgenic Huntington's disease mice. Using bromodeoxyuridine (BrdU), we found a progressive decrease in the number of proliferating cells in the dentate gyrus of R6/2 mice. This reduction was detected in pre-symptomatic mice, and by 11.

Spontaneous epileptic rats show changes in sleep architecture and hypothalamic pathology.

Purpose: The goal of the present study was to investigate the relationship between sleep, hypothalamic pathology, and seizures in spontaneous epileptic rats.

Methods: Rats were implanted with radiotelemetry transmitters for measuring electrocorticogram (ECoG) and stimulation electrodes in the hippocampus. Epileptogenesis was triggered by 2 h of electical stimulation-induced self-sustained status epilepticus (SSSE).

Behavioral characterization of a unilateral 6-OHDA-lesion model of Parkinson's disease in mice.

Parkinson's disease (PD) is one of the most common neurodegenerative disorders. Several toxin-induced animals models simulate the motor deficits occurring in PD. Among them, the unilateral 6-hydroxydopamine (6-OHDA) model is frequently used in rats and has the advantage of presenting side-biased motor impairments.

Proteolysis of NR2B by calpain in the hippocampus of epileptic rats.

Overactivation of N-methyl-D-aspartate receptors is known to mediate excitotoxicity due to excessive entry of calcium, leading to the activation of several calcium-dependent enzymes. Calpains are calcium-activated proteases that appear to play a role in excitotoxic neuronal death. Several cellular proteins are substrates for these proteases, particularly the N-methyl-D-aspartate receptor.

Forebrain acetylcholine regulates adult hippocampal neurogenesis and learning.

Hippocampus-mediated learning enhances neurogenesis in the adult dentate gyrus (DG), and this process has been suggested to be involved in memory formation. The hippocampus receives abundant cholinergic innervation and acetylcholine (ACh) plays an important role in learning and Alzheimer's disease (AD) pathophysiology. Here, we show that a selective neurotoxic lesion of forebrain cholinergic input with 192 IgG-saporin reduces DG neurogenesis with a concurrent impairment in spatial memory.

Measurement of cortical and hippocampal epileptiform activity in freely moving rats by means of implantable radiotelemetry.

Implanted radiotelemetry has been used for the measurement of cortical electroencephalogram (EEG), locomotor activity, body temperature and cardiovascular parameters. This technique allows high quality data acquisition from freely moving animals with no complications of externalised apparatus. This paper focuses on the methodology for short and long-term monitoring of epileptiform activity by simultaneous cortical EEG, hippocampal (HC) EEG and electromyogram (EMG) in rats.

No evidence for new dopaminergic neurons in the adult mammalian substantia nigra.

A recent report by Zhao et al. [Zhao, M., Momma, S.

Harnessing endogenous stem cells to treat neurodegenerative disorders of the basal ganglia.

New neurons are continuously generated in selective regions of the normal adult mammalian brain. Recent evidence suggests that neural stem or progenitor cells located in the subventricular zone lining of the lateral ventricles can be induced to proliferate and migrate to the adjacent striatum following brain insults or growth factor treatment. This ability to incorporate new cells into the striatum gives the potential of repairing and restoring basal ganglia functions in Parkinson's and Huntington's diseases.

Status epilepticus severity influences the long-term outcome of neurogenesis in the adult dentate gyrus.

Status epilepticus (SE) is characterized by continual seizure activity that can vary widely in the intensity of convulsions. We induced seizures by applying continuous electrical stimulation to the hippocampus in adult rats to explore the effects of three different SE states on neurogenesis and neuronal death in the hippocampus. Rats exhibiting the most severe SE state (fully convulsive) demonstrated profound increases in cell proliferation in the dentate gyrus (DG) at 1 week post-insult, but the majority of the new neurons had died at 4 weeks.

Electroconvulsive seizures induce endothelial cell proliferation in adult rat hippocampus.

Background: Electroconvulsive seizures, an animal model for electroconvulsive treatment, induce a strong increase in neurogenesis in the dentate gyrus of adult rats. Hippocampal neurogenesis has previously been described as occurring in an angiogenic niche. This study examines the effect of electroconvulsive seizures on proliferation of vascular cells in rat hippocampus.

Anterograde delivery of brain-derived neurotrophic factor to striatum via nigral transduction of recombinant adeno-associated virus increases neuronal death but promotes neurogenic response following stroke.

To explore the role of brain-derived neurotrophic factor for survival and generation of striatal neurons after stroke, recombinant adeno-associated viral vectors carrying brain-derived neurotrophic factor or green fluorescent protein genes were injected into right rat substantia nigra 4-5 weeks prior to 30 min ipsilateral of middle cerebral artery occlusion. The brain-derived neurotrophic factor-recombinant adeno-associated viral transduction markedly increased the production of brain-derived neurotrophic factor protein by nigral cells. Brain-derived neurotrophic factor was transported anterogradely to the striatum and released in biologically active form, as revealed by the hypertrophic response of striatal neuropeptide Y-positive interneurons.

Caspase-mediated death of newly formed neurons in the adult rat dentate gyrus following status epilepticus.

A large proportion of cells that proliferate in the adult dentate gyrus under normal conditions or in response to brain insults exhibit only short-term survival. Here, we sought to determine which cell death pathways are involved in the degeneration of newly formed neurons in the rat dentate gyrus following 2 h of electrically induced status epilepticus. We investigated the role of three families of cysteine proteases, caspases, calpains, and cathepsins, which can all participate in apoptotic cell death.

Electroconvulsive seizures increase hippocampal neurogenesis after chronic corticosterone treatment.

Major depression is often associated with elevated glucocorticoid levels. High levels of glucocorticoids reduce neurogenesis in the adult rat hippocampus. Electroconvulsive seizures (ECS) can enhance neurogenesis, and we investigated the effects of ECS in rats where glucocorticoid levels were elevated in order to mimic conditions seen in depression.

Neuronal apoptosis after brief and prolonged seizures.

Evidence has accumulated that apoptotic cell death contributes to brain damage following experimental seizures. A substantial number of degenerating neurons within limbic regions display morphological features of apoptosis following prolonged seizures evoked by systemic or local injections of kainic acid, systemic injections of pilocarpine and sustained stimulation of the perforant path. Although longer periods of seizures consistently result in brain damage, it has previously not been clear whether brief single or intermittent seizures lead to cell death.