Brain research
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Neuropathic pain has been described as the "most terrible of all tortures which a nerve wound may inflict" and arises as a consequence of nerve injury either of the peripheral or central nervous system. Following peripheral nerve injury, a cascade of events in the primary afferents leads to peripheral sensitization resulting in spontaneous nociceptor activity, decreased threshold and increased response to supra-threshold stimuli. ⋯ The peripheral nerve injury has been reported to induce neuroplastic changes in different brain regions including the anterior cingulate cortex, insular cortex, ventrolateral orbitofrontal area, amygdala, striatum, thalamus, hypothalamus, rostral ventromedial medulla, periaqueductal gray, pons (locus coeruleus), red nucleus, and medulla oblongata. The present review article discusses the involvement of these different brain areas in the development of peripheral nerve injury-induced neuropathic pain.
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Anxiety symptoms are one of the most common mental health conditions in childhood. Children and adolescents with Autism Spectrum Disorders (ASD) are at risk for developing mental health symptoms and anxiety in particular, especially when compared with their peers - both in the general population as well as when compared to youth with other developmental disabilities. Cognitive behavior therapy (CBT) has been identified as the treatment of choice in addressing anxiety symptoms in the general population, and an emerging body of literature indicates that modified CBT for youth with ASD can be effective in reducing anxiety symptoms. ⋯ However, the majority of these studies only briefly describe the parent's role, and little mention is made with regard to how the parent's role evolves over time as children age into adolescence. In this paper, the parent's role in the treatment of anxiety symptoms in children and adolescents with high-functioning ASD will be discussed with a particular emphasis on considerations for parents of teenagers. Specific recommendations for parent involvement will be provided.
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Kisspeptin has recently been identified as a key neuroendocrine gatekeeper of reproduction and is essential for the initiation of human puberty and maintenance of adult reproduction. Kisspeptin neurons appear to be integrative sensors, as they respond to changes in numerous internal and external factors including nutrient and fat status, stress and sex steroids, thus providing a link between these factors and reproduction. ⋯ These demonstrate an essential role for kisspeptin in GnRH neuron firing, GnRH pulsatile secretion, negative feedback by gonadal steroids, the onset of puberty, and the ovulatory LH surge. These studies establish that kisspeptin antagonists are powerful investigative tools and set the scene for more extensive physiological and pathophysiological studies as well as therapeutic intervention.
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The analysis of the functional correlates of "brain oscillations" has become an important branch of neuroscience. Although research on the functional correlates of brain oscillation has progressed to a high level, studies on cognitive disorders are rare and mainly limited to schizophrenia patients. ⋯ Furthermore, the effects of pharmaca and the influence of neurotransmitters in patients with cognitive disorders are also reviewed. Following the review, a short synopsis is given related to the analysis of brain oscillations.
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The lateral reticular nucleus (LRN) and locus coeruleus-subcoeruleus (LC/SC), brainstem structures which overlap the A1 and A6 noradrenergic nuclei respectively, have been implicated in descending modulation of spinal nociceptive transmission. The present studies were designed to examine the role of norepinephrine (NE) in the mediation of inhibition of the nociceptive tail flick reflex produced by focal electrical stimulation in the LRN and LC/SC. Spinal NE was depleted by intrathecal administration of 6-hydroxydopamine (6-OHDA; 20 micrograms) and the threshold electrical stimulation in the LRN and the LC/SC necessary to inhibit the tail flick reflex in lightly pentobarbital-anesthetized rats was determined 9 and 14 days later. ⋯ Binding of [3H]rauwolscine to lumbar spinal cord revealed an elevation in the estimated Bmax without a change in the estimated Kd of the high affinity binding component 9 days following 6-OHDA administration. This study demonstrates that spinal adrenoceptor denervation supersensitivity develops rapidly following intrathecal administration of 6-OHDA and compensates for the selective destruction of spinal noradrenergic nerve terminals. Thus, the absence of effect of NE depletion on the tail flick inhibitory stimulation threshold in the LRN and the LC/SC does not argue against the hypothesis that spinopetal NE-containing neurons in these brainstem loci are involved in modulation of spinal nociceptive transmission.