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Neuro–Endocrine–Immune Dysfunction in the Chronic Pain Patient
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Bliss and Lomo described long-term potentiation (LTP) in the hippocampus where brief high-frequency coincident input resulted in a persistent increase in synaptic efficacy.37 This phenomenon was later recorded in the spinal cord as part of the central sensitization process.38,39 This synaptic plasticity shares striking similarities with the process of memory.40 With LTP, the facilitation manifested after the stimulus—that is to say that for some time, only a low level of nociception was required to sustain the stimulation. Nociceptive inputs that are normally sub-threshold create excitation. This is distinct from wind-up where the facilitation occurs with continued stable but high-frequency stimulation.41 Long-term depression (LTD) is an opponent process to LTP. LTD occurs in response to weak or low-frequency stimulation.4
Animal Models of Down Syndrome and Other Genetic Diseases Associated with Mental Retardation
Published in Merlin G. Butler, F. John Meaney, Genetics of Developmental Disabilities, 2019
Angela J. Villar, Charles J. Epstein
Stereological morphometric studies of young and old Ts65Dn mice have demonstrated minor irregularities in some regions of the hippocampus of Ts65Dn mice, including reductions in the volume of CA2 and in the mean neuron number in the dentate gyrus (57). Microinjection of Lucifer yellow revealed the presence of “giant” spines on the dendrites of dentate gyrus and CA1 neurons which are present as early as postnatal day 21, as well as in mature animals (58). Interestingly, abnormal spines have also been described in the brains of children with DS (59). In addition, long-term potentiation (LTP) could not be elicited in Ts65Dn mice, presumably as a result of the influence of abnormal synaptic contacts on synaptic function (58,60,61). However, when inhibitory inputs were blocked with picrotoxin, LTP was restored. Long-term depression was also increased (60,61). These findings are indicative of abnormal synaptic plasticity in Ts65Dn (61).
Conclusions
Published in Julianne S. Oktay, Breast Cancer, 2013
For these daughters, the long-term impact was a chronic type of grieving. Although literature on grieving suggests that late adolescents are capable of normal grieving (going through the steps of denial, grieving, and restitution), the women in our study generally did not do so, in part, because they took on so many family responsibilities following the mother’s death. When they did return to activities common to their age group (e.g., education), they had a difficult time finding friends who could understand their bereavement. The result may have been a long-term depression. As adults, these women focused on the loss of the mother’s support, such as help with children/grandchildren, financial help, access to old recipes, help in emergencies, or simply support when the daughter felt overwhelmed.
Depression in disabling medical conditions – current perspectives
Published in International Review of Psychiatry, 2021
In conclusion, it is established that depression is a common problem among people with long-term disabling medical conditions and can entail additional disability and other complications leading to a deterioration in general health. Long-term depression might be associated with an increased risk of subsequent physical health problems, although the nature of that relationship and its underlying mechanisms remain unclear. Further evidence on this topic will be paramount to inform clinical practice, particularly for mental health and primary care settings. Meanwhile, patients presenting with long-term depression would benefit from regular physical health checks, and psychosocial and psychotherapeutic programmes promoting social support and a healthier lifestyle.
Cortical excitability in epilepsy and the impact of antiepileptic drugs: transcranial magnetic stimulation applications
Published in Expert Review of Neurotherapeutics, 2020
The interaction between TMS and cerebral cortex is much more complex than the hypothesized effect of TMS on the simple canonical microcircuit model of the neocortex particularly in pathological conditions (including epilepsy) which are characterized by structural or functional changes in cerebral cortex. This model is composed of excitatory pyramidal cells of layers II, III, and V of the cerebral neocortex, inhibitory interneurons, and cortico-cortical and thalamocortical inputs. rTMS induces strong depolarization of the superficial excitatory cells of the canonical microcircuit leading to the recruitment of fully synchronized clusters of excitatory neurons, including pyramidal tract neurons in layer V and inhibitory neurons producing a high frequency (∼670 Hz) repetitive discharge of the corticospinal axons. The inhibitory circuits are crucial to maintain the firing of the excitatory networks [25]. rTMS also alters neurotransmitter systems, hormonal axes, and synaptic plasticity via LTP (improve cell-cell communication) and LTD (long-lasting inhibition of cell–cell communications). The long-term forms of synaptic plasticity that are complex and involve coordinated pre- and post-synaptic mechanisms. Long-term depression exhibits many features congruent with those of slow rTMS, including frequency dependence, spread to functionally linked cortical regions, additive efficacy, and extended duration of effects. Long term (days to weeks) effects have also been observed with TMS administration reflected as sustained changes in neurotransmitter release, signaling pathways, and gene expression. rTMS acts on the genetic apparatus of neurons, glial cells, and may prevent neuronal death. rTMS has neurotrophic effects on dendritic growth and sprouting and the synthesis of some peptides (as brain-derived neurotrophic factor or BDNF and glial fibrillary acidic protein or GFAP), and regulates the expression of some genes, such as cfos, c-jung, which are important for neuronal plasticity and synaptic sprouting. Furthermore, rTMS is capable to alter the reactivity of free radical molecules [116].