ABSTRACT
Transcranial magnetic stimulation (TMS) is a non-invasive, non-pharmacological technique that is able to modulate cortical activity beyond the stimulation period. The residual aftereffects are akin to the plasticity mechanism of the brain and suggest the potential use of TMS for therapy. For years, TMS has been shown to transiently improve symptoms of neuropsychiatric disorders, but the underlying neural correlates remain elusive. Recently, there is evidence that altered connectivity of brain network dynamics is the mechanism underlying symptoms of various neuropsychiatric illnesses. By combining TMS and electroencephalography (EEG), the functional connectivity patterns among brain regions, and the causal link between function or behaviour and a specific brain region can be determined. Nonetheless, the brain network connectivity are highly complex and involve the dynamics interplay among multitude of brain regions. In this review article, we present previous TMS-EEG co-registration studies, which explore the functional connectivity patterns of human cerebral cortex. We argue the possibilities of neural correlates of long-term potentiation/ depression (LTP-/LTD)-like mechanisms of synaptic plasticity that drive the TMS aftereffects as shown by the dissociation between EEG and motor evoked potentials (MEP) cortical output. Here, we also explore alternative explanations that drive the EEG oscillatory modulations post TMS. The precise knowledge of the neurophysiological mechanisms underlying TMS will help characterise disturbances in oscillatory patterns, and the altered functional connectivity in neuropsychiatric illnesses.
ABSTRACT
Artemisia princeps (AP) is a flowering perennial used as a traditional medicine and dietary supplement across East Asia. No study has yet assessed its effects on synaptic plasticity in hippocampus and much less in a model of ovarian hormone deficiency. We examined the influence of chronic oral AP ethanol extract treatment in ovariectomized rats on the induction of long-term depression in a representative synapse (CA3-CA1) of the hippocampus. Ovariectomized rats demonstrated lower trabecular mean bone mineral densities than sham, validating the establishment of pathology. Against this background of pathology, AP-treated ovariectomized rats exhibited attenuated long-term depression (LTD) in CA1 relative to water-treated controls as measured by increased field excitatory post-synaptic potentials (fEPSP) activation averages over the post-stimulation period. While pathological significance of long-term depression (LTD) in ovariectomized rats is conflicting, that AP treatment significantly affected its induction offers justification for further study of its influences on plasticity and its related disorders.
Subject(s)
Animals , Female , Rats , Artemisia , Bone Density , Depression , Dietary Supplements , Ethanol , Asia, Eastern , Flowers , Hippocampus , Medicine, East Asian Traditional , Medicine, Traditional , Models, Animal , Neuronal Plasticity , Ovariectomy , Pathology , Plants, Medicinal , Plastics , SynapsesABSTRACT
Objective To explore the role of cyclooxgense-2 (COX-2) in tetrahydrocannabinol (THC)-induced inhibition of long-term depression (LTD) in CA1 area in vitro. Methods The hippocampal slices were prepared at 24 h after intraperitoneal injection of Δ~9-THC (10 mg/kg) or COX-2 inhibitor NS398 (10 mg/kg). Field excitatory post-synaptic potentials (fEPSP) were recorded in the stratum radiatum of the CA1 area in vitro to observe the effect of NS398, a selective inhibitor of COX-2, on the THC-induced inhibition of LTD and THC's effect on membrane excitability in pyramidal neurons by using the whole-cell patch clamp technique. Results ① Low-frequency stimulation (1 Hz, 15 min) induced-LTD in CA1 area was significantly attenuated by Δ9-THC. ② Δ~9-THC did not affect the basal synaptic transmission and membrane excitability (including membrane resting potentials, input resistance and firing property). ③ THC-induced inhibition of LTD was reversed by NS398. ④ THC-induced inhibition of LTD was robustly impaired in COX-2 knockout mice. Conclusion THC-induced inhibition of LTD in CA1 area was mediated via COX-2.
ABSTRACT
Objective To explore the role of cyclooxgense-2(COX-2) in tetrahydrocannabinol(THC)-induced inhibition of long-term depression(LTD) in CA1 area in vitro.Methods The hippocampal slices were prepared at 24 h after intraperitoneal injection of ?9-THC(10 mg/kg) or COX-2 inhibitor NS398(10 mg/kg).Field excitatory post-synaptic potentials(fEPSP) were recorded in the stratum radiatum of the CA1 area in vitro to observe the effect of NS398,a selective inhibitor of COX-2,on the THC-induced inhibition of LTD and THC's effect on membrane excitability in pyramidal neurons by using the whole-cell patch clamp technique. Results ① Low-frequency stimulation(1 Hz,15 min) induced-LTD in CA1 area was significantly attenuated by ?9-THC.② ?9-THC did not affect the basal synaptic transmission and membrane excitability(including membrane resting potentials,input resistance and firing property).③ THC-induced inhibition of LTD was reversed by NS398.④ THC-induced inhibition of LTD was robustly impaired in COX-2 knockout mice.Conclusion THC-induced inhibition of LTD in CA1 area was mediated via COX-2.