Changes In Efficacy Of Transmission Research Articles

Concurrent Electroencephalography Recording During Transcranial Alternating Current Stimulation (tACS)

Oscillatory brain activities are considered to reflect the basis of rhythmic changes in transmission efficacy across brain networks and are assumed to integrate cognitive neural processes. Transcranial alternating current stimulation (tACS) holds the promise to elucidate the causal link between specific frequencies of oscillatory brain activity and cognitive processes. Simultaneous electroencephalography (EEG) recording during tACS would offer an opportunity to directly explore immediate neurophysiological effects of tACS. However, it is not trivial to measure EEG signals during tACS, as tACS creates a huge artifact in EEG data. Here we explain how to set up concurrent tACS-EEG experiments. Two necessary considerations for successful EEG recording while applying tACS are highlighted. First, bridging of the tACS and EEG electrodes via leaking EEG gel immediately saturates the EEG amplifier. To avoid bridging via gel, the viscosity of the EEG gel is the most important parameter. The EEG gel must be viscous to avoid bridging, but at the same time sufficiently fluid to create contact between the tACS electrode and the scalp. Second, due to the large amplitude of the tACS artifact, it is important to consider using an EEG system with a high resolution analog-to-digital (A/D) converter. In particular, the magnitude of the tACS artifact can exceed 100 mV at the vicinity of a stimulation electrode when 1 mA tACS is applied. The resolution of the A/D converter is of importance to measure good quality EEG data from the vicinity of the stimulation site. By following these guidelines for the procedures and technical considerations, successful concurrent EEG recording during tACS will be realized.

Concurrent Electroencephalography Recording During Transcranial Alternating Current Stimulation (tACS).

Oscillatory brain activities are considered to reflect the basis of rhythmic changes in transmission efficacy across brain networks and are assumed to integrate cognitive neural processes. Transcranial alternating current stimulation (tACS) holds the promise to elucidate the causal link between specific frequencies of oscillatory brain activity and cognitive processes. Simultaneous electroencephalography (EEG) recording during tACS would offer an opportunity to directly explore immediate neurophysiological effects of tACS. However, it is not trivial to measure EEG signals during tACS, as tACS creates a huge artifact in EEG data. Here we explain how to set up concurrent tACS-EEG experiments. Two necessary considerations for successful EEG recording while applying tACS are highlighted. First, bridging of the tACS and EEG electrodes via leaking EEG gel immediately saturates the EEG amplifier. To avoid bridging via gel, the viscosity of the EEG gel is the most important parameter. The EEG gel must be viscous to avoid bridging, but at the same time sufficiently fluid to create contact between the tACS electrode and the scalp. Second, due to the large amplitude of the tACS artifact, it is important to consider using an EEG system with a high resolution analog-to-digital (A/D) converter. In particular, the magnitude of the tACS artifact can exceed 100 mV at the vicinity of a stimulation electrode when 1 mA tACS is applied. The resolution of the A/D converter is of importance to measure good quality EEG data from the vicinity of the stimulation site. By following these guidelines for the procedures and technical considerations, successful concurrent EEG recording during tACS will be realized.

Activity-dependent Synaptic Plasticity and Metaplasticity in Spinal Motor Networks

Throughout life, neuronal network properties are modulated according to both external and internal stimuli. These adaptive capabilities of the central nervous system (CNS) have been generically termed "plasticity". One prominent form of CNS plasticity is the capability of synapses to change their strength. Synaptic strength is not a constant value but depends at each moment on the synapse's past activity. These changes in transmission efficacy are called activity-dependent synaptic plasticity (ADSP) and result in an increase (potentiation) or a decrease (depression) in synaptic strength. The ability of synapses to express one type of ADSP can change as a function of previous plasticity and previous activation of synapses. This plasticity of synaptic plasticity has been termed metaplasticity. ADSP and metaplasticity are now regarded as essential mechanisms for normal information processing in neuronal networks. Rhythmic activities such as locomotion are generated by rhythmically active central neuronal networks called central pattern generators (CPGs) that possess the intrinsic ability to generate rhythmic and organized activity in the absence of sensory inputs. The CPG activity arises from a complex dynamic interaction between synaptic transmission, intrinsic membrane properties and neuromodulatory inputs. A growing body of evidence suggests that the spinal cord matches the plastic and metaplastic properties found in other parts of the CNS, both under normal conditions and after spinal cord injury. Here, findings describing ADSP and its neuromodulation in vertebrate sensorimotor networks are reviewed, followed by a discussion of the potential role of ADSP and neuromodulation in the physiology and pathophysiology of motor circuit assembly.

Voluntary Motor Output Is Altered by Spike-Timing-Dependent Changes in the Human Corticospinal Pathway

Repeated pairs of timed presynaptic and postsynaptic potentials cause lasting changes in efficacy of transmission at many synapses. The corticospinal tract is the major pathway controlling voluntary movement in humans, and corticospinal neurons have monosynaptic connections to motoneurons of many muscles. We hypothesized that corticospinal transmission in humans could be altered by delivering, to the corticospinal-motoneuronal synapses, timed pairs of presynaptic volleys (produced by cortical stimulation) and antidromic postsynaptic volleys (by peripheral nerve stimulation). To test corticospinal transmission, electrical cervicomedullary stimuli evoked motor responses [cervicomedullary motor-evoked potentials (CMEPs)] in biceps brachii before and for 1 h after conditioning with 50 paired cortical and peripheral nerve stimuli. Seven interstimulus intervals (ISIs) of conditioning stimulus pairs were tested on different days. With one ISI (+3 ms; cortical before peripheral nerve stimulation), CMEPs were significantly increased in size by 33 +/- 30% (mean +/- SD; n = 7) from 4 until 32 min after conditioning. With two other ISIs (-13 ms, +22 ms), CMEPs were decreased from approximately 30 until 60 min after conditioning (by 25 +/- 23% and 27 +/- 32%; n = 8). The remaining ISIs produced no changes. In a second study, subjects performed weak bilateral voluntary elbow flexion contractions before and after conditioning of the right elbow flexors. Conditioning ISIs that increased or decreased CMEPs similarly increased or decreased voluntary force and EMG on the right. Thus, depending on their timing, repeated paired stimuli can potentiate or depress corticospinal transmission, and these changes are functionally relevant. We suggest that bidirectional spike-timing-dependent plasticity can be induced at corticospinal-motoneuronal synapses and can influence voluntary motor output.

Postsynaptic control of the induction of long-term changes in efficacy of transmission at neocortical synapses in slices of rat brain.

1. Long-term potentiation (LTP) is an enduring, activity-induced increase in the efficacy of synaptic transmission, which has been considered as a possible neural substrate for learning. Recent experiments have shown that LTP can be induced in hippocampal CA1 neurons when a presynaptic volley is paired repetitively with depolarization of the postsynaptic cell, brought about with intracellularly applied depolarizing current pulses (20, 33). We have repeated these experiments in neocortical neurons, in transverse slices of rat sensorimotor cortex in vitro. 2. Stable intracellular recordings were obtained from 28 neurons (mean resting potential -78 mV, mean spike amplitude 95 mV, mean input resistance 41 M omega) mostly in layers V and VI. Two different afferent pathways were stimulated alternately at 0.2 Hz to evoke subthreshold composite excitatory postsynaptic potentials (EPSPs). One micromolar bicuculline methiodide was added to the bathing medium in most experiments. 3. Repetitive pairing of one afferent volley with a coincident intracellular depolarizing current pulse (100-200 ms long) of a magnitude sufficient to make the neuron fire 6 to 13 action potentials/pulse, gave rise after 30-50 pairings in 4 neurons to a significant enduring increase in the amplitude of the paired EPSP. The increase persisted without decrement for as long as the recording continued (range 15-50 min after the pairing ended) but the amplitude of the unpaired EPSP was unchanged. During the LTP, the membrane potential and the apparent input resistance of the postsynaptic neurons were also unchanged. 4. In two cells a significant prolonged depression of the paired EPSP was induced while the unpaired EPSP was unaffected. Membrane potential and input resistance were not changed. In the remaining 22 cells neither the paired nor the unpaired EPSP was altered. 5. Brief, tetanic stimulation was applied to one afferent pathway in 11 of the neurons in which postsynaptic stimulation had been ineffective. A variety of effects was produced (LTP, depression, or posttetanic potentiation). All the effects of tetanic stimulation were confined to the stimulated pathway. 6. We conclude that LTP can be produced in some neocortical neurons by pairing a presynaptic volley with postsynaptic depolarization, in an experimental paradigm that conforms to Hebb's (17) model of associative conditioning. Depression of the paired EPSP was produced in other cells with the same experimental design.(ABSTRACT TRUNCATED AT 400 WORDS)

Alteration in dentate neuronal activities associated with perforant path kindling: I. Long-term potentiation of excitatory synaptic transmission

One candidate for the neuronal mechanism of kindling is the facilitation of excitatory synaptic transmission. The population EPSP component of the perforant pathdentate field potential is strongly potentiated by the first few kindling stimulations applied to the perforant path. As kindling proceeds further, however, subsequent changes in transmission efficacy have been a source of controversy. The present study reexamines these changes in transmission efficacy of the perforant path-dentate granule cell synapses during and after perforant path kindling using improved methods of analysis of the field potentials recorded in freely moving rats. The slope of the regression line of the population EPSPs on a range of stimulus strength values was found to be enhanced by the first kindling stimulation and then continued to increase gradually with subsequent kindling stimulations, indicating a cumulative increase in synaptic transmission efficacy throughout the period of kindling. The potentiated excitatory synaptic transmission lasted for at least 1 month after the cessation of kindling. On the other hand, the kindling stimulations produced a progressive increase in the x-intercept of the regression line, indicating an increase in the minimal EPSP threshold. These two effects seem to account for the apparent discrepancy between previous studies, each of which measured the population EPSP at a fixed stimulus strength.