scholarly journals mGluR5-dependent acetylcholine, serotonin, and norepinephrine mediated modulation of synaptic eligibility traces into LTD in mice visual cortex

2021 ◽  
Author(s):  
Shumsuzzaman Khan
Keyword(s):  
Visual Cortex ◽  
Ex Vivo ◽  
Brain Slices ◽  
Low Frequency ◽  
Decay Kinetics ◽  
Low Frequency Stimulation ◽  
Long Term Changes ◽  
Frequency Stimulation ◽  
Mouse Visual Cortex

Abstract In reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.

scholarly journals NMDAR-independent acetylcholine, serotonin, and norepinephrine mediated modulation of synaptic eligibility traces into LTD in mice visual cortex

2020 ◽  
Author(s):  
Shumsuzzaman Khan
Keyword(s):  
Visual Cortex ◽  
Ex Vivo ◽  
Brain Slices ◽  
Low Frequency ◽  
Decay Kinetics ◽  
Low Frequency Stimulation ◽  
Long Term Changes ◽  
Frequency Stimulation ◽  
Mouse Visual Cortex

AbstractIn reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.

Brain-derived neurotrophic factor blocks long-term depression in rat visual cortex

1996 ◽  
Vol 76 (6) ◽  
pp. 4198-4201 ◽  
Author(s):  
Y. Akaneya ◽  
T. Tsumoto ◽  
H. Hatanaka
Keyword(s):  
Visual Cortex ◽  
Neurotrophic Factor ◽  
Tyrosine Kinases ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
Brain Derived Neurotrophic Factor ◽  
Long Term Depression ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

1. Brain-derived neurotrophic factor (BDNF) has been reported to play a role in long-term potentiation (LTP) in hippocampus, but whether it is involved also in long-term depression (LTD) is not yet known. In this study, we tested whether BDNF and its gene family, nerve growth factor (NGF), have any effect on synaptic transmission and LTD in visual cortical slices of young rats. 2. An application of BDNF at the concentration of 20 ng/ml did not significantly change layer II/III field responses evoked by layer IV stimulation at 0.1 Hz, although at 200 ng/ml it enhanced responses. BDNF at 20 ng/ml prevented LTD of field responses from being induced by low-frequency stimulation (1 Hz for 15 min) of layer IV. NGF did not have such effects in the same concentration range as that of BDNF. 3. The action of BDNF was antagonized by K252a, an inhibitor of receptor tyrosine kinases. When K252a alone was applied to slices, LTD of stronger magnitude than in control slices was induced by low-frequency stimulation. 4. These results suggest that endogeneous BDNF may prevent synapses from being depressed by low-frequency inputs in the developing visual cortex.

Low-frequency stimulation at the troughs of theta-oscillation induces long-term depression of previously potentiated CA1 synapses

1996 ◽  
Vol 75 (2) ◽  
pp. 877-884 ◽  
Author(s):  
P. T. Huerta ◽  
J. E. Lisman
Keyword(s):  
Hippocampal Slices ◽  
Field Potential ◽  
Low Frequency ◽  
Long Term Depression ◽  
Low Frequency Stimulation ◽  
Bath Application ◽  
Stable Conditions ◽  
Theta Frequency ◽  
Frequency Stimulation

1. The induction of long-term weakening of synaptic transmission in rat hippocampal slices was examined in CA1 synapses during cholinergic modulation. 2. Bath application of the cholinergic agonist carbachol (50 microM) activated an oscillation of the local field potential in the theta-frequency range (5-12 Hz), termed theta. It was previously shown that a stimulation train of 40 single shocks (at 0.1 Hz) to the Schaffer collateral-commisural afferents, each synchronized with positive peaks of theta, caused homosynaptic long-term enhancement in CA1. Furthermore, long-term depression (LTD) was sporadically observed when the stimulation train was given at negative troughs of theta. Here we have sought to determine stable conditions for LTD induction during theta. 3. Synaptic weakening was reliably obtained, by giving 40 shocks (at 0.1 Hz) at theta-troughs, only in pathways that had been previously potentiated. This decrement, termed theta-LTD, was synapse specific because it did not occur in an independent pathway not stimulated during theta. The interval between the initial potentiating tetanus and theta-LTD induction could be as long as 90 min. 4. theta-LTD could be saturated; after consecutive episodes of theta-LTD induction, no significant further depression was obtained. Moreover, theta-LTD could be reversed by tetanic stimulation. 5. theta-LTD could prevent the induction of LTD by 600-900 pulses at 1 Hz. This suggests that the two protocols may share common mechanisms at the synaptic level. 6. We conclude that single presynaptic spikes that occur at low frequency and are properly timed to the troughs of theta may be a relevant mechanism for decreasing the strength of potentiated synapses.

scholarly journals The significance of Gerta Vrbová's low-frequency stimulation experiment

2021 ◽  
Author(s):  
Dirk Pette
Keyword(s):  
Low Frequency ◽  
Basic Research ◽  
Contractile Properties ◽  
Scientific Cooperation ◽  
Low Frequency Stimulation ◽  
Slow Twitch Muscle ◽  
Frequency Stimulation ◽  
Time Courses ◽  
Fast Twitch

An inspiring scientific cooperation has come to an end, when Gerta Vrbová, an internationally renowned researcher in the field of neuromuscular interactions, passed away on October 2, 2020. Comparative EMG studies had led Gerta to suggest that different contractile properties of fast- and slow-twitch muscle fibers relate to specific firing patterns of their motoneurones. In support of her hypothesis, long term stimulation of fast-twitch muscles with a stimulus pattern resembling that of slow motoneurones, were shown to induce a pronounced fast-to-slow shift in contractile properties. In our cooperation which started in 1970, and also in cooperation with others, Gerta's experiment proved to be an ideal model for the study of neurally controlled changes in phenotype characteristics at various levels of molecular and cellular organization, their time courses and ranges. It has become most important in basic research on the adaptive potential or plasticity of muscle.

Robust Changes of Afferent-Induced Excitation in the Rat Spinal Dorsal Horn After Conditioning High-Frequency Stimulation

2000 ◽  
Vol 83 (4) ◽  
pp. 2412-2420 ◽  
Author(s):  
Hiroshi Ikeda ◽  
Tatsuya Asai ◽  
Kazuyuki Murase
Keyword(s):  
Dorsal Horn ◽  
High Frequency ◽  
Low Frequency ◽  
Single Pulse ◽  
High Frequency Stimulation ◽  
Neuronal Excitation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Stimulation Of

We investigated the neuronal plasticity in the spinal dorsal horn and its relationship with spinal inhibitory networks using an optical-imaging method that detects neuronal excitation. High-intensity single-pulse stimulation of the dorsal root activating both A and C fibers evoked an optical response in the lamina II (the substantia gelatinosa) of the dorsal horn in transverse slices of 12- to 25-day-old rat spinal cords stained with a voltage-sensitive dye, RH-482. The optical response, reflecting the net neuronal excitation along the slice-depth, was depressed by 28% for more than 1 h after a high-frequency conditioning stimulation of A fibers in the dorsal root (3 tetani of 100 Hz for 1 s with an interval of 10 s). The depression was not induced in a perfusion solution containing an NMDA antagonist,dl-2-amino-5-phosphonovaleric acid (AP5; 30 μM). In a solution containing the inhibitory amino acid antagonists bicuculline (1 μM) and strychnine (3 μM), and also in a low Cl−solution, the excitation evoked by the single-pulse stimulation was enhanced after the high-frequency stimulation by 31 and 18%, respectively. The enhanced response after conditioning was depotentiated by a low-frequency stimulation of A fibers (0.2–1 Hz for 10 min). Furthermore, once the low-frequency stimulation was applied, the high-frequency conditioning could not potentiate the excitation. Inhibitory transmissions thus regulate the mode of synaptic plasticity in the lamina II most likely at afferent terminals. The high-frequency conditioning elicits a long-term depression (LTD) of synaptic efficacy under a greater activity of inhibitory amino acids, but it results in a long-term potentiation (LTP) when inhibition is reduced. The low-frequency preconditioning inhibits the potentiation induction and maintenance by the high-frequency conditioning. These mechanisms might underlie robust changes of nociception, such as hypersensitivity after injury or inflammation and pain relief after electrical or cutaneous stimulation.

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