scholarly journals BDNF Controls Bidirectional Endocannabinoid Plasticity at Corticostriatal Synapses

2019 ◽  
Vol 30 (1) ◽  
pp. 197-214 ◽  
Author(s):  
Giuseppe Gangarossa ◽  
Sylvie Perez ◽  
Yulia Dembitskaya ◽  
Ilya Prokin ◽  
Hugues Berry ◽  
...  
Keyword(s):  
Low Frequency ◽  
Dorsal Striatum ◽  
Brain Structures ◽  
Spike Timing ◽  
Procedural Learning ◽  
Receptor Kinase ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Corticostriatal Plasticity

AbstractThe dorsal striatum exhibits bidirectional corticostriatal synaptic plasticity, NMDAR and endocannabinoids (eCB) mediated, necessary for the encoding of procedural learning. Therefore, characterizing factors controlling corticostriatal plasticity is of crucial importance. Brain-derived neurotrophic factor (BDNF) and its receptor, the tropomyosine receptor kinase-B (TrkB), shape striatal functions, and their dysfunction deeply affects basal ganglia. BDNF/TrkB signaling controls NMDAR plasticity in various brain structures including the striatum. However, despite cross-talk between BDNF and eCBs, the role of BDNF in eCB plasticity remains unknown. Here, we show that BDNF/TrkB signaling promotes eCB-plasticity (LTD and LTP) induced by rate-based (low-frequency stimulation) or spike-timing–based (spike-timing–dependent plasticity, STDP) paradigm in striatum. We show that TrkB activation is required for the expression and the scaling of both eCB-LTD and eCB-LTP. Using 2-photon imaging of dendritic spines combined with patch-clamp recordings, we show that TrkB activation prolongs intracellular calcium transients, thus increasing eCB synthesis and release. We provide a mathematical model for the dynamics of the signaling pathways involved in corticostriatal plasticity. Finally, we show that TrkB activation enlarges the domain of expression of eCB-STDP. Our results reveal a novel role for BDNF/TrkB signaling in governing eCB-plasticity expression in striatum and thus the engram of procedural learning.

scholarly journals BDNF controls bidirectional endocannabinoid-plasticity at corticostriatal synapses

2019 ◽  
Author(s):  
Giuseppe Gangarossa ◽  
Sylvie Perez ◽  
Yulia Dembitskaya ◽  
Ilya Prokin ◽  
Hugues Berry ◽  
...  
Keyword(s):  
Low Frequency ◽  
Dorsal Striatum ◽  
Brain Structures ◽  
Spike Timing ◽  
Procedural Learning ◽  
Two Photon ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Corticostriatal Plasticity

ABSTRACTThe dorsal striatum exhibits bidirectional corticostriatal synaptic plasticity, NMDAR- and endocannabinoids-(eCB)-mediated, necessary for the encoding of procedural learning. Therefore, characterizing factors controlling corticostriatal plasticity is of crucial importance. Brain-derived neurotrophic factor (BDNF) and its receptor, the tropomyosine receptor kinase-B (TrkB), shape striatal functions and their dysfunction deeply affect basal ganglia. BDNF/TrkB signaling controls NMDAR-plasticity in various brain structures including striatum. However, despite cross-talks between BDNF and eCBs, the role of BDNF in eCB-plasticity remains unknown. Here, we show that BDNF/TrkB signaling promotes eCB-plasticity (LTD and LTP) induced by rate-based (low-frequency stimulation) or spike-timing-based (spike-timing-dependent plasticity, STDP) paradigm in striatum. We show that TrkB activation is required for the expression and the scaling of both eCB-LTD and eCB-LTP. Using two-photon imaging of the dendritic spines combined with patch-clamp recordings, we show that TrkB activation induces an intracellular calcium boost, thus increasing eCB synthesis and release. We provide a mathematical model for the dynamics of the signaling pathways involved in corticostriatal plasticity. Finally, we show that TrkB activation allows an enlargement of the domain of expression of eCB-STDP. Our results reveal a novel role for BDNF/TrkB signaling in governing eCB-plasticity expression in striatum, and thus the engram of procedural learning.

Role of fascia in maintenance of muscle tension and pressure

1981 ◽  
Vol 51 (2) ◽  
pp. 317-320 ◽  
Author(s):  
S. R. Garfin ◽  
C. M. Tipton ◽  
S. J. Mubarak ◽  
S. L. Woo ◽  
A. R. Hargens ◽  
...  
Keyword(s):  
High Frequency ◽  
Muscle Tension ◽  
Fluid Pressure ◽  
Low Frequency ◽  
Testing Procedure ◽  
Force Transducer ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

The effect of fasciotomy on muscle tension (measured by a force transducer attached to the tendon) and interstitial fluid pressure (measured by Wick catheters in the muscle belly) was studied in the anterolateral compartments of 13 dog hindlimbs. Muscle tension and pressure were monitored in the tibialis cranialis muscle after low- and high-frequency stimulation of the peroneal nerve to produce twitch- and tetanic-type contractions. Fasciotomy decreased muscle force during the low-frequency stimulation by 16% (35.3 +/- 4.9 to 28.4 +/- 3.9 N) and during the high-frequency stimulation by 10% (60.8 %/- 4.9 to 54.8 +/- 3.9 N). Muscle pressure decreased 50% after fasciotomy under both conditions, 15 +/- 2 to 6 +/- 1 mmHg and 84 +/- 17 to 41 +/- 8 mmHg), respectively. Repeated functional evaluations during the testing procedure indicated that muscle fatigue was not a major factor in these results. It was concluded that fascia is important in the development of muscle tension and changes in interstitial pressure. Furthermore, the results raised questions concerning the merits of performing a fasciotomy for athletes with a compartment syndrome.

The role of galanin receptors in anticonvulsant effects of low-frequency stimulation in perforant path–kindled rats

Neuroscience ◽  
2007 ◽  
Vol 150 (2) ◽  
pp. 396-403 ◽  
Author(s):  
M. Sadegh ◽  
J. Mirnajafi-Zadeh ◽  
M. Javan ◽  
Y. Fathollahi ◽  
M. Mohammad-Zadeh ◽  
...  
Keyword(s):  
Low Frequency ◽  
Perforant Path ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Galanin Receptors ◽  
Anticonvulsant Effects

The role of 5-HT1A receptors of hippocampal CA1 region in anticonvulsant effects of low-frequency stimulation in amygdala kindled rats

2018 ◽  
Vol 196 ◽  
pp. 119-125 ◽  
Author(s):  
Alireza Gharib ◽  
Zeinab Sayyahi ◽  
Alireza Komaki ◽  
Victoria Barkley ◽  
Abdolrahman Sarihi ◽  
...  
Keyword(s):  
Low Frequency ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Low Frequency Stimulation ◽  
Hippocampal Ca1 ◽  
Frequency Stimulation ◽  
Anticonvulsant Effects

Fatigue and damage to the masseter muscle by prolonged low-frequency stimulation in the rat

2005 ◽  
Vol 50 (12) ◽  
pp. 1005-1013 ◽  
Author(s):  
Konosuke Yamasaki ◽  
Shuitsu Harada ◽  
Itsuro Higuchi ◽  
Mitsuhiro Osame ◽  
Gakuji Ito
Keyword(s):  
Masseter Muscle ◽  
Low Frequency ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

scholarly journals MONOSYNAPTIC REFLEX RESPONSE OF INDIVIDUAL MOTONEURONS AS A FUNCTION OF FREQUENCY

1957 ◽  
Vol 40 (3) ◽  
pp. 435-450 ◽  
Author(s):  
David P. C. Lloyd
Keyword(s):  
High Frequency ◽  
Temporal Summation ◽  
Low Frequency ◽  
Stimulation Frequency ◽  
Monosynaptic Reflex ◽  
Reflex Response ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Frequency Of Stimulation

An assemblage of individual motoneurons constituting a synthetic motoneuron pool has been studied from the standpoint of relating monosynaptic reflex responses to frequency of afferent stimulation. Intensity of low frequency depression is not a simple function of transmitter potentiality. As frequency of stimulation increases from 3 per minute to 10 per second, low frequency depression increases in magnitude. Between 10 and approximately 60 per second low frequency depression apparently diminishes and subnormality becomes a factor in causing depression. At frequencies above 60 per second temporal summation occurs, but subnormality limits the degree of response attainable by summation. At low stimulation frequencies rhythm is determined by stimulation frequency. Interruptions of rhythmic firing depend solely upon temporal fluctuation of excitability. At high frequency of stimulation rhythm is determined by subnormality rather than inherent rhythmicity, and excitability fluctuation leads to instability of response rhythm. In short, whatever the stimulation frequency, random excitability fluctuation is the factor disrupting rhythmic response. Monosynaptic reflex response latency is stable during high frequency stimulation as it is in low frequency stimulation provided a significant extrinsic source of random bombardment is not present. In the presence of powerful random bombardment discharge may become random with respect to monosynaptic afferent excitation provided the latter is feeble. When this occurs it does so equally at low frequency and high frequency. Thus temporal summation is not a necessary factor. There is, then, no remaining evidence to suggest that the agency for temporal summation in the monosynaptic system becomes a transmitting agency in its own right.

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