Abstract
Previous studies have demonstrated that brain-derived neurotrophic factor (BDNF) is one of the diffusible messengers for enhancing synaptic transmission in the hippocampus. Less information is available about the possible roles of BDNF in the anterior cingulate cortex (ACC). In the present study, we used 64-electrode array field recording system to investigate the effect of BDNF on ACC excitatory transmission. We found that BDNF enhanced synaptic responses in a dose-dependent manner in the ACC in C57/BL6 mice. The enhancement was long-lasting, and persisted for at least 3 h. In addition to the enhancement, BDNF also recruited inactive synaptic responses in the ACC. Bath application of the tropomyosin receptor kinase B (TrkB) receptor antagonist K252a blocked BDNF-induced enhancement. L-type voltage-gated calcium channels (L-VGCC), metabotropic glutamate receptors (mGluRs), but not NMDA receptors were required for BDNF-produced enhancement. Moreover, calcium-stimulated adenylyl cyclase subtype 1 (AC1) but not AC8 was essential for the enhancement. A selective AC1 inhibitor NB001 completely blocked the enhancement. Furthermore, BDNF-produced enhancement occluded theta burst stimulation (TBS) induced long-term potentiation (LTP), suggesting that they may share similar signaling mechanisms. Finally, the expression of BDNF-induced enhancement depends on postsynaptic incorporation of calcium-permeable AMPA receptors (CP-AMPARs) and protein kinase Mζ (PKMζ). Our results demonstrate that cortical BDNF may contribute to synaptic potentiation in the ACC.
Highlights
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family which plays a diverse, and broad, role in regulating neuronal structure and function in the central nervous system [1]
We found that BDNF induced synaptic enhancement in the anterior cingulate cortex (ACC) slice with four active channels showing long-term enhancement lasting over 3 h (Fig. 1E) and two active channels showing a short-term enhancement lasting less than 2 h (Fig. 1F), with one channel remaining unchanged throughout the entire recording period (Fig. 1G)
CP‐AMPARs and protein kinase Mζ (PKMζ) were involved in BDNF induced synaptic enhancement In the ACC, changes in postsynaptic AMPARs contribute to the expression of theta burst stimulation (TBS) induced L-long-term potentiation (LTP), and the application of a CP-AMPAR antagonist 3 h after induction reduced synaptic potentiation [13]
Summary
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family which plays a diverse, and broad, role in regulating neuronal structure and function in the central nervous system [1]. Cumulative data has demonstrated that BDNF is crucially involved in synaptic plasticity in the adult brain [2]. ACC is a key cortical area for processing painful and emotional information [8,9,10,11]. Adult synapses in the ACC are highly plastic, and both presynaptic release of glutamate and postsynaptic excitatory responses can undergo long-term potentiation (LTP) [8, 12]. Inhibition or genetic deletion of key molecules required for triggering LTP produces analgesic effects in animal models of chronic pain as well as emotional fear, anxiety, and depression [13, 14].
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