Abstract
Voltage-gated Ca2+ (CaV) channels are transmembrane proteins comprising three subfamilies named CaV1, CaV2 and CaV3. The CaV3 channel subfamily groups the low-voltage activated Ca2+ channels (LVA or T-type) a significant role in regulating neuronal excitability. CaV3 channel activity may lead to the generation of complex patterns of action potential firing such as the postinhibitory rebound (PIR). In the adult spinal cord, these channels have been found in dorsal horn interneurons where they control physiological events near the resting potential and participate in determining excitability. In motoneurons, CaV3 channels have been found during development, but their functional expression has not yet been reported in adult animals. Here, we show evidence for the presence of CaV3 channel-mediated PIR in motoneurons of the adult turtle spinal cord. Our results indicate that Ni2+ and NNC55-0396, two antagonists of CaV3 channel activity, inhibited PIR in the adult turtle spinal cord. Molecular biology and biochemical assays revealed the expression of the CaV3.1 channel isotype and its localization in motoneurons. Together, these results provide evidence for the expression of CaV3.1 channels in the spinal cord of adult animals and show also that these channels may contribute to determine the excitability of motoneurons.
Highlights
Motoneurons are efferent neurons that originate in the spinal cord and synapse with muscle fibers to control muscle contraction [1]
It is acknowledged that postinhibitory rebound (PIR) may be mediated by the activation of two types of ion channels known as hyperpolarization-activated cyclic nucleotide-gated (HCN) and low voltage-activated (LVA) Ca2+ channels [3,5,6]
In addition to their contribution to the rebound firing of action potential (AP), HCN channels are the dominant molecular component of the hyperpolarization-activated current (Ih) that play a major role in pacemaking activity [2,6,7], while LVA Ca2+ channels can modulate neuronal excitability by opening in response to small membrane depolarization
Summary
Motoneurons are efferent neurons that originate in the spinal cord and synapse with muscle fibers to control muscle contraction [1]. Motoneurons may generate an action potential (AP) firing pattern known as postinhibitory rebound (PIR) when the membrane potential returns to its resting value [2]. It is acknowledged that PIR may be mediated by the activation of two types of ion channels known as hyperpolarization-activated cyclic nucleotide-gated (HCN) and low voltage-activated (LVA) Ca2+ channels [3,5,6]. In addition to their contribution to the rebound firing of APs, HCN channels are the dominant molecular component of the hyperpolarization-activated current (Ih) that play a major role in pacemaking activity [2,6,7], while LVA Ca2+ channels ( known as CaV3.1, CaV3.2 and CaV3.3) can modulate neuronal excitability by opening in response to small membrane depolarization. In addition to promote rebound firing, CaV3 channels regulate lowamplitude intrinsic neuronal oscillations, promote Ca2+ entry, and boost synaptic signals [5,8,9]
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