| Medial geniculate body (MGB) consists of ventral division of MGB (MGBv), dorsal division of MGB (MGBd) and medial division of MGB (MGBm) in thalamus. Learning-induced frequency-specific receptive field plasticity can be evoked in MGB neurons, which depends on activation of muscarinic cholinergic receptor (mAChR). However, the cellular mechanism remains unclear. Thus, using in vitro whole-cell patch clamp recordings and biocytin staining, I investigated the electrophysiological properties of MGB neurons in mice and the effects of cholinergic receptor activation on membrane properties and its mechanism. The results are as follows:1.99 MGB neurons were obtained, including 36 MGBv neurons,34 MGBd neurons and 29 MGBm neurons. The resting membrane potential (RMP) and active threshold showed significant differences among neurons of different subnuclei (unpaired t-test, p< 0.05). Two firing patterns including bursting (16.2%,16/99) and tonic (83.8%,83/99) were identified based on the responses to depolarizing current. Tonic firing mainly occurred in MGBv neurons (94.4%,34/36) while bursting firing in MGBm neurons (31.0%,9/29). All MGB neurons had depolarizing rebounds at the offset of hyperpolarizing currents. Some neurons (17.2%,17/99) also showed hyperpolarization-activated inward current (Ih) to hyperpolarizing currents.2. Carbachol (CCh,5μM) was used to investigate the effects of cholinergic receptor activation on electrophysiological properties of 65 MGB neurons, including 25 MGBv neurons,20 MGBd neurons, and 20 MGBm neurons. The membrane potentials were depolarized, hyperpolarized or no change. The percentages of depolarization are 84% (21/25) in MGBv,45%(9/20) in MGBd and 40%(8/20) in MGBm. The percentages of hyperpolarization and no change are 12%(3/25),4%(1/25) in MGBv,35%(7/20),20% (4/20) in MGBd and 45%(9/20),15%(3/20) in MGBm.3. Bath application of CCh together with positive current injection were able to induce persistent activities (PA) of neural memebrane, which was characterized by continuous depolarization and increased spiking after current injection. The PA was induced in 63.1%(41/65) of all recorded neurons. The percentage of neurons with PA was84%(21/25) in MGBv,60%(12/20) in MGBd and 40%(8/20) in MGBm.The PA frequency of MGBv neurons, comparable to MGBm neruons, was higher than that of MGBd neurons (unpaired t-test, p< 0.05) Comparing to short duration (200 ms) of current injection, long current injection (2 s) yielded higherfrequency during PA (unpaired t-test,p< 0.05).4. Different channel blockers were applied to investigate the induction mechanisms of PA. The results showed that PA was blocked by muscarinic acetylcholine receptor (mAChR) antagonist atropine (10 μM) (n=12, paired t-test, p<0.01). Fast synaptic blockers kynurenic acid (KA,2 mM) and picrotoxin (100μM) partially blocked PA (n=13), they significantly reduced PA frequency and amplitude of depolarization (n=13, paired t-test, p<0.05), but facilitated PA of some neurons (n=3) with the increasing of PA frequency and amplitude of depolarization.Overall, MGB neurons from the three subnuclei were significantly differentin RMP and active threshold and responded differently to CCh. mAChR activation and depolarizaitons were able to induce PA in MGB neurons. Pharmalogical experiemnts indicated that PA in different thalamic subnuclei may share the same mechanism. PA depended on the activation of mAChR as well as fast synaptic transmission which suggested a result of interaction between intrinsic properties and neural circuits. This study provided insights for us to understandthe cellularmechanism of learing-induced auditory plasticity. |
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