TY - JOUR
T1 - Long-term potentiation of intrinsic excitability in LV visual cortical neurons
AU - Cudmore, Robert H.
AU - Turrigiano, Gina G.
PY - 2004/7
Y1 - 2004/7
N2 - Neuronal excitability has a large impact on network behavior, and plasticity in intrinsic excitability could serve as an important information storage mechanism. Here we ask whether postsynaptic excitability of layer V pyramidal neurons from primary visual cortex can be rapidly regulated by activity. Whole cell current-clamp recordings were obtained from visual cortical slices, and intrinsic excitability was measured by recording the firing response to small depolarizing test pulses. Inducing neurons to fire at high-frequency (30-40 Hz) in bursts for 5 min in the presence of synaptic blockers increased the firing rate evoked by the test pulse. This long-term potentiation of intrinsic excitability (LTP-IE) lasted for as long as we held the recording (>60 min). LTP-IE was accompanied by a leftward shift in the entire frequency versus current (F-I) curve and a decrease in threshold current and voltage. Passive neuronal properties were unaffected by the induction protocol, indicating that LTP-IE occurred through modification in voltage-gated conductances. Reducing extracellular calcium during the induction protocol, or buffering intracellular calcium with bis-(o-aminophenoxy)- N,N,N′, N′-tetraacetic acid, prevented LTP-IE. Finally, blocking protein kinase A (PKA) activation prevented, whereas pharmacological activation of PKA both mimicked and occluded, LTP-IE. This suggests that LTP-IE occurs through postsynaptic calcium influx and subsequent activation of PKA. Activity-dependent plasticity in intrinsic excitability could greatly expand the computational power of individual neurons.
AB - Neuronal excitability has a large impact on network behavior, and plasticity in intrinsic excitability could serve as an important information storage mechanism. Here we ask whether postsynaptic excitability of layer V pyramidal neurons from primary visual cortex can be rapidly regulated by activity. Whole cell current-clamp recordings were obtained from visual cortical slices, and intrinsic excitability was measured by recording the firing response to small depolarizing test pulses. Inducing neurons to fire at high-frequency (30-40 Hz) in bursts for 5 min in the presence of synaptic blockers increased the firing rate evoked by the test pulse. This long-term potentiation of intrinsic excitability (LTP-IE) lasted for as long as we held the recording (>60 min). LTP-IE was accompanied by a leftward shift in the entire frequency versus current (F-I) curve and a decrease in threshold current and voltage. Passive neuronal properties were unaffected by the induction protocol, indicating that LTP-IE occurred through modification in voltage-gated conductances. Reducing extracellular calcium during the induction protocol, or buffering intracellular calcium with bis-(o-aminophenoxy)- N,N,N′, N′-tetraacetic acid, prevented LTP-IE. Finally, blocking protein kinase A (PKA) activation prevented, whereas pharmacological activation of PKA both mimicked and occluded, LTP-IE. This suggests that LTP-IE occurs through postsynaptic calcium influx and subsequent activation of PKA. Activity-dependent plasticity in intrinsic excitability could greatly expand the computational power of individual neurons.
UR - http://www.scopus.com/inward/record.url?scp=3042636619&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3042636619&partnerID=8YFLogxK
U2 - 10.1152/jn.01059.2003
DO - 10.1152/jn.01059.2003
M3 - Article
C2 - 14973317
AN - SCOPUS:3042636619
SN - 0022-3077
VL - 92
SP - 341
EP - 348
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
IS - 1
ER -