Blockade of cyclic AMP-dependent protein kinase does not prevent the reverse ocular dominance shift in kitten visual cortex.
Blockade of cyclic AMP-dependent protein kinase does not prevent the reverse ocular dominance shift in kitten visual cortex.
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DOI：
10.1152/jn.00313.2003
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发表时间：
2003-08
影响因子：
2.5
通讯作者：
S. Shimegi;Q. Fischer;Yupeng Yang;Hiromichi Sato;N. Daw
中科院分区：
文献类型：
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作者：
S. Shimegi;Q. Fischer;Yupeng Yang;Hiromichi Sato;N. Daw
单眼剥夺（MD）是视皮层发育的关键时期，导致神经元双眼反应丧失，向睁开眼转移，即正常的眼优势（OD）转移。然而，当MD与蝇蕈醇对视觉皮层的慢性失活相结合时，神经元的OD分布向剥夺眼转移（反向OD转移）。我们以前已经证明，正常的OD偏移被蛋白激酶A（PKA）抑制剂，8-氯腺苷-3 '，5'-环硫代磷酸，RP异构体（RP-8-Cl-cAMPS），长期输注到小猫视觉皮层取消。在这项研究中，我们研究了这种抑制剂对反向OD偏移的影响。MD和蝇蕈醇输注到6周龄小猫的视觉皮层中的组合引起了与先前研究中所见相当的反向OD偏移。然而，在PKA抑制剂与蝇蕈醇同时输注时也观察到反向OD偏移。在层IV中观察到最强的OD偏移，无论PKA抑制剂的存在与否。这表明，突触前和突触后活动的分离，主要发生在丘脑皮质突触，诱导反向OD偏移和抑制PKA不阻止它。推测，抑制PKA在沉默皮层没有效果。我们的结论是：1）PKA的激活是不需要的反向OD位移的诱导，和2）的细胞内信号转导机制的基础MD诱导OD可塑性之间的正常和反向OD位移不同。
Monocular deprivation (MD) during the critical period for the development of visual cortex causes a loss of binocular response of neurons and a shift to the open eye, a normal ocular dominance (OD) shift. However, when MD is combined with chronic inactivation of the visual cortex by muscimol, the OD distribution of the neurons shifts to the deprived eye (reverse OD shift). We have previously shown that the normal OD shift is abolished by chronic infusion of the protein kinase A (PKA) inhibitor, 8-chloroadenosine-3', 5'-cyclic monophosphorothioate, Rp-isomer (Rp-8-Cl-cAMPS), into kitten visual cortex. In this study, we investigated the effect of this inhibitor on the reverse OD shift. Combination of MD and muscimol infusion into the visual cortex of 6-wk-old kittens caused a reverse OD shift that was comparable to that seen in previous studies. However, a reverse OD shift was also seen with concurrent infusion of the PKA inhibitor with muscimol. The strongest OD shift was observed in layer IV regardless of the presence or absence of the PKA inhibitor. This suggests that the dissociation of pre- and postsynaptic activities, which occurs mainly at thalamocortical synapses, induces the reverse OD shift and that inhibition of PKA does not prevent it. Presumably, an inhibition of PKA has no effect in silent cortex. We conclude that 1) an activation of PKA is not required for the induction of the reverse OD shift, and 2) the intracellular signaling mechanism underlying MD-induced OD plasticity differs between normal and reverse OD shifts.