Dodt H U, Pawelzik H, Zieglgänsberger W
Clinical Neuropharmacology, Max-Planck-Institute for Psychiatry, Munich, F.R.G.
Brain Res. 1991 Apr 5;545(1-2):307-11. doi: 10.1016/0006-8993(91)91303-i.
The effects of noradrenaline (NA) and alpha- and beta-adrenergic agonists on neocortical neurons in rat brain slices were studied by intracellular recording. NA added to the perfusion medium decreased the orthodromically evoked excitatory postsynaptic potential (EPSP) and increased the neuronal excitability on current injection. The decrease of the EPSP by NA was mimicked by alpha-adrenoceptor activation. The beta-adrenergic agonist, isoprenaline, increased the neuronal excitability to current injections similarly to NA. In addition, isoprenaline markedly increased the amplitude of a late component of the EPSP (I-EPSP). The increase of the I-EPSP was long-lasting (up to 90 min). Since this late component of the EPSP is blocked by the NMDA (N-methyl-D-aspartate)-antagonist APV (D-2-amino-5-phosphonovalerate), an enhancement of this excitatory synaptic transient via beta-adrenoceptors may be relevant for the facilitatory effect of NA on neuronal plasticity.
通过细胞内记录研究了去甲肾上腺素（NA）以及α和β肾上腺素能激动剂对大鼠脑片新皮质神经元的影响。添加到灌流介质中的NA降低了顺向诱发的兴奋性突触后电位（EPSP），并增加了电流注入时神经元的兴奋性。NA对EPSP的降低作用可被α肾上腺素受体激活所模拟。β肾上腺素能激动剂异丙肾上腺素与NA类似地增加了电流注入时神经元的兴奋性。此外，异丙肾上腺素显著增加了EPSP晚期成分（I-EPSP）的幅度。I-EPSP的增加是持久的（长达90分钟）。由于EPSP的这种晚期成分被NMDA（N-甲基-D-天冬氨酸）拮抗剂APV（D-2-氨基-5-磷酸戊酸）阻断，因此通过β肾上腺素受体增强这种兴奋性突触瞬变可能与NA对神经元可塑性的促进作用有关。
