Leresche N, Asprodini E, Emri Z, Cope D W, Crunelli V
Neurobiologie Cellulaire, Institut des Neurosciences, UMR CNRS 7624, Université Pierre et Marie Curie, Paris, France.
Neuroscience. 2000;98(3):513-22. doi: 10.1016/s0306-4522(00)00107-x.
The action of somatostatin on GABA-mediated transmission was investigated in cat and rat thalamocortical neurons of the dorsal lateral geniculate nucleus and ventrobasal thalamus in vitro. In the cat thalamus, somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons and on the postsynaptic response elicited in these cells by bath or iontophoretic application of (+/-)baclofen (5-10 microM) or GABA, respectively. However, somatostatin (1-10 microM) decreased by a similar amount (45-55%) the amplitude of electrically evoked GABA(A) and GABA(B) inhibitory postsynaptic potentials in 71 and 50% of neurons in the lateral geniculate and ventrobasal nucleus, respectively. In addition, the neuropeptide abolished spontaneous bursts of GABA(A) inhibitory postsynaptic potentials in 85% of kitten lateral geniculate neurons, and decreased (40%) the amplitude of single spontaneous GABA(A) inhibitory postsynaptic potentials in 87% of neurons in the cat lateral geniculate nucleus. Similar results were obtained in the rat thalamus. Somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons in this species, or on the outward current elicited by puff-application of (+/-)baclofen (5-10 microM). However, in 57 and 22% of neurons in the rat lateral geniculate and ventrobasal nuclei, respectively, somatostatin (1 microM) reduced the frequency, but not the amplitude, of miniature GABA(A) inhibitory postsynaptic currents by 31 and 37%, respectively. In addition, the neuropeptide (1 microM) decreased the amplitude of evoked GABA(A) inhibitory postsynaptic currents in 20 and 55% of rat ventrobasal neurons recorded in normal conditions and during enhanced excitability, respectively: this effect was stronger on bursts of inhibitory postsynaptic currents(100% decrease) than on single inhibitory postsynaptic currents (41% decrease). These results demonstrate that in the sensory thalamus somatostatin inhibits GABA(A)- and GABA(B)-mediated transmission via a presynaptic mechanism, and its action is more prominent on bursts of GABAergic synaptic currents/potentials.
在体外对猫和大鼠背外侧膝状核及腹侧基底丘脑的丘脑皮质神经元中生长抑素对γ-氨基丁酸（GABA）介导的传递作用进行了研究。在猫的丘脑中，生长抑素（10微摩尔）对丘脑皮质神经元的被动膜特性以及分别通过浴槽给药或离子电渗法施加（±）巴氯芬（5 - 10微摩尔）或GABA在这些细胞中引发的突触后反应均无影响。然而，生长抑素（1 - 10微摩尔）分别使外侧膝状核和腹侧基底核中71%和50%的神经元中电诱发的GABA(A)和GABA(B)抑制性突触后电位的幅度降低了相似的量（45 - 55%）。此外，该神经肽消除了85%的小猫外侧膝状核神经元中GABA(A)抑制性突触后电位的自发爆发，并使猫外侧膝状核中87%的神经元中单个自发GABA(A)抑制性突触后电位的幅度降低了40%。在大鼠丘脑中也获得了类似结果。生长抑素（10微摩尔）对该物种丘脑皮质神经元的被动膜特性或通过微量给药（±）巴氯芬（5 - 10微摩尔）引发的外向电流均无影响。然而，在大鼠外侧膝状核和腹侧基底核中分别有57%和22%的神经元，生长抑素（1微摩尔）使微小GABA(A)抑制性突触后电流的频率分别降低了31%和37%，但幅度未降低。此外，该神经肽（1微摩尔）在正常条件下和兴奋性增强时分别使记录到的20%和55%的大鼠腹侧基底神经元中诱发的GABA(A)抑制性突触后电流的幅度降低：这种作用对抑制性突触后电流的爆发（降低100%）比对单个抑制性突触后电流（降低41%）更强。这些结果表明，在感觉丘脑中生长抑素通过突触前机制抑制GABA(A)和GABA(B)介导的传递，并且其作用在GABA能突触电流/电位的爆发上更为突出。
