Tepper J M, Martin L P, Anderson D R
Center for Molecular and Behavioral Neuroscience, Aidekman Research Center, Rutgers, State University of New Jersey, Newark 07102, USA.
J Neurosci. 1995 Apr;15(4):3092-103. doi: 10.1523/JNEUROSCI.15-04-03092.1995.
Evidence from electrophysiological studies has suggested an inhibitory interaction between GABAergic neurons in substantia nigra pars reticulata and dopaminergic neurons in pars compacta. However, that this inhibitory interaction is due to a projection from pars reticulata to pars compacta has never been demonstrated directly, nor has the GABAergic neuron that mediates the interaction been identified either electrophysiologically or anatomically. To more closely examine interactions between substantia nigra pars reticulata GABA neurons and dopaminergic neurons, single unit extracellular recordings were obtained from antidromically identified nigrostriatal neurons and their response to antidromic activation of nigral GABAergic projection neurons observed. Stimulation of superior colliculus or thalamus produced a short latency inhibition of dopaminergic neurons. This inhibition was blocked by local application of bicuculline but not 2-hydroxysaclofen. Bicuculline caused most dopaminergic neurons to fire in a bursty mode, whereas saclofen caused most dopaminergic neurons to fire in a pacemaker-like mode. The thalamic-evoked inhibition was not affected by kainate lesions of the globus pallidus, but these lesions produced effects on firing pattern identical to those produced by saclofen. These data demonstrate a short latency inhibition of nigral dopaminergic neurons mediated by GABAA receptors that arises from the axon collaterals of pars reticulata projection neurons. We propose a model in which the firing pattern of nigral dopaminergic neurons in vivo is modulated differentially by disinhibition of GABAA inputs arising from pars reticulata projection neuron axon collaterals and disinhibition of pallidonigral GABAergic inputs mediated by GABAB receptors.
电生理研究的证据表明，黑质网状部的γ-氨基丁酸（GABA）能神经元与致密部的多巴胺能神经元之间存在抑制性相互作用。然而，这种抑制性相互作用是否源于网状部向致密部的投射，从未得到直接证实，介导这种相互作用的GABA能神经元在电生理或解剖学上也未被鉴定出来。为了更深入地研究黑质网状部GABA神经元与多巴胺能神经元之间的相互作用，我们从经逆向鉴定的黑质纹状体神经元获得了单单位细胞外记录，并观察了它们对黑质GABA能投射神经元逆向激活的反应。刺激上丘或丘脑可使多巴胺能神经元产生短潜伏期抑制。局部应用荷包牡丹碱可阻断这种抑制，但2-羟基舒必利则不能。荷包牡丹碱使大多数多巴胺能神经元以爆发式模式放电，而舒必利则使大多数多巴胺能神经元以起搏器样模式放电。丘脑诱发的抑制不受苍白球海人藻酸损伤的影响，但这些损伤对放电模式产生的影响与舒必利产生的影响相同。这些数据表明，由网状部投射神经元的轴突侧支介导的GABAA受体对黑质多巴胺能神经元产生短潜伏期抑制。我们提出了一个模型，其中黑质多巴胺能神经元在体内的放电模式受到来自网状部投射神经元轴突侧支的GABAA输入去抑制和由GABAB受体介导的苍白球-黑质GABA能输入去抑制的差异调节。
