Buckby L E, Lacey M G
Department of Pharmacology, Division of Neuroscience, The Medical School, University of Birmingham, Vincent Drive, Edgbaston, Birmingham B15 2TT, UK.
Exp Brain Res. 2001 Nov;141(2):146-52. doi: 10.1007/s002210100841.
Extracellularly recorded field potentials, evoked by stimulation of cortico-nucleus accumbens border, were recorded in the nucleus accumbens (NAcc) in horizontal slices of rat ventral forebrain. The field excitatory postsynaptic potential (EPSP) event (N2) was calcium dependent, blocked by tetrodotoxin (1 microM), and reduced by over 70% by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), the antagonist of AMPA-type glutamate receptors. The EPSP amplitude was enhanced by either of the GABA(A) receptor antagonists, picrotoxin (10 microM; by 252+/-33%, n=18) and bicuculline methiodide (20 microM; by 216+/-34%, n=4). Additionally, picrotoxin (3-50 microM) and bicuculline methiodide (20 microM) promoted epileptiform activity within the NAcc, manifest as the emergence of additional late components, N3, N4 and N5, in the evoked synaptic waveform. In slices with the frontal cortex removed, picrotoxin (10-50 microM) and bicuculline methiodide (20 microM) were unable to promote epileptiform activity within the NAcc, although a smaller increase in the peak amplitude of the field EPSP (163+/-18%, n=6) was observed at the highest concentrations of picrotoxin (50 microM). Histological examination of the slice demonstrated that in such decorticated slices, the piriform cortex (PC) had been removed. We propose that stimulation of the cortico-NAcc border not only evokes an orthodromic EPSP in the NAcc, but also causes antidromic activation of cortical tissue. Disinhibition by GABA(A) antagonists of circuits intrinsic to the cortex, possibly the piriform cortex, is the principal cause of the facilitation of the EPSP and of regenerative epileptiform activity in NAcc evoked by stimulation of cortical input.
在大鼠腹侧前脑水平切片的伏隔核（NAcc）中，记录了由刺激皮质 - 伏隔核边界诱发的细胞外记录场电位。场兴奋性突触后电位（EPSP）事件（N2）依赖于钙，被河豚毒素（1微摩尔）阻断，并且被AMPA型谷氨酸受体拮抗剂6 - 氰基 - 7 - 硝基喹喔啉 - 2,3 - 二酮（CNQX）（10微摩尔）降低了70%以上。EPSP幅度被两种GABA(A)受体拮抗剂增强，印防己毒素（10微摩尔；增强252±33%，n = 18）和甲磺酸荷包牡丹碱（20微摩尔；增强216±34%，n = 4）。此外，印防己毒素（3 - 50微摩尔）和甲磺酸荷包牡丹碱（20微摩尔）促进了伏隔核内的癫痫样活动，表现为在诱发的突触波形中出现额外的晚期成分N3、N4和N5。在切除额叶皮质的切片中，印防己毒素（10 - 50微摩尔）和甲磺酸荷包牡丹碱（20微摩尔）无法促进伏隔核内的癫痫样活动，尽管在印防己毒素最高浓度（50微摩尔）时观察到场EPSP峰值幅度有较小增加（163±18%，n = 6）。切片的组织学检查表明，在这种去皮质切片中，梨状皮质（PC）已被切除。我们提出，刺激皮质 - 伏隔核边界不仅在伏隔核中诱发顺行性EPSP，还会导致皮质组织的逆行性激活。GABA(A)拮抗剂对皮质固有回路（可能是梨状皮质）的去抑制作用是刺激皮质输入诱发伏隔核中EPSP促进和再生性癫痫样活动的主要原因。
