INTERACTIONS BETWEEN D-ALA-MET-ENKEPHALIN, A10 DOPAMINERGIC-NEURONS, AND SPONTANEOUS BEHAVIOR IN THE RAT
INTERACTIONS BETWEEN D-ALA-MET-ENKEPHALIN, A10 DOPAMINERGIC-NEURONS, AND SPONTANEOUS BEHAVIOR IN THE RAT
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DOI：
10.1016/s0166-4328(80)80047-7
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发表时间：
1980-01-01
影响因子：
2.7
通讯作者：
IVERSEN, SD
中科院分区：
文献类型：
--
作者：
KELLEY, AE;STINUS, L;IVERSEN, SD
研究了阿片肽与腹侧被盖区多巴胺能神经元的相互作用。分析VTA输注D-Ala-Met-脑啡酰胺（DALA）的行为后果。DALA引起的剂量依赖性增加在光电池笼和圆形走廊测量的自发活动。在旷场和洞箱中的观察显示，DALA诱导的行为刺激的特征在于增强的运动，饲养和孔访问的数量，而梳理时间和孔访问的持续时间减少。DALA诱导的刺激被纳洛酮逆转，并被6-OHDA（6-羟基多巴胺）破坏DA-A10末端完全阻断。同时VTA输注DALA可增强D-Amphetamine诱导的行为激活，这表明对DALA的行为反应依赖于DA-A10神经元活性。据推测，阿片受体的刺激对DA-A10神经元的抑制性输入施加突触前抑制（例如，GABA或树突状DA），从而释放多巴胺能活性。在VTA输注DALA后4 h、1 d和6 d，D-苯丙胺反应强烈减弱，仅在14 d恢复正常。这种持久的修饰可能反映了阿片神经元活性的降低，从而释放了对DA-A10神经元的抑制。内源性阿片肽可能对多巴胺能中皮质边缘系统有调节作用。
The interaction between opioid peptides and dopaminergic A10 (DA-A10) neurons in the ventral tegmental area (VTA) was studied. The behavioral consequences of VTA infusion of D-Ala-Met-enkephalinamide (DALA) were analyzed. DALA elicited a dose-dependent increase in locomotor activity measured in photocell cages and the circular corridor. Observations in the open field and in a hole box revealed that DALA-induced behavioral stimulation was characterized by enhancement of locomotion, rearing and number of hole visits, while grooming time and duration of hole visits were decreased. DALA-induced stimulation was reversed by naloxone, and was completely blocked by 6-OHDA (6-hydroxydopamine) destruction of DA-A10 terminals. D-Amphetamine-induced behavioral activation was potentiated by simultaneous VTA infusion of DALA which indicates that the behavioral response to DALA is dependent on DA-A10 neuronal activity. It is postulated that stimulation of opiate receptors exerts a presynaptic inhibition of an inhibitory input to DA-A10 neurons (e.g., GABA or dendritic DA), thus releasing dopaminergic activity. The D-amphetamine response was strongly attenuated 4 h, 1 and 6 days after VTA infusion of DALA, and returned to normal only at 14 days. This long-lasting modification may reflect decreased activity of opioid neurons, releasing the inhibition of DA-A10 neurons. Apparently endogenous opioid peptides may exert a modulatory influence on the dopaminergic mesocorticolimbic system.