Neuroscience Research Centre and Department of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Islamic Republic of Iran.
Neuroscience. 2011 Jan 13;172:139-52. doi: 10.1016/j.neuroscience.2010.10.031. Epub 2010 Oct 20.
The cerebellum, which controls coordinated and rapid movements, is a potential target for the deleterious effects of drugs of abuse including cannabis (i.e. marijuana, cannabinoids). Prenatal exposure to cannabinoids has been documented to cause abnormalities in motor and cognitive development, but the exact mechanism of this effect at the cellular level has not been fully elucidated. Previous studies indicate that cannabinoids are capable of modulating synaptic neurotransmission. In addition to altering synaptic activity, cannabinoid exposure may also change intrinsic neuronal properties. In the present study several different approaches including behavioral assays, extracellular field potential recordings and whole-cell patch clamp recordings, were used to address whether maternal exposure to the CB1 cannabinoid receptor agonist WIN 55-212-2 (WIN) affects the intrinsic electrophysiological properties of Purkinje neurons. WIN treatment of pregnant rats produced a significant decrease in the rearing frequency, total distance moved and mobility of the offspring, but significantly increased the time of the righting reflex, the grooming frequency and immobility. Neuromotor function, as assessed in the grip test and balance beam test, was also significantly impaired in prenatally WIN-treated group. Prenatal exposure to WIN increased the amplitude of population spikes (PS) recorded from the cerebellar Purkinje cell layer of offspring following synaptic blockage. WIN treatment of pregnant rats also profoundly affected the intrinsic properties of Purkinje neurons in offspring. This treatment increased the firing regularity, firing frequency, amplitude of afterhyperpolarization (AHP), the peak amplitude of action potential and the first spike latency, but decreased significantly the time to peak and duration of action potentials, the instantaneous firing frequency, the rate of rebound action potential and the voltage "sag" ratio. These results raise the possibility that maternal exposure to cannabinoids may profoundly affect the intrinsic membrane properties of cerebellar Purkinje neurons of offspring by altering the membrane excitability through modulation of intrinsic ion channels.
小脑控制协调和快速运动,是滥用药物(如大麻,大麻素)的有害影响的潜在靶点。有文献记录表明,产前暴露于大麻素会导致运动和认知发育异常,但这种细胞水平的影响的确切机制尚未完全阐明。先前的研究表明,大麻素能够调节突触神经传递。除了改变突触活性外,大麻素暴露还可能改变内在神经元特性。在本研究中,我们使用了几种不同的方法,包括行为测定、细胞外场电位记录和全细胞膜片钳记录,以确定母体暴露于 CB1 大麻素受体激动剂 WIN 55-212-2(WIN)是否会影响浦肯野神经元的内在电生理特性。WIN 处理怀孕大鼠会显著降低幼仔的举升频率、总移动距离和移动性,但显著增加翻正反射、梳理频率和不动性的时间。在抓握试验和平衡梁试验中评估的神经运动功能也明显受损。产前 WIN 暴露增加了突触阻断后从小脑浦肯野细胞层记录的群体锋电位(PS)的幅度。WIN 处理怀孕大鼠也深刻地影响了后代浦肯野神经元的内在特性。这种处理增加了放电规律、放电频率、后超极化(AHP)幅度、动作电位峰值幅度和第一峰潜伏期,但显著降低了动作电位的峰值时间和持续时间、瞬时放电频率、反弹动作电位的速率和电压“凹陷”比。这些结果表明,母体暴露于大麻素可能通过调节内在离子通道来改变膜兴奋性,从而深刻地影响后代小脑浦肯野神经元的内在膜特性。