Starr M S, Summerhayes M
Neuroscience. 1983 Dec;10(4):1171-83. doi: 10.1016/0306-4522(83)90107-0.
Rotational behaviour was initiated in naive rats by injecting muscimol into one substantia nigra pars reticulata, or in unilaterally 6-hydroxydopamine-treated rats with systemic or intracaudate apomorphine. Electrolytic or kainic acid lesions were made in one or both ventromedial nuclei of the thalamus and their effects on the components of circling studied. A unilateral ventromedial electrolesion imposed a weak ipsilateral posture and occasionally elicited weak ipsiversive circling acutely, but not chronically. Challenging these rats with a large subcutaneous dose of apomorphine invariably provoked ipsiversive circling, however old was the lesion. Bilateral electrolesions caused slight hypoactivity. Kainic acid treatments of one or both ventromedial thalami produced uncontrolled hypermotility initially, with subsequent loss of ventromedial neurones and recovery of normal motor behaviour. No form of ventromedial lesion affected the incidence of stereotypy. Acute (but not chronic) contralateral or ipsilateral ventromedial electrolesions, or both, slowed muscimol and apomorphine-induced circling (often in different ways) through complex changes in posture and/or locomotor drive. Animals lesioned during the course of a circling episode often showed the biggest changes in circling to begin with, only to recover minutes later. Rapidly circling rats were sometimes more readily inhibited than slowly circling rats. Toxin injury of the ventromedial nucleus appeared to suppress muscimol and not apomorphine circling. Any ventromedial lesion (electrical or chemical, acute or chronic), if positioned opposite a contraversive circling stimulus, intensified the associated posture. Ipsilateral lesions tended to abolish posture altogether or, like bilateral treatments, to suppress locomotion. Sham operations had none of these effects. Acute electrical lesions and drug-induced inhibition of one or both ventromedial thalami were more or less identical in their effects on rat circling behaviour, save that bilateral muscimol injection caused profound catalepsy while lesions did not. It is suggested that the ventromedial thalamus is more concerned with the registration of striatal dopamine-mediated behaviours in drug-stimulated than in spontaneously behaving rats, and that other output pathways may rapidly compensate for any impairment of function in the ventromedial nuclei.
通过向一侧黑质网状部注射蝇蕈醇,或在单侧6-羟基多巴胺处理的大鼠中全身性或尾状核内注射阿扑吗啡,可引发未处理大鼠的旋转行为。在丘脑的一个或两个腹内侧核进行电解或 kainic 酸损伤,并研究其对转圈各组成部分的影响。单侧腹内侧电解损伤会导致轻度的同侧姿势,偶尔会急性引发轻度的同侧旋转,但不会长期存在。然而,无论损伤时间多久,用大剂量皮下注射阿扑吗啡刺激这些大鼠总会引发同侧旋转。双侧电解损伤会导致轻微的活动减少。对丘脑腹内侧核的一侧或两侧进行 kainic 酸处理最初会导致不受控制的活动亢进,随后腹内侧神经元丧失,运动行为恢复正常。任何形式的腹内侧损伤均不影响刻板行为的发生率。急性(而非慢性)对侧或同侧腹内侧电解损伤,或两者皆有,会通过姿势和/或运动驱动的复杂变化减缓蝇蕈醇和阿扑吗啡诱导的转圈(通常方式不同)。在转圈过程中受到损伤的动物,起初转圈变化通常最大,但几分钟后就会恢复。快速转圈的大鼠有时比慢速转圈的大鼠更容易受到抑制。腹内侧核的毒素损伤似乎会抑制蝇蕈醇诱导的转圈,但不会抑制阿扑吗啡诱导的转圈。任何腹内侧损伤(电损伤或化学损伤,急性或慢性),如果位于与反向转圈刺激相对的位置,会增强相关的姿势。同侧损伤往往会完全消除姿势,或者像双侧处理一样,抑制运动。假手术没有这些效果。急性电损伤和药物诱导对丘脑腹内侧核一侧或两侧的抑制对大鼠转圈行为的影响大致相同,只是双侧注射蝇蕈醇会导致深度僵住,而损伤则不会。有人认为,在药物刺激的大鼠中,丘脑腹内侧核更关注纹状体多巴胺介导行为的记录,而在自发行为的大鼠中则不然,并且其他输出通路可能会迅速补偿腹内侧核功能的任何损伤。