Jackson Jesse, Dickson Clayton T, Bland Brian H
Behavioral Neuroscience Research Group, Department of Psychology, The University of Calgary, 2500 University Drive, Calgary, Alberta, Canada T2N 1N4.
J Neurophysiol. 2008 Jun;99(6):3009-26. doi: 10.1152/jn.00065.2008. Epub 2008 Apr 24.
Evidence has accumulated suggesting that the median raphe (MR) mediates hippocampal theta desynchronization. However, few studies have evaluated theta-related neural circuitry during MR manipulation. In urethane-anesthetized rats, we investigated the effects of MR stimulation on hippocampal field and cell activity using high-frequency (100 Hz), theta burst (TBS), and slow-frequency electrical stimulation (0.5 Hz). We demonstrated that high-frequency stimulation of the MR did not elicit deactivated patterns in the forebrain, but rather elicited low-voltage activity in the neocortex and small-amplitude irregular activity (SIA) in the hippocampus. Both hippocampal phasic theta-on and -off cells were inhibited by high-frequency MR stimulation, although MR stimulation failed to affect cells that had neither state or phase relationships with theta field activity. TBS of the MR-induced theta field activity phase locked to the stimulation. Slow-frequency stimulation elicited a state-dependent reset of theta phase through a short-latency inhibition (5 ms) in phasic theta-on cells. Subpopulations of phasic theta-on cells responded in either oscillatory or nonoscillatory patterns to MR pulses, depending on their intraburst interval. off cells exhibited a state-dependent modulation of cell firing occurring preferentially during nontheta. The magnitude of MR-induced reset varied as a function of the phase of the theta oscillation when the pulse was administered. Therefore high-frequency stimulation of the MR appears to disrupt hippocampal theta through a state-dependent, short-latency inhibition of rhythmic cell populations in the hippocampus functioning to switch theta oscillations to an activated SIA field state.
越来越多的证据表明中缝正中核（MR）介导海马θ波去同步化。然而，很少有研究评估在操纵MR期间与θ波相关的神经回路。在氨基甲酸乙酯麻醉的大鼠中，我们使用高频（100Hz）、θ波爆发（TBS）和低频电刺激（0.5Hz）研究了MR刺激对海马场和细胞活动的影响。我们证明，高频刺激MR不会在前脑中引发失活模式，而是在新皮层中引发低电压活动，并在海马中引发小幅度不规则活动（SIA）。高频MR刺激抑制了海马的相位θ波开启和关闭细胞，尽管MR刺激未能影响与θ波场活动既无状态关系也无相相关系的细胞。MR的TBS诱导的θ波场活动与刺激锁相。低频刺激通过对相位θ波开启细胞的短潜伏期抑制（5毫秒）引发θ波相位的状态依赖性重置。相位θ波开启细胞的亚群根据其爆发间期对MR脉冲以振荡或非振荡模式做出反应。关闭细胞在非θ波期间优先表现出细胞放电的状态依赖性调制。当施加脉冲时，MR诱导的重置幅度随θ波振荡的相位而变化。因此，高频刺激MR似乎通过对海马中有节奏的细胞群进行状态依赖性的短潜伏期抑制来破坏海马θ波，这种抑制作用是将θ波振荡转换为激活的SIA场状态。
