Long-term increases in neuronal activity in the motor cortex evoked by simultaneous stimulation of the thalamus and somatosensory cortex in cats

Experiments on anesthetized cats were used to study the activity of motor cortex neurons (field 4γ) in response to separate and simultaneous stimulation of the ventrolateral nucleus of the thalamus and the somatosensory cortex (field 2) of the brain. Long-term potentiation of motor cortex neuron activity in response to simultaneous stimulation of the ventrolateral nucleus and somatosensory cortex arose only in regions receiving corticocortical projections from the stimulation site in the somatosensory cortex of the brain, while regions lacking corticocortical projections from the somatosensory cortex showed no such effect. Experiments demonstrated that the duration of increased motor cortex neuron activity following stimulation of the ventrolateral nucleus of the thalamus and somatosensory cortex was greater than one hour after recording was started. These data led to the conclusion that simultaneous stimulation of corticocortical and thalamocortical afferents can alter the level of neuronal activity in the motor cortex only in regions with convergent sensory inputs from the thalamus and somatosensory cortex of the brain. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 84, No. 5–6, pp. 460–468, May–June, 1998.     

延髓腹外侧区微量注射L-NAME对内脏-减压反应的影响

目的观察延髓腹外侧区头端（RVLM）和尾端（CVLM）微量注射N-硝基-L-精氨酸甲酯（L-NAME）对内脏-减压反应的影响,探讨静注L-NAME使该反应产生翻转的中枢机制。方法用电刺激内脏大神经传入纤维的方法模拟内脏痛,比较RVLM和CVLM微量注射L-NAME前后刺激神经时血压的变化情况。结果RVLM给药后基础血压升高（P<0.01）;给药前刺激神经时为降压反应,△MBP=-（26.19±6.77）mmHg（1mmHg=0.133kPa）,而给药后刺激时血压下降的效应被抵消,△MBP=-（15.56±6.63）mmHg（P<0.01）。CVLM给药后基础血压降低（P<0.01）,给药前刺激神经时为降压反应,△MBP=-（28.78±11.71）mmHg,而给药后刺激时血压仍下降,但△MBP=-（16.63±9.30）mmHg（P<0.01）。若提前注入L-Arg,可以取消L-NAME的作用,即基础血压和刺激后的反应性血压的变化均恢复到原来的水平。结论RVLM和CVLM微量注射L-NAME可部分抵消内脏-减压反应,提前注入L-精氨酸（L-Arg）可以取消L-NAME的上述作用。表明VLM参与了内脏-减压反应并通过中枢NO通路起作用;静注L-NAME引起的翻转作用则是由于抑制了内源性NO的生成。     

The orexinergic neurons receive synaptic input from C1 cells in rats

The C1 cells, located in the rostral ventrolateral medulla (RVLM), are activated by pain, hypoxia, hypoglycemia, infection, and hypotension and elicit cardiorespiratory stimulation, adrenaline and adrenocorticotropic hormone (ACTH) release, and arousal. The orexin neurons contribute to the autonomic responses to acute psychological stress. Here, using an anatomical approach, we consider whether the orexin neurons could also be contributing to the autonomic effects elicited by C1 neuron activation. Phenylethanolamine N‐methyl transferase‐immunoreactive (PNMT‐ir) axons were detected among orexin‐ir somata, and close appositions between PNMT‐ir axonal varicosities and orexin‐ir profiles were observed. The existence of synapses between PNMT‐ir boutons labeled with diaminobenzidine and orexinergic neurons labeled with immunogold was confirmed by electron microscopy. We labeled RVLM neurons with a lentiviral vector that expresses the fusion protein ChR2‐mCherry under the control of the catecholaminergic neuron‐selective promoter PRSx8 and obtained light and ultrastructural evidence that these neurons innervate the orexin cells. By using a Cre‐dependent adeno‐associated vector and TH‐Cre rats, we confirmed that the projection from RVLM catecholaminergic neurons to the orexinergic neurons originates predominantly from PNMT‐ir catecholaminergic (i.e., C1 cells). The C1 neurons were found to establish predominantly asymmetric synapses with orexin‐ir cell bodies or dendrites. These synapses were packed with small clear vesicles and also contained dense‐core vesicles. In summary, the orexin neurons are among the hypothalamic neurons contacted and presumably excited by the C1 cells. The C1–orexin neuronal connection is probably one of several suprabulbar pathways through which the C1 neurons activate breathing and the circulation, raise blood glucose, and facilitate arousal from sleep. J. Comp. Neurol. 522:3834–3846, 2014. © 2014 Wiley Periodicals, Inc.     

Inducción del temblor mandibular por lesión electrolítica del estriado ventrolateral y por el tratamiento subcrónico con haloperidol en rata macho: un contraste electromiográfico

Introduction

Tremulous jaw movement (TJMs) in rats can be induced pharmacologically by striatal dopaminergic manipulation or electrolytic lesion of ventrolateral striatum (VLS). This tremor has neurochemical, anatomical and electromyographic (EMG) characteristics similar to those of tremor in Parkinson patients. However, the EMG characteristics of tremors generated by electrolytic lesion to the VLS have not yet been studied.

Method

This study used electromyography to describe tremulous jaw movement generated by bilateral electrolytic lesion in the VLS and compare it to tremors induced using subchronic IP treatment with haloperidol, a dopaminergic D2 receptor antagonist. The experimental groups contained rats with a lesion in the ventrolateral striatum and rats on subchronic haloperidol treatment; the control group received only the vehicle. The EMG signal from the temporal muscle was recorded at baseline and during TJMs in all groups.

Results

TMJ frequencies were heterogeneous among the groups. Rats with VLS lesion showed higher amplitude and frequency values than the haloperidol-treated rats. Amplitudes at baseline also differed among the groups.

Conclusions

We conclude that TMJs associated with electrolytic lesion to the VLS show a higher frequency and amplitude than tremors induced by haloperidol. This may be related to the way striatum neurons are affected.     

Facilitation and attenuation of a visceral nociceptive reflex from the rostroventral medulla in the rat

BACKGROUND & AIMS: Noxious inputs from somatic tissue are subject to biphasic descending modulation from the rostroventral medulla (RVM). In the present study, we investigated descending facilitatory and inhibitory influences from the RVM on a visceral nociceptive reflex. METHODS: The visceromotor response (VMR), a contraction of peritoneal musculature during noxious colorectal distention (80 mm Hg, 20 seconds), was quantified as the integrated electromyogram. RESULTS: At 22 sites in the RVM, electrical stimulation produced biphasic effects, facilitating the VMR at low (5, 10, and 25 microA) and inhibiting it at greater (>50 microA) intensities of stimulation. Electrical stimulation at all intensities tested (5-200 microA) in other sites in the RVM only inhibited (30 sites) or only facilitated (12 sites) the VMR to colorectal distention. Activation of glutamatergic receptors in the RVM replicated the effects of electrical stimulation. Reversible blockage (intraspinal lidocaine injection) or irreversible transection of spinal funiculi revealed that descending facilitatory influences from the RVM were conveyed in the ventrolateral/ventral funiculus, whereas descending inhibitory influences were contained in the dorsolateral funiculi. CONCLUSIONS: Spinal visceral nociceptive reflexes are subject to facilitatory modulation from the RVM, providing the basis for a mechanism by which visceral sensations can be enhanced from supraspinal sites.     

注意缺陷多动障碍儿童动态功能连接的功能磁共振成像研究

目的:探索注意缺陷多动障碍儿童静态以及动态功能连接的异常。方法:收集智商高于80的6～16岁符合DSM-IV诊断的注意缺陷多动障碍儿童97例(男78例,女19例)和年龄匹配的正常对照儿童74例(男45例,女29例)的静息态功能磁共振成像数据,比较两组全脑静态功能连接和动态功能连接指标。结果:注意缺陷多动障碍组的静态功能连接与正常对照组的差异无统计学意义(P>0.05),注意缺陷多动障碍组腹外侧前额叶与全脑其他脑区功能连接的模式变异性大于正常对照组[(0.65±0.07)%vs.(0.60±0.08)%,P<0.01]。结论:动态分析提示腹外侧前额叶是注意缺陷多动障碍的关键脑区,为理解疾病的脑机制提供可能的新视角。     

Role of the cholinergic mechanisms of the ventrolateral preoptic area of the hypothalamus in regulating the state of sleep and waking in pigeons

Maintenance of waking in pigeons was found to be linked with the mechanisms of activation of muscarinic (M-) cholinergic receptors of the ventrolateral preoptic area of the hypothalamus. “Muscarinic” waking was characterized by an increase in the power of the EEG spectrum at 0.75–12 Hz and an increase in brain temperature. Activation of nicotinic (N-) cholinergic receptors in this area was associated with an increase in the duration of slow sleep, a decrease in the spectral EEG power at 0.75–7 Hz, and a decrease in brain temperature in this state; hyperactivation of these receptors led to the development of waking, where waking episodes were associated with significant decreases in brain temperature. Blockade of M-and N-cholinergic receptors resulted in changes in the sleep-waking cycle and thermoregulation which were oppose to those seen on receptor activation. It is suggested that M-and N-cholinergic receptors of the ventrolateral preoptic area of the pigeon hypothalamus are involved in regulating sleep and waking, their effects being associated with influences on the GABAergic system of this area. __________ Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 93, No. 2, pp. 189–200, February, 2007.     

GABA_A受体部分介导丙泊酚在中脑导水管周围灰质腹外侧区的致痛觉过敏作用

目的观察丙泊酚在vlPAG对大鼠伤害性感受的影响及GABAA受体在其中可能的作用。方法Sprague-Daw ley(SD)♀大鼠随机分组,丙泊酚(Propofol,Pro)和荷包牡丹碱(B icucu lline,B ic)采用中脑导水管周围灰质腹外侧区(ven-trolateral portion of the PAG,vlPAG)注射。行为学实验采用热板法和福尔马林实验,分别以舔后爪潜伏时间(Hot-p latelatency,HPL)和疼痛(累计)评分为指标。免疫组化方法观察丙泊酚在vlPAG对福尔马林单侧足底皮下注射诱发的脊髓背角Fos蛋白表达的影响。结果行为学部分:两种疼痛模型中丙泊酚(10 g.L-1)vlPAG注射引起痛敏(P<0.01)。热板法实验中,丙泊酚vlPAG微量注射的痛敏作用可被相同部位预先注射25 mg.L-1B ic在10和20 m in时间点分别拮抗70%和71%(均P<0.01),在30和40 m in完全拮抗。在福尔马林实验中,丙泊酚vlPAG微量注射使福尔马林疼痛评分增加,此作用可被B ic(25 mg.L-1)在60 m in拮抗57%(P<0.05)。免疫组化部分中,丙泊酚vlPAG微量注射使福尔马林引起的脊髓背角各层FLI阳性细胞数明显增多(P<0.01),B ic vlPAG微量注射(25 mg.L-1)可部分拮抗丙泊酚vlPAG微量注射的作用(P<0.01)。结论在大鼠vlPAG微量注射丙泊酚能产生痛敏作用;GABAA受体部分介导了丙泊酚的以上作用。     

针刺对高血压大鼠延髓头端腹外侧区氧化应激水平影响的研究

目的:从自由基来源和清除的角度探讨针刺对自发性高血压大鼠(SHR)延髓头端腹外侧区(RVLM)中氧化应激水平影响的潜在机制.方法:15只Wistar(WKY)大鼠为正常组,45只SHR大鼠随机分为高血压组、针刺组和非穴组.针刺组取"太冲穴"直刺,非穴组取非穴位浅刺,治疗1次/d,共14 d.采用遥测技术检测针刺对血压的...