Conditioned and unconditioned forelimb reflex systems in the cat: involvement of the intermediate cerebellum

 Temporary inactivation of the cerebellar interposed nuclei was used to assess the role of the intermediate cerebellum in the performance of forelimb cutaneo-muscular reflexes in the cat. The following types of reflexive responses were evaluated: the classically conditioned and unconditioned forelimb withdrawal responses and the forelimb tactile placing, hopping and magnet responses. The experiments tested the hypothesis that the intermediate cerebellum is involved in the performance of all the above forelimb reflexes. The forelimb withdrawal reflex was classically conditioned in a newly developed paradigm in which animals were first operantly conditioned to stand on four elevated platforms. Trained animals were microinjected with a γ-aminobutyric acid (GABA) agonist, muscimol, in the interposed nuclei, and the effects of inactivation of the intermediate cerebellar output on the forelimb reflexes were examined. The main findings of these experiments are that unilateral muscimol inactivation of the interposed nuclei in the cat abolished the expression of the classically conditioned limb flexion reflex, suppressed the performance of the unconditioned withdrawal reflex and, in parallel, downregulated the tactile placing, hopping and magnet postural responses in the ipsilateral forelimb. These observations are inconsistent with concepts indicating exclusive involvement of the intermediate cerebellum in the classically conditioned reflexes elicited by aversive stimuli. On the contrary, they support the hypothesis of a more global involvement of this structure in learned and unlearned defensive flexion reflexes and in automatic postural response systems. Received: 29 July 1996 / Accepted: 26 September 1996     

A Thalamic Contribution to Arousal-induced, Non-photic Entrainment of the Circadian Clock of the Syrian Hamster

It is well established that the circadian clock of the suprachiasmatic nuclei (SCN) is entrained by light. More recently, the potent effects of arousing, non-photic cues on the clock have been recognized. The neural mediators of non-photic entrainment are yet to be identified. To examine the contribution of the thalamic intergeniculate leaflet (IGL) and its NPY-immunopositive projection, the geniculo-hypothalamic tract to non-photic entrainment by arousal, male Syrian hamsters received lesions of the IGL (IGLX) which ablated NPY-immunoreactivity in the SCN. Their circadian responses to both photic and non-photic cues were then tested. Lesions resulted in a delay in the timing of activity onset following lights out, but had no effect on the behavioural or cellular circadian responses to phase-advancing light pulses presented at circadian time (CT) CT19 (where CT12 represents the time of activity onset). Injection with a benzodiazepine (chlordiazepoxide, 100 mg/kg) at CT6 suppressed wheel-running, increased general locomotion of intact controls and induced large phase advances of the circadian rhythm of wheel-running. Chlordiazepoxide also inhibited wheel-running in lesioned animals, but there was no significant increase in general locomotion and the lesioned animals did not phase advance. Serial arousal by injection of saline at intervals of 23.5 h for 6 days entrained the circadian rhythm of wheel-running of intact hamsters and was associated with an increase in general locomotor activity. Entrainment by serial arousal was abolished by IGLX. However, the lesioned animals did show a clear behavioural response to every presentation of the non-photic cue. These results show that the IGL is a necessary component of the neural pathways mediating both arousal- and benzodiazepine-induced non-photic entrainment.     

Pyramidal cells in primary auditory cortex project to cochlear nucleus in rat

Recent work has demonstrated that the auditory cortex in rat sends direct projections to the auditory nuclei of the brainstem, including the cochlear nucleus and superior olive. To determine the cortical origin of the projections to cochlear nucleus, Fast Blue, a retrograde fluorescent tracer, was injected into the cochlear nucleus. Labeled cells in the forebrain were then studied with light microscopy and mapped. The projection was found to originate from large pyramidal neurons in layer V of primary auditory cortex. The projection was predominantly ipsilateral, and no labeled neurons were found in other cortical areas. These data imply that primary auditory cortex exerts influence over ascending auditory information at the earliest stages of the central auditory system.     

Suppression of the jaw-opening reflex by periaqueductal gray stimulation is decreased by paramedian brainstem lesions

Electrical stimulation of the midbrain periaqueductal gray region (PAG) suppresses the tooth pulp-evoked jaw-opening reflex (TP-JOR). In the present study the pathways that mediate this suppression were investigated by placing brainstem lesions in lightly anesthetized cats. Parasagittal lesions that interrupted the afferent and efferent connections of the medullary and pontine raphe nuclei attenuated (but did not abolish) suppression of the TP-JOR evoked by PAG stimulation. This result provides further evidence that medial brainstem structures partially mediate the effects of PAG stimulation in the trigeminal system.     

Modulation of dopamine function by glycine in the nucleus accumbens of the brain of the rat

The effects of glycine on the phasic changes in locomotor activity in the rat, caused by a persistent infusion of dopamine (DA) into the nucleus accumbens (ACB) were investigated. Dopamine (25 μg/24 hr), infused into the nucleus accumbens for 13 days, caused hyperactivity, with two peaks occurring on days 3–4 and 9–11. Glycine (12.5 or 25 μg/24 hr) infused into the nucleus accumbens on its own did not alter the locomotor activity, yet when infused at the same time as DA (25 μg/24 hr), glycine (12.5 or 25 μg/24 hr) inhibited the development of the first peak of hyperactivity induced by DA, with no effect on the second peak. A larger dose of glycine (50 μg/24 hr), infused alone, significantly increased locomotor activity, and a combination of this dose with DA (25 μg/24 hr), led to a temporal shift in the response to DA such that the first peak of hyperactivity was delayed to “fuse” with the second peak. The locomotor response to a threshold dose of DA (6.25 μg/24 hr) plus glycine (50 μg/24 hr) was no greater than could be accounted for by the hyperactivity response to glycine alone (50 μg/24 hr). Strychnine (10 μg/24 hr), infused into the nucleus accumbens, produced no alteration in locomotor activity. Similarly, when infused together with DA (25 μg/24 hr), strychnine (10 μg/24 hr) caused no significant alteration in the phasic hyperactivity induced by DA. However, strychnine (10 μg/24 hr), infused together with DA and glycine (25 and 12.5 μg/24 hr respectively), prevented the inhibition by glycine of the first peak of hyperactivity induced by DA. The results indicate that while glycine may not normally exert a tonic modulatory influence on those mechanisms in the nucleus accumbens which regulate locomotor activity, when applied exogenously glycine can partially moderate the locomotor response to DA, through an action on strychnine-sensitive receptors.     

Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. II. New synapse formation in the medial amygdaloid nucleus by fibers from the bed nucleus of the stria terminalis

The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 ± 0.1 (mean±S.E.M.) per unit area (2500 μm² in the molecular layer, and 3/0 ± 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 ± 0.6 per unit area in the molecular layer and 4.5 ± 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury.     

损毁下丘脑不同脑区对折断腿骨所致血浆皮质酮变化的影响

清醒sprague-Dawley雄性大鼠64只,以折断胫腓骨造成应激。观察非内侧基底下丘脑脑区损毁对应激前(Bo)、后(Bs)血浆皮质酮变化的影响。以Bs/Bo及Bs-Bo的值衡量应激反应的大小。根据所损毁脑区的部位及范围将动物分为6组:假手术组、室旁核损毁组、室旁核部分损毁组、室旁核少量损毁组、下丘脑前部—视前区损毁组、下丘脑后部损毁组。用统计学方法比较了6组动物的Bs/Bo及Bs-B0值,以及根据4例室旁核完全损毁动物仍保持有应激反应的事实,我们得出结论:(1)在清醒大鼠的损伤性应激反应中,下丘脑室旁核较其他非基底内侧下丘脑区具有较重要的作用。(2)室旁核以外的促肾上腺皮质激素释放因子神经元可能也参与应激反应。     

大鼠下丘脑室旁核及其邻近区域至室管膜的传出联系

用20只Wistar大鼠以PHA—L免疫组织化学顺行追踪技术研究了下丘脑室旁核及其邻近区域对脑室系统室管膜的传出联系。在脑室系统某些部位的室管膜层或其下方见有丰富的标记纤维并见许多膨结和终末膨突。这些纤维似乎参与形成室管膜上、下丛,构成脑—脑脊液神经体液回路的重要环节。     

兔孤束核区微量注射γ-氨基丁酸的降压效应

在53只乌拉坦麻醉家兔身上,观察到延髓孤束核(NTS)区注射γ-氨基丁酸(GABA)使血压显著下降,安定(DZ)有相似的降压效应,荷包牡丹碱(BIC)和印防己毒素(PIC)则使血压升高;促甲状腺素释放激素(TRH)和甲硫脑啡肽(MTP)对血压无明显影响;延髓的另一些区域应用GABA等药物后血压变化不明显;提示GABA能神经递质系统参与心血管活动的抑制性中枢调节,NTS区是其作用部位之一。     

The effect of bacterial melanin on electrical activity of neurons of the substantia nigra under conditions of GABA generation

The changes in spike activity of single neurons of the compact part of the substantia nigra, evoked by nucleus caudatus stimulation under conditions of long-term registration of the single and multiple, isolated and combined actions of GABA, GABA-amide, glutamine, and ethanolamine-O-sulfate (EOS) were studied in albino rats. Inhibition of poststimulus activity under GABA action was recorded and the inhibitory effect of GABA-amide was revealed. Primary excitatory and subsequent inhibitory effects of glutamine in combination with EOS were shown. The subsequent administration of bacterial melanin, synthesized by a mutant culture of Bacillus thuringiensis (BT-M) evoked a clear-cut and prolonged excitatory reaction during all the combined actions of GABA, GABA-amide, glutamine, and EOS. Preliminary administration of BT-M abolished the inhibitory poststimulus effects of GABA, GABA-amide, and EOS, as well as glutamine-induced excitation.