Effects of neuroactive peptide urocortin on STN neuron's spontaneousdischarge and relationship with CRF-2R / 中国药理学通报

Aim To investigate the effects of endocrinal petptide urocortin on subthalamic nucleus (STN) neuron''s discharge, also observe the convergence effect of UCN with dopamine (DA) and glutamate (GLU), so as to understand the regulation effects of UCN and its mechanism in Parkinson''s disease (PD).Methods Forty Sprague-Dawley rats were used in this experiment.Nerve electrophysiology method-microiontophoresis was used to observe the effects of UCN on STN neuron firing rates and firing wave.Astressin (AST, the blocker of CRF receptor 2), protein kinase A (PKA) were used to observe the effects of UCN whether via CRF-2R and PKA signal pathway.Moreover, given UCN during the period of DA and GLU, the effects of UCN on DA and GLU in STN neurons were determined.Results During the period of using the UCN, UCN could inhibit the firing rate of 82％ (27/33) STN neuron (P<0.01), and the firing discharge rates were reduced from(3.65±0.27)Hz to (2.05±0.33) Hz (P<0.01).However, the inhibitory effects of UCN in STN could be antagonized by AST.Given UCN during the period of microiontophoresis of inhibitory neurotransmitter (DA) and excited neurotransmitter (GLU), UCN could enhance the effects of DA and attenuate the excitatory effects of GLU (P<0.01).Conclusion UCN and GLU/DA in STN, UCN play inhibitory and regulated effects on STN neurotransmitters(DA and GLU)via CRF-2 receptor and PKA signal pathway.

Effects of Low-Frequency Stimulation of Pedunculopontine Nucleus on Spontaneous Discharges of Globus Pallidus Internus / 天津医药

Objective To explore the mechanism of the low-frequency electrical stimulate on pedunculopontine nu-cleus to treat the Parkinson (PD) through observinge the low-frequency electrical stimulation of Pedunculopontine Nucleus (PPN) in PD rat model and the effects of neurotransmitters (GPi) neurons discharge in the medial part of the globus pallidus. Methods Thirty SD rats were randomly assigned to the control group and the PD model group, with 15 in each group. PD model was established through injecting 6-OHDA into Substantia nigra compact (SNc) of black rat. Effect of low frequency electrical stimulation, micro-electrophoresis glutamate (Glu) and its receptor blocking breaking agent MK-801,γ-aminobu-tyric acid (GABA) and its receptor antagonist bicuculline (BIC) on discharge of rat neuron GPi was examined using extracel-lular unit recording methods through seven glass microelectrode recording. Results When stimulated by low frequency electrical stimulation of PPN, reactions from the control group and neuronal response GPi in PD rats were inhibited. The aver-age discharge frequency was reduced compared to pre-stimulation (P < 0.01). Micro-electrophoresis and BIC Glu excite neurons while microiontophoresis MK-801 and GABA restrain neurons. In the background of micro-electrophoresis BIC’s excitatory effects on neuron, low-frequency electrical stimulation on PPN reduced neuronal firing frequency. And in the background of inhibition effect of micro-electrophoresis MK-801, low-frequency stimulation PPN further restrain neuronal discharge frequency. Conclusion Low frequency electrical stimulation inhibits GPi PPN neuronal activity probably though regulating neurons projecting to the Glu and GABA nerve pathways in GPi neuron.

Glycine enhances glutamate-induced excitation in ventromedial hypothalamic neurons in Awake rats.

The finding that glycine potentiates N-methyl-D-aspartate (NMDA) receptor-mediated responses, has tremendously changed our understanding of glutamatergic synaptic transmission in the brain. Although the phenomenon has been confirmed in number of preparations, it is yet to be demonstrated in awake animals. Further, the controversy that glycine binding sites of NMDA receptor are saturated in vivo or not, can be best verified in awake animals. Here, we have demonstrated that glycine enhanced glutamate-induced neuronal discharges in the ventromedial nucleus of the hypothalamus of awake behaving rats using microiontophoresis technique, suggesting that the glycine binding sites of NMDA receptor are not saturated under physiological conditions.

Effects of iontophoretically applied substance P, calcitonin gene-related peptide on excitability of dorsal horn neurones in rats

Spontaneous pain, allodynia and hyperalgesia are well known phenomena following peripheral nerve or tissue injury, and it is speculated that secondary hyperalgesia and allodynia, are generally thought to depend on a hyperexcitability (sensitization) of neurons in the dorsal horn. It is supposed that the sensitization may be due to various actions of neurotransmitters (SP, CGRP, excitatory amino acids) released from the primary afferent fibers. In this study, we examined effects of the iontophoretically applied SP and CGRP on the response to EAA receptor agonists (NMDA and non-NMDA) in the WDR dorsal horn neurones and see if the effects of SP or CGRP mimic the characteristic response pattern known in various pain models. The main results are summarized as follows: 1) SP specifically potentiated NMDA response. 2) CGRP non-specifically potentiated both NMDA and AMPA responses. Potentiation of NMDA response, however, was significantly greater than that of AMPA response. 3) 50% of SP applied cells and 15.8% of CGRP applied cells showed reciprocal changes(potentiation of NMDA response and suppression of AMPA response). These results are generally consistent with the sensitization characteristics in diverse pain models and suggests that the modulatory effects of SP and CGRP on NMDA and non-NMDA (AMPA) response are, at least in part, contribute to the development of sensitization in various pain models.

The responses of RU486 to the effects of corticosterone sulfate on cardiovascular neurons in the rostral ventrolateral medulla of rats / 中国药理学通报

0.05), but completely (3 neurons) or partially (9 neurons) blocked the excitatory effect induced by CORT. CONCLUSION CORT had rapid excitatory effects on the Caldiovascular neuronsin the RVLM. RU 486 had no responses to the baseline activity of the cardiovascular neurons, and but completely or partially blocked the effect of CORT on the cardiovascular neurons.

Effects of Microiontophoretically Applied Some Different Transmitter Receptor Antagonists on the Evoked Response of “Pain” Units of Hypothalamic Paraventricular Nucleus / 第二军医大学学报

Effects of microiontophoretically applied transmitter receptor antagonists on the evoked response of “pain” units of PVN in rats by sciatic stimulation were observed. The results showed: (l)The evoked response of 7 out of 38 PVN “pain” units could be blocked by atropine (7/38); 5 out of 27 by hexamethonium; 6 out of 31 by phentolamine (6/31); and 4 out of 25 by propranolol (4/25). Seventeen out of 52 were blocked by cyproheptadine (17/52), but 3 out of 52 were augmented by cyproheptadine (3/52). (2) The evoked response of the same “pain” unit could be blocked by two antagonists: the evoked response of 2 out of 27 PVN “pain” units could be blocked by atropine and cyprohepadine; 3 out of 20 by hexamethonium and cyproheptadine; 2 out of 25 by prepamolol and cyproheptadine. These results suggest that the noxious somatic input to PVN involves 5-HT, cholinergic and adrenergic transmitter receptor mechanisms and that the convergence of various transmitter systems on PVN “pain” unit is indicated.