ABSTRACT
Aim To investigate the inhibitory effects of urocortin2 (UCN2) on ventral tegmental area (VTA) nervous activity of morphine addiction rats and the mechanism. Methods Morphine addiction rats and the microiontophoresis method were used to observe the effects of UCN2 on VTA neuron′s spontaneous dis-charge changing rule, as well as the inhibitory effects of UCN2 on DA neuron′s cluster spontaneous dis-charge, to identify UCN2 and DA on the same VTA neuron. Morever, the inhibitor of corticotropin-regula-ting factor′s receptor ( CRF-2 R ) and the blocker of protein kinase A ( PKA ) , AST-2 B and H89 , were used to investigate the effects of UCN2 on VTA neuron′s of morphine addiction rats. Results UCN2 could inhibit the firing rate 82% (31/38) of the tested VTA neuron ( P<0. 01 ) , the discharge frequency changed from (20. 89 ± 2. 86) Hz to (13. 66 ± 3. 93) Hz (P<0. 01). Further, the inhibitor of PKA, AST-2B and H89 could ablolish the inhibitory effects of UCN2 . Morever, the excitatory firing of VTA neurons was at-tenuated by addition of UCN2 , while AST application could inhibit the UCN2′s inhibitory effects. Conclu-sion UCN2 could regulate the effects of VTA via PKA pathway and may thereby contribute to the improvement of drug addiction.
ABSTRACT
Aim The goal is to make a further comprehension of the pathogenesis of Parkinsons disease (PD) and hence add further knowledge for PD diagnosis by observing the functions of nitric oxide (NO) in striatum (STR). Method Microelectrodes were used to observe the effects of sodium nitroprusside (SNP), L-glutamic acid (GLU) and ?-aminobutyric acid (GABA) on STR neurons' spontaneous firing rates, and at the same time, we observed the effects of NO on GLU and GABA. Results 77% (51/66) of the tested neurons were excited by SNP, NO synthase inhibitor L-NAME antagonized the excitatory effect of SNP. Duringthe periods of microelectrophoresis GLU and GABA, SNP amplified the excitatory effect of GLU and weakened the inhibitory effect of GABA. L-NAME antagonized the excitatory effect of GLU.Conclusion These results demonstrated clearly that NO, GLU and GABA functions might converge in the same STR neurons. NO and GLU functions are excitatory whereas GABA function is inhibitory on the firing activities in STR neurons.
ABSTRACT
Objective To observe the modulation of met enkephalin (ME) and naloxone (NLX) on the excitatory effects of kainic acid (KA) and glutamic acid (GLU) in hippocampus of rats and to explore the possible mechanism of the effects of ME in the KA epilepsy model. Methods A total of 45 healthy Wistar rats were anesthetized with 1% sodium pentobarbital (3 ml/kg intraperitoneal injection). After endotracheal intubation, the animal was mounted onto a SN 1stereotaxic apparatus (Narishige) and routine craniotomy was performed. Then the animal was immobilized by 0.01% curare (1 mg/kg) after it woke up. The peripheral pipettes of a multiple pipette microelectrode were used for microelectrophoretic application of drugs; the central pipette was used for extracellular recording of the hippocampal unit discharges (HUDs). Results ①ME excited most of the HUDs; opioid receptor antagonist NLX could reverse the excitatory effects of met enkephalin. NLX applied alone had no effects on the firing rate of HUDs. ②KA and GLU excited the HUDs intensively but ME and NLX could modulate their excitatory effects. Conclusion ME may promote the development of epilepsy by modulating the excitatory effects of KA and GLU in hippocampus.