Modulation of gamma-aminobutyric acid on painful sense in central nervous system of morphine-dependent rats / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To observe the effects of gamma-aminobutyric acid (GABA) on the electric activities of pain-excited neurons (PEN) in nucleus accumbens (NAc) in central nervous system (CNS) of morphine-dependent rats.</p><p><b>METHODS</b>After GABA or the GABA(A)-receptor antagonist, bicuculline (Bic), was injected into cerebral ventricles or NAc, right sciatic nerve was stimulated by electrical pulses, which was considered as traumatic pain stimulation. Extracellular recordings methods were used to record the electric activities of PEN in NAc.</p><p><b>RESULTS</b>When GABA was injected into intracerebroventricle (ICV) as well as NAc, it could decrease the pain-evoked discharge frequency and prolong the latency of PEN. Bic could interdict the above effects of GABA on the electric activities of PEN.</p><p><b>CONCLUSION</b>Exogenous GABA might have an inhibitory effect on the central pain adjustment. Furthermore, GABA and GABA(A) receptor participate and mediate the traumatic information transmission process in CNS.</p>

Phentolamine antagonizes the effects of norepinephrine on the activity of pain-related neurons in the parafascicular nucleus of morphine-dependent rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To examine the antagonization of phentolamine against the effects of norepinephrine (NE) on the activity of pain-related neurons in the parafascicular nucleus of morphine-dependent rats.</p><p><b>METHODS</b>Electric impulses were applied as nociceptive stimulus to the right sciatic nerve of morphine-dependent rats, and the discharges of the pain-related neurons in the parafascicular nucleus were recorded by extracellular recording method with glass microelectrodes.</p><p><b>RESULTS</b>Intracerebroventricular injection of norepinephrine resulted in the inhibition of evoked response of the pain-excited neurons as well as the excitation of evoked response of the pain-inhibiting neurons. Both the inhibitory effect on the electric discharges of the pain-excited neurons and the excitatory effect on the pain-inhibiting neurons of norepinephrine were almost completely blocked by intracerebroventricular administration of phentolamine.</p><p><b>CONCLUSION</b>Phentolamine antagonizes the inhibitory effect of norepinephrine on the activity of pain-related neurons in the parafascicular nucleus in morphine-dependent rats, and norepinephrine may play an important role in the integration of the pain signal through the alpha-receptors.</p>

Effect of acetylcholine on pain-related electric activities in hippocampal CA1 area of normal and morphinistic rats / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To examine the effect of acetylcholine (ACh) on the electric activities of pain-excitation neurons (PEN) and pain-inhibitation neurons (PIN) in the hippocampal CA1 area of normal rats or morphinistic rats, and to explore the role of ACh in regulation of pain perception in CA1 area under normal condition and morphine addiction.</p><p><b>METHODS</b>The trains of electric impulses applied to sciatic nerve were set as noxious stimulation. The discharges of PEN and PIN in the CA1 area were recorded extracellularly by glass microelectrode. We observed the influence of intracerebroventricular (i.c.v.) injection of ACh and atropine on the noxious stimulation-evoked activities of PEN and PIN in the CA1 area.</p><p><b>RESULTS</b>Noxious stimulation enhanced the electric activity of PEN and depressed that of PIN in the CA1 area of both normal and addiction rats. In normal rats, ACh decrease the pain-evoked discharge frequency of PEN, while increased the frequency of PIN. These effects reached the peak value at 4 min after injection of ACh. In morphinistic rats, ACh also inhibited the PEN electric activity and potentialized the PIN electric activity, but the maximum effect appeared at 6 min after administration. The ACh-induced responses were significantly blocked by muscarinic receptor antagonist atropine.</p><p><b>CONCLUSION</b>Cholinergic neurons and muscarinic receptors in the hippocampal CA1 area are involved in the processing of nociceptive information and they may play an analgesia role in pain modulation. Morphine addiction attenuated the sensitivity of pain-related neurons to the noxious information.</p>

Differential effects of dopamine on pain-related electric activities in normal rats and morphinistic rats / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To investigate the influence of dopamine (DA) and DA receptor's antagonist on the transmission of noxious information in the central nervous system of normal rats or morphinistic rats.</p><p><b>METHODS</b>The influence of DA on the electric activity of the pain-excited neuron (PEN) in the caudate nucleus (Cd) of normal rats or morphinistic rats was recorded after the sciatic nerve was noxiously stimulated.</p><p><b>RESULTS</b>DA shortened the average latency of the evoked discharge of PEN in the Cd of normal rats, indicating that DA could increase the activity of PEN and pain sensitivity in normal rats. This effect could be inhibited by Droperidol. DA increased the average latency of the evoked discharge of PEN in the Cd of morphinistic rats, indicating that DA could inhibit the activity of PEN and pain sensitivity in morphinistic rats.</p><p><b>CONCLUSION</b>The responses to painful stimulation were completely opposite between normal rats and morphinistic rats after the intracerebroventricular injection of DA.</p>

Influence of glutamate and NMDA-receptor antagonist MK-801 on the electric activities of pain-excitation neurons in the nucleus accumbens of rats / 生理学报

The experiment explored the influence of glutamic acid (Glu) and the NMDA-receptor antagonist dizocilpine maleate (MK-801) on the pain-evoked responses of pain-excitation neurons (PEN) in the nucleus accumbens (NAc) of rats. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The discharges of PEN in NAc were recorded by glass microelectrode. We observed the influence of intracerebroventricular (icv) injection of Glu and microinjection of MK-801 into the NAc on the noxious stimulation-evoked activities of PEN in NAc. The results showed that the noxious stimulation potentiated the electric activities of PEN in NAc. Intracerebroventricular injection of Glu (10 nmol/10 microl) increased the frequency of the discharge of PEN evoked by the noxious stimulation in NAc, the Glu-induced response was blocked by the injection of MK-801 (1.0 nmol/0.5 microl) into NAc. MK-801 partly inhibited the response of PEN upon the noxious stimulation. It is therefore suggested that the facilitatory effect of Glu on PEN response in NAc to the noxious stimulation is mediated by NMDA receptors, and that Glu and NMDA receptors are involved in the modulation of nociceptive information transmission in the NAc.

The relation between amygdaloid nucleus in rats and pain modulation / 中国应用生理学杂志

<p><b>AIM</b>To research the influence of noxious stimuli on the electric activities of pain-related neurons in several subnuclei of Amygdaloid Nucleus in rats.</p><p><b>METHODS</b>Trains of the electric impulses applied to the sciatic nerve were used as noxious stimuli. The discharges of neurons were channeled off by glass microelectrode.</p><p><b>RESULTS</b>Pain-related neurons existed in several subnuclei of Amygdaloid Nucleus. When the noxious stimuli were administered the frequency of discharges of pain-excited neurons (PEN) was increased while the frequency of pain-inhibited neurons (PIN) was decreased to the lowest level. The electric activities of PEN and PIN were matched with each other. Intraperitoneal injection of morphine (10 mg/kg) antagonized the effects of noxious stimuli on the pain-related neurons.</p><p><b>CONCLUSION</b>Several subnuclei of Amygdaloid Nucleus play an essential role in perceiving, integrating and transmitting the pain impulses. They are a part of the central nervous system in which pain information is controlled and managed.</p>