Search

Our previous work have demonstrated that the stimulation of somatosensory area II (Sm II) of cerebral cortex or N. accumbens (NAc) could activate nucleus raphe magnus (NRM), producing analgesia. The aim of this work is to study whether the effect of activation of Sm II on neurons in NRM is related to NAc. The spontaneous discharges of NRM neurons and their nociceptive responses induced by stimulation of tail tip were recorded extracellularly with glass microelectrode. The effects of stimulation of Sm II on the NRM neurons were observed before and after lesion of NAc. Before lesion of NAc, the stimulation of Sm II could activate NRM neurons, obviously increasing the firing rates in 0-10 minutes after stimulation (P < 0.05-0.01), and their nociceptive responses were decreased in 0-10 and 20 minutes (P < 0.01-0.001). After lesion of NAc, the firing rates having no clear change, and their nociceptive responses were even slightly enhanced. It is suggested that the effect of activation of Sm II on NRM neurons may need the relay via the NAc.

We have reported that many cases of Hb H disease have a complication of iron overload without a history of multiple blood transfusion or prolonged iron therapy. We determined their iron absorption by 59Fe whole body counting in 13 such cases. Also 10 normal subjects were studied as a control group. The results showed a significant increase in iron absorption to 20.3%, in contrast to 6.9% in the normal control. This was further documented by their RBC incorporation (i.e. the percentage of orally administered) 59Fe recovered in the total RBC mass) on day 14 (13.7% vs 6.1%). The degree of ineffective erythropoiesis might not be severe considering their similar 59Fe utilization by RBC (i.e. the percentage of absorbed 59Fe recovered in the RBC) to the normals (86.3% vs. 84.3%).

The actions of a gamma-aminobutyric acid B (GABAB) agonist, (-)-baclofen, on the electrophysiological properties of neurons and synaptic transmission in the spinal dorsal horn (laminae I-IV) were examined by using intracellular recordings in spinal cord slice from young rats. In addition, the effects of baclofen on the dorsal root stimulation-evoked outflow of glutamate and aspartate from the spinal dorsal horn were examined by using high performance liquid chromatography (HPLC) with flourimetric detection. Superfusion of baclofen (5 nM to 10 microM) hyperpolarized, in a stereoselective and bicuculline-insensitive manner, the majority (86%) of tested neurons. The hyperpolarization was associated with a decrease in membrane resistance and persisted in a nominally zero-Ca2+, 10 mM Mg(2+)- or a TTX-containing solution. Our findings indicate that the hyperpolarizing effect of baclofen is probably due to an increase in conductance to potassium ions. Baclofen decreased the direct excitability of dorsal horn neurons, enhanced accommodation of spike discharge, and reduced the duration of Ca(2+)-dependent action potentials. Baclofen depressed, or blocked, excitatory postsynaptic potentials evoked by electrical stimulation of the dorsal roots. Spontaneously occurring synaptic potentials were also reversibly depressed by baclofen. Whereas baclofen did not produce any consistent change in the rate of the basal outflow of glutamate and aspartate, the stimulation-evoked release of the amino acids was blocked. The present results suggest that baclofen, by activating GABAB receptors, may modulate spinal afferent processing in the superficial dorsal horn by at least two mechanisms: (1) baclofen depresses excitatory synaptic transmission primarily by a presynaptic mechanism involving a decrease in the release of excitatory amino acids, and (2) at higher concentrations, the hyperpolarization and increased membrane conductance may contribute to the depressant effect of baclofen on excitatory synaptic transmission in the rat spinal dorsal horn.

The purpose of the present work is to study whether the analgesia of "Zusanli" EA was mainly produced by its noxious effect. The antidromic C waves on N. peroneus communis innervating the area of "Zusanli" point were recorded. When "Zusanli" point was stimulated by trains of stimuli, the amplitude of the antidromic C wave was obviously decreased due to collision with the orthodromic stimulation. It was suggested that EA of "Zusanli" could excite some C fibers. It was observed that when the stimulation intensity reached the threshold of C fiber, the NRM neurons were obviously activated, and when it reached or exceeded the intensity for producing the maximal C wave, the NRM neurons were highly activated. Therefore, EA analgesia is probably produced mainly by its noxious stimulus component, especially carried by C fibers, via a negative feedback mechanism in modulating pain.