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214 Effects of various type of local anesthetic on Ca2+-activated GK+ in sympathetic ganglion cells
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DEPOLARIZATION AND ENHANCEMENT OF MONOSYIIAPTIC EPSP BY IS,3RACPD IN SPINAL MOTONEURONS. HIROYUKI GOTANI. MIYUKI KUNO, FUSAO A N D SHIUSHI MATSUURA. DePt. of Phvsiol.. Osaka City Univ. Med. Sch.. Osaka 545. JaDan.
Glutamate, a candidate for excitatory transmitter at synapses b e t w e e n frog spinal motoneurons and the descending lateral column fibers (LC), occasionally enhances the monosynaptic e x c i t a t o r y postsynaptic potentials (EPSPs). Here we analyzed effects of iS,3R-I-Aminocyclopentane-l,3-dicarboxylic acid (IS,3R-ACPD), a metabotropic glutamate receptor agonist, on membrane potential and amplitude of LC-EPSPS. "The whole spinal cord of the frog was isolated under anesthesia with sodium p e n t o b a r b i t o n e and was i n t r a - a r t e r i a l l y p e r f u s e d w i t h oxygenated Ringer solution. IS,3R-ACPD(5-50 ~M) d e p o l a r i z e d about two thirds of the cells (ACPD potential, 5-35 mV with 5 ~M), associated with increment in input conductance. EPSP reduced on the rising phase of the ACPD potential, but then enhancement of EPSP a p p e a r e d and lasted over the decay phase. At lower concentrations (<5 NM), EPSP w a s enhanced w i t h o u t apparent depolarization. These results suggest that IS,3R-ACPD enhances EPSP via mechanisms different from those responsible for ACPD potentials.
213
PROPERTY OF SLOW EPSPS IN SUBSTANTIA GELATINOSA (SG) NEURONS EVOKED BY PRIMARY A8 FIBERS IN ADULT RAT SPINAL CORD SLICES. YOHICHI YAJIRI, MEGUMU YOSHIMURA AND SYOGORO NISHI, Dept. of Physiol., Kurume Univ. Sch. of Med., Kunlme 830. JaPan.
The slow EPSPs evoked by primary afferent A~ fiber stimulation were recorded intracellularly from SG neurons in transverse or horizontal slices of the spinal cord in which an attached dorsal root was retained. The slow EPSPs were inducible in 20% of SG neurons by single low-intensity stimulation which was sufficient to excite the A5 fibers. In many SG neurons, the slow EPSPs were associated with a decrease in membrane resistance and were increased in amplitude witL membrane hyperpolarization. These primary afferent induced slow EPSPs were abolished by CNQX and APV. In contrast, those evoked by focal stimulation were depressed but not abolished by CNQX and APV. The slow EPSPs were not likely mediated by NMDA receptors, since the NMDA-induced depolarization was, in contrast to the slow EPSPs, associated with an increase in input resistance and decreased in amplitude with membrane hyperpolarization. The slow EPSPs were not affected by GDP-13-S applied intracellularly.These observations suggest that the A~ fibers make glutamatergic synapses with interneurons presynaptic to SG neurons. A subset of these intemeurons release a substance that generates the slow EPSPs in SG neurons. Focal stimulation would stimulate the intemeurons directly responsible for generating the slow EPSP in SG neurons and also stimulate other nervous elements including A8 fibers terminating onto the interneurons above-mentioned.
214
EFFECTS OF VARIOUS TYPE OF LOCAL ANESTHETIC ON C a 2 + - A C T I V A T E D GK+ IN SYMPATHETIC GANGLION CELLS. KOHSUKE SOMEII, WILLI~4 K RIKER2, KAZUHIKO NARA~ AKIHIRO TOCHINAI I, AND TAKASHI A SUZUKI1. iDept, of Oral Physiol., Sch. of Dent., Iwate Medical University. Morioka, Iwate 020 JAPAN and 2Dept. of Pharmacol., Sch. of Med., The Oregon Health Sciences University. 3181 S.W. Sam Jackson Park Road, Portland, Oregon 92701~3098, U.S.A. Caffeine induces an oscillatory Ca2+-activa%ed GK+ in frog ganglion cells, evident as rhythmic membrane hyperpolarizations (P~H). We examined the effects of procaine, cocaine, lidocaine, carbocaine, or tetracaine on intracellularly recorded (K+-citrate electrodes) RMH induced by caffeine. Procaine abolished RM~ 18/60 cells, cocaine in 1/21, tetracaine in 6/8, lidocaine in 0/43, and carbocaine in 0/21. In the cell with persistent ~MH the amplitudes ~nd frequencies were reduced. Ester-type local anesthetics (procaine, cocaine, tetracaine) appear to be more potent than amido--type (lidocaine, carbocaine) in blocking C a 2 + - a c t i v a t e d GK+ increase. Local anesthetic interference with Ca2+ mobilization is suggested by equipotency of local anesthetics for block of-spikes ,and miniature spontaneous synaptic potentials, but unequal potencies for block of RMH, and reversal of local ~nesthetic block by ATP (but not adenosine). The results that local anesthetics may depress the rise in [Ca2+]i that triggers GK+ , particularly since extracellular ATP, which can i~crease cell Ca2+, reverse the tetracaine or procaine block.
212 ~CA}~RA.
~hgj~o-ku,
DEPOLARIZATION AND ENHANCEMENT OF MONOSYIIAPTIC EPSP BY IS,3RACPD IN SPINAL MOTONEURONS. HIROYUKI GOTANI. MIYUKI KUNO, FUSAO A N D SHIUSHI MATSUURA. DePt. of Phvsiol.. Osaka City Univ. Med. Sch.. Osaka 545. JaDan.
Glutamate, a candidate for excitatory transmitter at synapses b e t w e e n frog spinal motoneurons and the descending lateral column fibers (LC), occasionally enhances the monosynaptic e x c i t a t o r y postsynaptic potentials (EPSPs). Here we analyzed effects of iS,3R-I-Aminocyclopentane-l,3-dicarboxylic acid (IS,3R-ACPD), a metabotropic glutamate receptor agonist, on membrane potential and amplitude of LC-EPSPS. "The whole spinal cord of the frog was isolated under anesthesia with sodium p e n t o b a r b i t o n e and was i n t r a - a r t e r i a l l y p e r f u s e d w i t h oxygenated Ringer solution. IS,3R-ACPD(5-50 ~M) d e p o l a r i z e d about two thirds of the cells (ACPD potential, 5-35 mV with 5 ~M), associated with increment in input conductance. EPSP reduced on the rising phase of the ACPD potential, but then enhancement of EPSP a p p e a r e d and lasted over the decay phase. At lower concentrations (<5 NM), EPSP w a s enhanced w i t h o u t apparent depolarization. These results suggest that IS,3R-ACPD enhances EPSP via mechanisms different from those responsible for ACPD potentials.
213
PROPERTY OF SLOW EPSPS IN SUBSTANTIA GELATINOSA (SG) NEURONS EVOKED BY PRIMARY A8 FIBERS IN ADULT RAT SPINAL CORD SLICES. YOHICHI YAJIRI, MEGUMU YOSHIMURA AND SYOGORO NISHI, Dept. of Physiol., Kurume Univ. Sch. of Med., Kunlme 830. JaPan.
The slow EPSPs evoked by primary afferent A~ fiber stimulation were recorded intracellularly from SG neurons in transverse or horizontal slices of the spinal cord in which an attached dorsal root was retained. The slow EPSPs were inducible in 20% of SG neurons by single low-intensity stimulation which was sufficient to excite the A5 fibers. In many SG neurons, the slow EPSPs were associated with a decrease in membrane resistance and were increased in amplitude witL membrane hyperpolarization. These primary afferent induced slow EPSPs were abolished by CNQX and APV. In contrast, those evoked by focal stimulation were depressed but not abolished by CNQX and APV. The slow EPSPs were not likely mediated by NMDA receptors, since the NMDA-induced depolarization was, in contrast to the slow EPSPs, associated with an increase in input resistance and decreased in amplitude with membrane hyperpolarization. The slow EPSPs were not affected by GDP-13-S applied intracellularly.These observations suggest that the A~ fibers make glutamatergic synapses with interneurons presynaptic to SG neurons. A subset of these intemeurons release a substance that generates the slow EPSPs in SG neurons. Focal stimulation would stimulate the intemeurons directly responsible for generating the slow EPSP in SG neurons and also stimulate other nervous elements including A8 fibers terminating onto the interneurons above-mentioned.
214
EFFECTS OF VARIOUS TYPE OF LOCAL ANESTHETIC ON C a 2 + - A C T I V A T E D GK+ IN SYMPATHETIC GANGLION CELLS. KOHSUKE SOMEII, WILLI~4 K RIKER2, KAZUHIKO NARA~ AKIHIRO TOCHINAI I, AND TAKASHI A SUZUKI1. iDept, of Oral Physiol., Sch. of Dent., Iwate Medical University. Morioka, Iwate 020 JAPAN and 2Dept. of Pharmacol., Sch. of Med., The Oregon Health Sciences University. 3181 S.W. Sam Jackson Park Road, Portland, Oregon 92701~3098, U.S.A. Caffeine induces an oscillatory Ca2+-activa%ed GK+ in frog ganglion cells, evident as rhythmic membrane hyperpolarizations (P~H). We examined the effects of procaine, cocaine, lidocaine, carbocaine, or tetracaine on intracellularly recorded (K+-citrate electrodes) RMH induced by caffeine. Procaine abolished RM~ 18/60 cells, cocaine in 1/21, tetracaine in 6/8, lidocaine in 0/43, and carbocaine in 0/21. In the cell with persistent ~MH the amplitudes ~nd frequencies were reduced. Ester-type local anesthetics (procaine, cocaine, tetracaine) appear to be more potent than amido--type (lidocaine, carbocaine) in blocking C a 2 + - a c t i v a t e d GK+ increase. Local anesthetic interference with Ca2+ mobilization is suggested by equipotency of local anesthetics for block of-spikes ,and miniature spontaneous synaptic potentials, but unequal potencies for block of RMH, and reversal of local ~nesthetic block by ATP (but not adenosine). The results that local anesthetics may depress the rise in [Ca2+]i that triggers GK+ , particularly since extracellular ATP, which can i~crease cell Ca2+, reverse the tetracaine or procaine block.