Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
Synaptic Vesicle Depletion in Reticulospinal Axons is Reduced by 5‐hydroxytryptamine : Direct Evidence for Presynaptic Modulation of Glutamatergic Transmission. / Shupliakov, O.; Pieribone, V. A.; Gad, H.; Brodin, L.
в: European Journal of Neuroscience, Том 7, № 5, 01.01.1995, стр. 1111-1116.Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
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TY - JOUR
T1 - Synaptic Vesicle Depletion in Reticulospinal Axons is Reduced by 5‐hydroxytryptamine
T2 - Direct Evidence for Presynaptic Modulation of Glutamatergic Transmission
AU - Shupliakov, O.
AU - Pieribone, V. A.
AU - Gad, H.
AU - Brodin, L.
PY - 1995/1/1
Y1 - 1995/1/1
N2 - 5‐hydroxytryptamine (5‐HT; serotonin) is known to depress glutamatergic synaptic transmission in the spinal cord of vertebrates. To test directly whether 5‐HT inhibits synaptic glutamate release, we examined its effect on the ultrastructure of synaptic vesicle clusters in giant reticulospinal axons in a lower vertebrate (lamprey; Lampetra fluviatilis). The size of these axons makes it possible to selectively expose only a part of the presynaptic element to 5‐HT, while another part of the same axon is maintained in control solution. Action potential stimulation at 20 Hz for 20 min caused a marked reduction in the number of synaptic vesicles in active zones maintained in control solution, while in the part exposed to 5‐HT (20 μM) the number of synaptic vesicles per active zone was ‐3‐fold higher. In contrast, 5‐HT had no effect on the number of vesicles in resting axons. To examine whether 5‐HT acts by reducing presynaptic Ca2+ influx, intra‐axonal recordings of Ba2+ potentials were performed. No reduction of the axonal Ba2+ potential could be detected after application of 20 or 200 pM 5‐HT. The present results show that 5‐HT reduces the rate of synaptic exocytosis in reticulospinal axons. The effect appears to be mediated by a mechanism distinct from the presynaptic Ca2+ channels.
AB - 5‐hydroxytryptamine (5‐HT; serotonin) is known to depress glutamatergic synaptic transmission in the spinal cord of vertebrates. To test directly whether 5‐HT inhibits synaptic glutamate release, we examined its effect on the ultrastructure of synaptic vesicle clusters in giant reticulospinal axons in a lower vertebrate (lamprey; Lampetra fluviatilis). The size of these axons makes it possible to selectively expose only a part of the presynaptic element to 5‐HT, while another part of the same axon is maintained in control solution. Action potential stimulation at 20 Hz for 20 min caused a marked reduction in the number of synaptic vesicles in active zones maintained in control solution, while in the part exposed to 5‐HT (20 μM) the number of synaptic vesicles per active zone was ‐3‐fold higher. In contrast, 5‐HT had no effect on the number of vesicles in resting axons. To examine whether 5‐HT acts by reducing presynaptic Ca2+ influx, intra‐axonal recordings of Ba2+ potentials were performed. No reduction of the axonal Ba2+ potential could be detected after application of 20 or 200 pM 5‐HT. The present results show that 5‐HT reduces the rate of synaptic exocytosis in reticulospinal axons. The effect appears to be mediated by a mechanism distinct from the presynaptic Ca2+ channels.
KW - exocytosis
KW - presynaptic inhibition
KW - serotonin
KW - spinal cord
UR - http://www.scopus.com/inward/record.url?scp=0029074686&partnerID=8YFLogxK
U2 - 10.1111/j.1460-9568.1995.tb01099.x
DO - 10.1111/j.1460-9568.1995.tb01099.x
M3 - Article
C2 - 7613617
AN - SCOPUS:0029074686
VL - 7
SP - 1111
EP - 1116
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
SN - 0953-816X
IS - 5
ER -
ID: 40836856