TY - JOUR
T1 - 5-HT-Mediated synaptic potentials in the dorsal raphe nucleus
T2 - Interactions with excitatory amino acid and GABA neurotransmission
AU - Pan, Z. Z.
AU - Colmers, W. F.
AU - Williams, J. T.
PY - 1989
Y1 - 1989
N2 - Intracellular recordings from neurons within dorsal raphe nucleus in slices from rat brain were used to study an inhibitory postsynaptic potential (IPSP) evoked by electrical stimulation. The IPSP was observed in ~70% of neurons, had a latency to onset of 40-65 ms, reached a peak in 350-400 ms, had a total duration of 1-2 s, and reversed polarity at the potassium equilibrium potential. This IPSP was blocked by spiperone (1 μM) and prolonged by fluoxetine (300 nM - 30 μM) suggesting that it was mediated by 5-hydroxytryptamine (5-HT). Superfusion with γ-aminobutyric acid (GABA) and excitatory amino acid receptor antagonists were used to block 'fast' synaptic potentials that preceded the IPSP such that it could be studied in isolation. Blockade of the GABA-mediated synaptic potentials increased the amplitude of the IPSP by 1.3-fold. The amplitude of the IPSP was reduced by 30% after blockade of the excitatory amino acid-mediated synaptic potential. The results indicate that the IPSP recorded in dorsal raphe neurons was caused by 5-HT released at least in part from indirect (synaptically induced) excitation of 5-HT-containing cells within the slice.
AB - Intracellular recordings from neurons within dorsal raphe nucleus in slices from rat brain were used to study an inhibitory postsynaptic potential (IPSP) evoked by electrical stimulation. The IPSP was observed in ~70% of neurons, had a latency to onset of 40-65 ms, reached a peak in 350-400 ms, had a total duration of 1-2 s, and reversed polarity at the potassium equilibrium potential. This IPSP was blocked by spiperone (1 μM) and prolonged by fluoxetine (300 nM - 30 μM) suggesting that it was mediated by 5-hydroxytryptamine (5-HT). Superfusion with γ-aminobutyric acid (GABA) and excitatory amino acid receptor antagonists were used to block 'fast' synaptic potentials that preceded the IPSP such that it could be studied in isolation. Blockade of the GABA-mediated synaptic potentials increased the amplitude of the IPSP by 1.3-fold. The amplitude of the IPSP was reduced by 30% after blockade of the excitatory amino acid-mediated synaptic potential. The results indicate that the IPSP recorded in dorsal raphe neurons was caused by 5-HT released at least in part from indirect (synaptically induced) excitation of 5-HT-containing cells within the slice.
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U2 - 10.1152/jn.1989.62.2.481
DO - 10.1152/jn.1989.62.2.481
M3 - Article
C2 - 2788717
AN - SCOPUS:0024364155
SN - 0022-3077
VL - 62
SP - 481
EP - 486
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 2
ER -