Glutamate mediates an inhibitory postsynaptic potential in dopamine neurons

Nature ◽  
10.1038/27919 ◽  
1998 ◽  
Vol 394 (6688) ◽  
pp. 78-82 ◽  
Author(s):  
C. D. Fiorillo ◽  
J. T. Williams
Keyword(s):  
Dopamine Neurons ◽  
Inhibitory Postsynaptic Potential ◽  
Postsynaptic Potential

A depolarizing inhibitory postsynaptic potential activated by synaptically released γ-aminobutyric acid under physiological conditions in rat hippocampal pyramidal cells

1988 ◽  
Vol 66 (8) ◽  
pp. 1100-1102 ◽  
Author(s):  
Paul Perreault ◽  
Massimo Avoli
Keyword(s):  
High Intensity ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Rat Hippocampus ◽  
Aminobutyric Acid ◽  
Afferent Stimulation ◽  
Inhibitory Postsynaptic Potential ◽  
Physiological Conditions ◽  
Ca1 Pyramidal Neurons ◽  
Postsynaptic Potential

We report that CA1 pyramidal neurons of the rat hippocampus respond to high intensity afferent stimulation by generating a late depolarizing potential that typically occurs between the early (fast) inhibitory postsynaptic potential (IPSP) and the late (slow) IPSP. This potential is reminiscent of the response seen after the application of 4-aminopyridine and can be blocked by bicuculline, indicating that GABAA receptors are involved in its generation.

The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia

1986 ◽  
Vol 56 (3) ◽  
pp. 823-834 ◽  
Author(s):  
P. A. Smith ◽  
F. F. Weight
Keyword(s):  
B Cells ◽  
Ringer Solution ◽  
Sympathetic Ganglia ◽  
Sympathetic Chain ◽  
C Cells ◽  
Inhibitory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Sucrose Gap ◽  
Paravertebral Sympathetic Ganglia ◽  
Stimulation Of

Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.

Selective Inhibition by Adenosine of mGluR IPSPs in Dopamine Neurons After Cocaine Treatment

2000 ◽  
Vol 83 (3) ◽  
pp. 1307-1314 ◽  
Author(s):  
Christopher D. Fiorillo ◽  
John T. Williams
Keyword(s):  
Dopamine Release ◽  
Metabotropic Glutamate Receptor ◽  
Selective Inhibition ◽  
Dopamine Neurons ◽  
Dopamine System ◽  
Extracellular Adenosine ◽  
Mesolimbic Dopamine System ◽  
Metabotropic Glutamate ◽  
Postsynaptic Potential ◽  
A1 Receptor

With repeated exposure to psychostimulants such as cocaine and amphetamine, long-lasting changes occur in the mesolimbic dopamine system that are thought to underlie continued drug-seeking and relapse. One consequence of repeated cocaine treatment is an increase in extracellular adenosine in the ventral tegmental area (VTA), which results in tonic inhibition of synaptic input to dopamine neurons. The synapse specificity of this increased adenosine tone was examined on glutamate- and GABA-mediated responses using the selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). The slow, metabotropic glutamate receptor (mGluR)-mediated inhibitory postsynaptic potential (IPSP) was enhanced by DPCPX only in slices from psychostimulant-treated animals. Under resting conditions, DPCPX was without effect on fast excitatory postsynaptic currents (EPSCs) in slices from saline- or cocaine-treated animals. However, in the presence of amphetamine, DPCPX did augment fast EPSCs in slices from cocaine-treated rats. Although DPCPX increased GABAB IPSPs, the magnitude of the increase was not altered by cocaine pretreatment, even in the presence of amphetamine. This suggests that the elevated adenosine tone induced by cocaine treatment acts preferentially on glutamate terminals. Furthermore, the inhibition of the mGluR IPSP by endogenous adenosine may result in more effective burst firing mediated by glutamate afferents in cocaine-treated rats, a phenomenon known to enhance dopamine release.

Sign in / Sign up

Export Citation Format

Share Document