Melatonin Receptor-Mediated Stimulation of Phosphoinositide Breakdown in Chick Brain Slices

Afferents from the nucleus accumbens (NAc) are a major source of input into the ventral pallidum (VP). Research reveals that these afferents are GABAergic, however, stimulation of these afferents induces both excitatory and inhibitory responses within the VP. These are likely to be partially mediated by enkephalin and substance P (SP), which are also released by these afferents, and are known to modulate VP neurons. However, less is known about the potentially differential effects stimulation of these afferents has on subpopulations of neurons within the VP and the cellular mechanisms by which they exert their effects. The current study aimed to research this further using brain slices containing the VP, stimulation of the NAc afferents, and multi-electrode array (MEA) recordings of their VP targets. Stimulation of the NAc afferents induced a pause in the tonic firing in 58% of the neurons studied in the VP, while 42% were not affected. Measures used to reveal the electrophysiological difference between these groups found no significant differences in firing frequency, coefficient of variation, and spike half-width. There were however significant differences in the pause duration between neurons in the dorsal and ventral VP, with stimulation of NAc afferents producing a significantly longer pause (0.48 ± 0.06 s) in tonic firing in dorsal VP neurons, compared to neurons in the ventral VP (0.21 ± 0.09 s). Pauses in the tonic firing of VP neurons, as a result of NAc afferent stimulation, were found to be largely mediated by GABAA receptors, as the application of picrotoxin significantly reduced their duration. Opioid agonists and antagonists were found to have no significant effects on the pause in tonic activity induced by NAc afferent stimulation. However, NK-1 receptor antagonists caused significant decreases in the pause duration, suggesting that SP may contribute to the inhibitory effect of NAc afferent stimulation via activation of NK-1 receptors.

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Differential conditioning of associative synaptic enhancement in hippocampal brain slices

Science ◽

10.1126/science.3952501 ◽

1986 ◽

Vol 232 (4746) ◽

pp. 85-87 ◽

Cited By ~ 105

Author(s):

Kelso ◽

TH Brown

Keyword(s):

Electrical Stimulation ◽

High Frequency ◽

Differential Conditioning ◽

Pyramidal Neurons ◽

Brain Slices ◽

Synaptic Inputs ◽

Hippocampal Synapses ◽

Stimulation Paradigm ◽

Stimulation Of

An electrophysiological stimulation paradigm similar to one that produces Pavlovian conditioning was applied to synaptic inputs to pyramidal neurons of hippocampal brain slices. Persistent synaptic enhancement was induced in one of two weak synaptic inputs by pairing high-frequency electrical stimulation of the weak input with stimulation of a third, stronger input to the same region. Forward (temporally overlapping) but not backward (temporally separate) pairings caused this enhancement. Thus hippocampal synapses in vitro can undergo the conditional and selective type of associative modification that could provide the substrate for some of the mnemonic functions in which the hippocampus is thought to participate.

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Propofol Suppresses Synaptic Responsiveness of Somatosensory Relay Neurons to Excitatory Input by Potentiating GABAA Receptor Chloride Channels

Molecular Pain ◽

10.1186/1744-8069-1-2 ◽

2005 ◽

Vol 1 ◽

pp. 1744-8069-1-2 ◽

Cited By ~ 28

Author(s):

Shui-Wang Ying ◽

Peter A Goldstein

Keyword(s):

Electrical Stimulation ◽

Chloride Channel ◽

Temporal Summation ◽

Brain Slices ◽

Excitatory Input ◽

Dependent Manner ◽

Sensory Stimuli ◽

Shunting Inhibition ◽

Stimulation Of ◽

Relay Neurons

Propofol is a widely used intravenous general anesthetic. Propofol-induced unconsciousness in humans is associated with inhibition of thalamic activity evoked by somatosensory stimuli. However, the cellular mechanisms underlying the effects of propofol in thalamic circuits are largely unknown. We investigated the influence of propofol on synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex (VB) to excitatory input in mouse brain slices, using both current- and voltage-clamp recording techniques. Excitatory responses including EPSP temporal summation and action potential firing were evoked in VB neurons by electrical stimulation of corticothalamic fibers or pharmacological activation of glutamate receptors. Propofol (0.6 – 3 μM) suppressed temporal summation and spike firing in a concentration-dependent manner. The thalamocortical suppression was accompanied by a marked decrease in both EPSP amplitude and input resistance, indicating that a shunting mechanism was involved. The propofol-mediated thalamocortical suppression could be blocked by a GABAA receptor antagonist or chloride channel blocker, suggesting that postsynaptic GABAA receptors in VB neurons were involved in the shunting inhibition. GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked in VB neurons by electrical stimulation of the reticular thalamic nucleus. Propofol markedly increased amplitude, decay time, and charge transfer of GABAA IPSCs. The results demonstrated that shunting inhibition of thalamic somatosensory relay neurons by propofol at clinically relevant concentrations is primarily mediated through the potentiation of the GABAA receptor chloride channel-mediated conductance, and such inhibition may contribute to the impaired thalamic responses to sensory stimuli seen during propofol-induced anesthesia.

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A dialogue between glia and neurons in the retina: modulation of neuronal excitability

Neuron Glia Biology ◽

10.1017/s1740925x0500013x ◽

2004 ◽

Vol 1 (3) ◽

pp. 245-252 ◽

Cited By ~ 26

Author(s):

ERIC A. NEWMAN

Keyword(s):

Synaptic Transmission ◽

Glial Cells ◽

Neuronal Excitability ◽

Ganglion Cells ◽

Brain Slices ◽

Müller Cells ◽

Muller Cells ◽

Signaling Mechanisms ◽

Bidirectional Signaling ◽

Stimulation Of

Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron–glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.

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