Synaptic properties of the lemniscal and paralemniscal pathways to the mouse somatosensory thalamus

Somatosensory information is thought to arrive in thalamus through two glutamatergic routes called the lemniscal and paralemniscal pathways via the ventral posterior medial (VPm) and posterior medial (POm) nuclei. Here we challenge the view that these pathways functionally represent parallel information routes. Using electrical stimulation and an optogenetic approach in brain slices from the mouse, we investigated the synaptic properties of the lemniscal and paralemniscal input to VPm and POm. Stimulation of the lemniscal pathway produced class 1, or “driver,” responses in VPm relay cells, which is consistent with this being an information-bearing channel. However, stimulation of the paralemniscal pathway produced two distinct types of responses in POm relay cells: class 1 (driver) responses in 29% of the cells, and class 2, or “modulator,” responses in the rest. Our data suggest that, unlike the lemniscal pathway, the paralemniscal one is not homogenous and that it is primarily modulatory. This finding requires major rethinking regarding the routes of somatosensory information to cortex and suggests that the paralemniscal route is chiefly involved in modulatory functions rather than simply being an information route parallel to the lemniscal channel.

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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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Dense arrays of micro-needles for recording and electrical stimulation of neural activity in acute brain slices

Journal of Neural Engineering ◽

10.1088/1741-2560/10/1/016007 ◽

2012 ◽

Vol 10 (1) ◽

pp. 016007 ◽

Cited By ~ 5

Author(s):

D E Gunning ◽

J M Beggs ◽

W Dabrowski ◽

P Hottowy ◽

C J Kenney ◽

...

Keyword(s):

Electrical Stimulation ◽

Neural Activity ◽

Brain Slices ◽

Dense Arrays ◽

Stimulation Of

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Evoked Neuronal Activity Accompanied by Transmitter Release Increases Oxygen Concentration in Rat Striatum in vivo but Not in vitro

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1992.87 ◽

1992 ◽

Vol 12 (4) ◽

pp. 629-637 ◽

Cited By ~ 22

Author(s):

Jayne B. Zimmerman ◽

Robert T. Kennedy ◽

R. Mark Wightman

Keyword(s):

Electrical Stimulation ◽

Caudate Nucleus ◽

Neuronal Activity ◽

Brain Slices ◽

Rat Striatum ◽

Initial Increase ◽

Striatal Slices ◽

Carbon Fiber Microelectrode ◽

Stimulation Of

Dopamine and oxygen (O2) were measured in the caudate nucleus of anesthetized rats and in striatal slices during electrical stimulation. Simultaneous electrochemical detection of dopamine and O2 was accomplished with fast-scan cyclic voltammetry at a Nafion-coated carbon-fiber microelectrode. Stimulation of the medial forebrain bundle resulted in synaptic overflow of dopamine in the caudate nucleus. At the same time, O2 concentration increased in the extracellular fluid with two separate phases. The amplitude of the initial increase directly correlated with the frequency of the stimulus, with the time of maximum concentration reproducible across a range of frequencies. The second increase occurred at later times with a more random amplitude and with a broad, variable shape. Agents which blocked vasodilation affected both phases: Atropine attenuated the initial increase, while the second feature was nearly absent after theophylline. Yohimbine and α-methyl- p-tyrosine did not affect the O2 responses. Local electrical stimulation of the slice preparation also resulted in dopamine overflow, but a prolonged decrease in O2 concentration accompanied this event. Striatal field stimulation in vivo produced changes in O2 concentration dependent on the relative position of the stimulating and working electrodes, but none of the responses resembled that seen in the caudate slice. Thus, while measurements in brain slices show O2 consumption as a result of stimulated neuronal activity, an apparent elevation of local cerebral blood flow during and after stimulation dominate the in vivo response.

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