Visualization of central neurons and recording of action potentials

C. Yamamoto; T. Chujo

doi:10.1007/bf00237605

Possible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phenethylamine on single facial motoneurons

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y86-220 ◽

1986 ◽

Vol 64 (10) ◽

pp. 1302-1309 ◽

Cited By ~ 7

Author(s):

Nicholas J. Penington ◽

R. J. Reiffenstein

Keyword(s):

Action Potentials ◽

Serotonin Receptor ◽

Facilitatory Effect ◽

Central Neurons ◽

Local Anaesthetic Effect ◽

Anaesthetized Rats ◽

Responses To Dopamine ◽

Single Unit Recordings ◽

Facial Motoneurons ◽

Anaesthetic Effect

2,5-Dimemoxy-4-methylamphetamine (DOM, "STP") is a potent hallucinogen, proposed to be a serotonin receptor agonist. Its effects have not previously been tested upon central neurons where serotonin is excitatory and serotonin antagonists are effective. Extracellular single unit recordings were obtained from facial motoneurons in anaesthetized rats, and drugs were applied from five-barrelled micropipettes by iontophoresis. Facial motoneurons were commonly silent. During subthreshold application of glutamate, firing could be induced by dopamine and DOM. As reported by others, serotonin and noradrenaline also excited facial motoneurons under these conditions. Methysergide antagonized responses to serotonin and DOM but not those to noradrenaline; methysergide could not usually discriminate between responses to serotonin and dopamine. Ketanserin reversibly antagonized (but could not discriminate between) responses to serotonin, dopamine, and noradrenaline. Chlorpromazine antagonized responses to dopamine at doses that did not alter serotonin-induced excitation, and responses to DOM were not reduced by doses of chlorpromazine, that had no local anaesthetic effect on action potentials elicited by DOM and serotonin. These results suggest that DOM is an agonist on at least one type of central serotonin receptor. This receptor may also be a ketanserin (5-HT2) binding site.

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Sodium sensitivity of KNa channels in mouse CA1 neurons

Journal of Neurophysiology ◽

10.1152/jn.00064.2021 ◽

2021 ◽

Author(s):

Richard Gray ◽

Daniel Johnston

Keyword(s):

Potassium Channels ◽

Action Potentials ◽

Single Channel ◽

Cell Types ◽

Channel Activity ◽

Ca1 Neurons ◽

Central Neurons ◽

The Family ◽

Excised Patches ◽

Inside Out

Potassium channels play an important role regulating transmembrane electrical activity in essentially all cell types. We were especially interested in those that determine the intrinsic electrical properties of mammalian central neurons. Over 30 different potassium channels have been molecularly identified in brain neurons, but there often is not a clear distinction between molecular structure and the function of a particular channel in the cell. Using patch-clamp methods to search for single potassium channels in excised inside-out (ISO) somatic patches with symmetrical potassium, we found that nearly all patches contained non-voltage-inactivating channels with a single-channel conductance of 100-200 pS. This conductance range is consistent with the family of sodium-activated potassium channels (Slo2.1, Slo2.2 or collectively, KNa). The activity of these channels was positively correlated with a low cytoplasmic Na+ concentration (2-20 mM). Cell-attached recordings from intact neurons, however, showed little or no activity of this K+ channel. Attempts to increase channel activity by increasing [Na+]i with bursts of action potentials or direct perfusion of Na+ through a whole-cell pipette had little effect on KNa channel activity. Furthermore, excised outside-out patches across a range of intracellular [Na+] showed less channel activity than we had seen with excised ISO patches. Blocking the Na+/K+ pump with ouabain increased the activity of the KNa channels in excised OSO patches to levels comparable to ISO excised patches. Our results suggest that despite their apparent high levels of expression the activity of somatic KNa channels is tightly regulated by the activity of the Na+/K+ pump.

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Polarity of varicosity initiation in central neuron mechanosensation

The Journal of Cell Biology ◽

10.1083/jcb.201606065 ◽

2017 ◽

Vol 216 (7) ◽

pp. 2179-2199 ◽

Cited By ~ 12

Author(s):

Yuanzheng Gu ◽

Peter Jukkola ◽

Qian Wang ◽

Thomas Esparza ◽

Yi Zhao ◽

...

Keyword(s):

Action Potentials ◽

Mechanosensitive Channel ◽

Neuronal Polarity ◽

Central Neuron ◽

Central Neurons ◽

New Feature ◽

Axonal Varicosity ◽

Physical And Chemical ◽

Stimulation Of

Little is known about mechanical regulation of morphological and functional polarity of central neurons. In this study, we report that mechanical stress specifically induces varicosities in the axons but not the dendrites of central neurons by activating TRPV4, a Ca2+/Na+-permeable mechanosensitive channel. This process is unexpectedly rapid and reversible, consistent with the formation of axonal varicosities in vivo induced by mechanical impact in a mouse model of mild traumatic brain injury. In contrast, prolonged stimulation of glutamate receptors induces varicosities in dendrites but not in axons. We further show that axonal varicosities are induced by persistent Ca2+ increase, disassembled microtubules (MTs), and subsequently reversible disruption of axonal transport, and are regulated by stable tubulin-only polypeptide, an MT-associated protein. Finally, axonal varicosity initiation can trigger action potentials to antidromically propagate to the soma in retrograde signaling. Therefore, our study demonstrates a new feature of neuronal polarity: axons and dendrites preferentially respond to physical and chemical stresses, respectively.

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Electrical Properties of Hypothalamic Neuroendocrine Cells

The Journal of General Physiology ◽

10.1085/jgp.47.4.691 ◽

1964 ◽

Vol 47 (4) ◽

pp. 691-717 ◽

Cited By ~ 136

Author(s):

E. R. Kandel

Keyword(s):

Action Potentials ◽

Sea Water ◽

Input Resistance ◽

Neuroendocrine Cells ◽

Membrane Properties ◽

Intracellular Recordings ◽

Effector Cells ◽

Central Neurons ◽

Hypothalamic Hormones ◽

Recurrent Collaterals

Goldfish hypothalamic neuroendocrine cells have been investigated with intracellular recordings. The cells showed resting potentials of 50 mv and action potentials up to 117 mv followed by a long lasting and prominent diphasic hyperpolarizing afterpotential. The action potential occurred in two steps indicating sequential invasion. "Total" neuron (input) resistance was measured to be 3.3 x 107 Ω and total neuron time constant was 42 msec. Orthodromic volleys, produced by olfactory tract stimulation, generated graded excitatory postsynaptic potentials. These neuroendocrine cells seem, therefore, to have electrical membrane properties that are similar to those of other central neurons. Antidromic volleys (pituitary stimulation) produced inhibitory post-synaptic potentials whose latency was only slightly longer than that of the antidromic spike indicating the presence of recurrent collaterals. This finding suggests that the concept of the neuroendocrine cell as a neuron whose axon forms contacts only on blood vessels and not on other neurons or effector cells is too restrictive. Perfusion of the gills with dilute (0.3 per cent) sea water produced an inhibition of spontaneous activity. This inhibition is discussed in relation to recent work which demonstrates that goldfish hypothalamic hormones facilitate Na+ influx across the gill membrane.

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