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Jack A. Boulant - One of the best experts on this subject based on the ideXlab platform.
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Temperature effects on neuronal membrane potentials and inward currents in rat Hypothalamic Tissue slices.
The Journal of physiology, 2005Co-Authors: Yanmei Zhao, Jack A. BoulantAbstract:Preoptic-anterior Hypothalamic (PO/AH) neurones sense and regulate body temperature. Although controversial, it has been postulated that warm-induced depolarization determines neuronal thermosensitivity. Supporting this hypothesis, recent studies suggest that temperature-sensitive cationic channels (e.g. vanilloid receptor TRP channels) constitute the underlying mechanism of neuronal thermosensitivity. Moreover, earlier studies indicated that PO/AH neuronal warm sensitivity is due to depolarizing sodium currents that are sensitive to tetrodotoxin (TTX). To test these possibilities, intracellular recordings were made in rat Hypothalamic Tissue slices. Thermal effects on membrane potentials and currents were compared in PO/AH warm-sensitive, temperature-insensitive and silent neurones. All three types of neurones displayed slight depolarization during warming and hyperpolarization during cooling. There were no significant differences in membrane potential thermosensitivity for the different neuronal types. Voltage clamp recordings (at -92 mV) measured the thermal effects on persistent inward cationic currents. In all neurones, resting holding currents decreased during cooling and increased during warming, and there was no correlation between firing rate thermosensitivity and current thermosensitivity. To determine the thermosensitive contribution of persistent, TTX-sensitive currents, voltage clamp recordings were conducted in the presence of 0.5 microm TTX. TTX decreased the current thermosensitivity in most neurones, but there were no resulting differences between the different neuronal types. The present study found no evidence of a resting ionic current that is unique to warm-sensitive neurones. This supports studies suggesting that neuronal thermosensitivity is controlled, not by resting currents, but rather by currents that determine rapid changes in membrane potential between successive action potentials.
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Cellular mechanisms for neuronal thermosensitivity in the rat hypothalamus.
The Journal of Physiology, 1996Co-Authors: John Griffin, M L Kaple, A. R. Chow, Jack A. BoulantAbstract:1. To study the basic mechanisms of neuronal thermosensitivity, rat Hypothalamic Tissue slices were used to record and compare intracellular activity of temperature-sensitive and -insensitive neurones. This study tested the hypothesis that different neuronal types have thermally dependent differences in the transient potentials that determine the interspike interval. 2. Most spontaneously firing neurones displayed depolarizing prepotentials that preceded each action potential. In warm-sensitive neurones, warming increased the rate of rise of the depolarizing prepotential which, in turn, decreased the interspike interval and increased the firing rate. In contrast, temperature had little or no effect on the rate of rise in prepotentials of temperature-insensitive neurones. 3. Prepotential depolarization can be due to increasing depolarizing conductances or decreasing hyperpolarizing conductances. These are differences in the ionic conductances responsible for prepotentials in temperature-sensitive and -insensitive neurones. In warm-sensitive neurones, the net ionic conductance decreased as the prepotential depolarized towards threshold, suggesting that the prepotential is primarily determined by a decrease in outward potassium conductances. In contrast, in low-slope temperature-insensitive neurones, the net conductance remained constant during the interspike interval, suggesting a more balanced combination of both depolarizing and hyperpolarizing conductances. 4. Transient outward potassium currents, including A-currents, are important determinants of neuronal firing rates. These currents were identified in all warm-sensitive neurones tested, as well as in many temperature-insensitive and silent neurones. Since warming increased the rates of inactivation of these currents, transient K+ currents may contribute to the temperature-dependent prepotentials of some Hypothalamic neurones.
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Temperature effects on membrane potential and input resistance in rat Hypothalamic neurones.
The Journal of Physiology, 1995Co-Authors: John Griffin, Jack A. BoulantAbstract:1. Whole-cell recordings were conducted in rat Hypothalamic Tissue slices to test the hypothesis that thermal changes in membrane potential contribute to neuronal thermosensitivity. Intracellular recordings of membrane potential and input resistance were made in eighty-two neurones, including twenty-four silent neurones and fifty-eight spontaneously firing neurones (22 warm-sensitive neurones and 36 temperature-insensitive neurones). Fifty-seven of the neurones were recorded in the preoptic and anterior hypothalamus. 2. Warm-sensitive neurones increased their firing rates during increases in temperature (1.07 +/- 0.06 impulses s-1 degree C-1), but their resting membrane potentials were not affected by temperature (0.06 +/- 0.06 mV degree C-1). Similarly, temperature did not affect the membrane potentials of temperature-insensitive neurones or silent neurones. 3. Silent neurones had significantly lower input resistances (256.9 +/- 20.0 M omega), compared with temperature-insensitive (362.6 +/- 57.2 M omega) and warm-sensitive neurones (392.2 +/- 50.0 M omega). Temperature had the same effect on all three types of neurones, such that resistance increased during cooling and decreased during warming. 4. If hyperpolarizing or depolarizing holding currents were applied to neurones, temperature caused changes in the membrane potentials. This spurious effect can be explained by thermally induced changes in the input resistance. 5. Measurements of electrode tip potentials indicated that artificial changes in membrane potential may also be recorded if grounding electrodes are not isolated from the changes in temperature. 6. These results suggest that physiological changes in resting membrane potentials do not determine neuronal warm sensitivity, and thermal changes in input resistance do not determine the primary differences between warm-sensitive and temperature-insensitive Hypothalamic neurones.
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Intracellular analysis of inherent and synaptic activity in Hypothalamic thermosensitive neurones in the rat.
The Journal of Physiology, 1991Co-Authors: M. C. Curras, Stephen R. Kelso, Jack A. BoulantAbstract:1. Intracellular neuronal activity was recorded in rat preoptic-anterior Hypothalamic Tissue slices. Thirty neurones were classified as warm sensitive, cold sensitive or temperature insensitive, based on their firing rate response to temperature changes. Seventy-seven per cent of the neurones were temperature insensitive, which included both spontaneously firing and silent neurones. Of all neurones, 10% were warm sensitive and 13% were cold sensitive. 2. Silent temperature-insensitive neurones had lower input resistances (126 +/- 21 M omega) than thermosensitive neurones (179 +/- 24 M omega). Regardless of neuronal type, however, resistance was inversely related to temperature. 3. Warm-sensitive neurones were characterized by a slow, depolarizing pre-potential, whose rate of rise was temperature dependent. This depolarizing potential disappeared during current-induced hyperpolarization, suggesting that intrinsic mechanisms are responsible for neuronal warm sensitivity. 4. Spike activity in cold-sensitive neurones correlated with putative excitatory and inhibitory postsynaptic potentials, whose frequency was thermosensitive. This suggests that cold sensitivity in these neurones depends on synaptic input from nearby neurones. 5. Like cold-sensitive neurones, action potentials of temperature-insensitive neurones often were preceded by short duration (less than 20 ms), rapidly rising pre-potentials, whose rates of rise were not affected by temperature. In some temperature-insensitive neurones, depolarizing current injection increased both firing rate (by 5-8 impulses s-1) and warm sensitivity, with pre-potentials having temperature-dependent rates of rise. We suggest that temperature-insensitive neurones employ two opposing, thermally dependent mechanisms: a voltage-dependent depolarizing conductance and a hyperpolarizing sodium-potassium pump.
Raymund A.c. Roos - One of the best experts on this subject based on the ideXlab platform.
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Daniel J Van Wamelen, Jasper J Anink, Robin Van Steenhoven, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Raymund A.c. RoosAbstract:To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. Postmortem cohort study. Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Jasper J Anink, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Daniel J Van Wamelen, Robin Van Steenhoven, Raymund A.c. RoosAbstract:STUDY OBJECTIVE To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. DESIGN Postmortem cohort study. PATIENTS Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. MEASUREMENTS AND RESULTS Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. CONCLUSIONS These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction.
Ralf Jockers - One of the best experts on this subject based on the ideXlab platform.
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Daniel J Van Wamelen, Jasper J Anink, Robin Van Steenhoven, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Raymund A.c. RoosAbstract:To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. Postmortem cohort study. Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Jasper J Anink, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Daniel J Van Wamelen, Robin Van Steenhoven, Raymund A.c. RoosAbstract:STUDY OBJECTIVE To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. DESIGN Postmortem cohort study. PATIENTS Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. MEASUREMENTS AND RESULTS Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. CONCLUSIONS These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction.
Daniel J Van Wamelen - One of the best experts on this subject based on the ideXlab platform.
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Daniel J Van Wamelen, Jasper J Anink, Robin Van Steenhoven, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Raymund A.c. RoosAbstract:To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. Postmortem cohort study. Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction
Daniel J Van Wamelen - One of the best experts on this subject based on the ideXlab platform.
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suprachiasmatic nucleus neuropeptide expression in patients with huntington s disease
Sleep, 2013Co-Authors: Jasper J Anink, Debora Angeloni, Ahmad N Aziz, Ralf Jockers, Franco Fraschini, Daniel J Van Wamelen, Robin Van Steenhoven, Raymund A.c. RoosAbstract:STUDY OBJECTIVE To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the Hypothalamic suprachiasmatic nucleus. DESIGN Postmortem cohort study. PATIENTS Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded Hypothalamic Tissue. MEASUREMENTS AND RESULTS Using postmortem paraffin-embedded Tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. CONCLUSIONS These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction.