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J A Boulant

Publications and source records attributed to J A Boulant.

At least 19 recordsLinked to original sources
PubMed2001

Synaptic and morphological characteristics of temperature-sensitive and -insensitive rat hypothalamic neurones.

1. Intracellular recordings were made from neurones in rat hypothalamic tissue slices, primarily in the preoptic area and anterior hypothalamus, a thermoregulatory region that integrates central and peripheral thermal information. The present study compared morphologies and local synaptic inputs of warm-sensitive and temperature-insensitive neurones. 2. Warm-sensitive neurones oriented their dendrites perpendicular to the third ventricle, with medial dendrites directed toward the periventricular region and lateral dendrites directed toward the medial forebrain bundle. In contrast, temperature-insensitive neurones generally oriented their dendrites parallel to the third ventricle. 3. Both warm-sensitive and temperature-insensitive neurones displayed excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). In most cases, EPSP and IPSP frequencies were not affected by temperature changes, suggesting that temperature-insensitive neurones are responsible for most local synapses within this hypothalamic network. 4. Two additional neuronal groups were identified: silent neurones having no spontaneous firing rates and EPSP-driven neurones having action potentials that are primarily dependent on excitatory synaptic input from nearby neurones. Silent neurones had the most extensive dendritic trees, and these branched in all directions. In contrast, EPSP-driven neurones had the fewest dendrites, and usually the dendrites were oriented in only one direction (either medially or laterally), suggesting that these neurones receive more selective synaptic input.

Animals↗
PubMed2001

Temperature-sensitive properties of rat suprachiasmatic nucleus neurons.

The hypothalamic suprachiasmatic nucleus (SCN) contains a heterogeneous population of neurons, some of which are temperature sensitive in their firing rate activity. Neuronal thermosensitivity may provide cues that synchronize the circadian clock. In addition, through synaptic inhibition on nearby cells, thermosensitive neurons may provide temperature compensation to other SCN neurons, enabling postsynaptic neurons to maintain a constant firing rate despite changes in temperature. To identify mechanisms of neuronal thermosensitivity, whole cell patch recordings monitored resting and transient potentials of SCN neurons in rat hypothalamic tissue slices during changes in temperature. Firing rate temperature sensitivity is not due to thermally dependent changes in the resting membrane potential, action potential threshold, or amplitude of the fast afterhyperpolarizing potential (AHP). The primary mechanism of neuronal thermosensitivity resides in the depolarizing prepotential, which is the slow depolarization that occurs prior to the membrane potential reaching threshold. In thermosensitive neurons, warming increases the prepotential's rate of depolarization, such that threshold is reached sooner. This shortens the interspike interval and increases the firing rate. In some SCN neurons, the slow component of the AHP provides an additional mechanism for thermosensitivity. In these neurons, warming causes the slow AHP to begin at a more depolarized level, and this, in turn, shortens the interspike interval to increase firing rate.

Action Potentials↗
PubMed2000

Role of the preoptic-anterior hypothalamus in thermoregulation and fever.

Lesion and thermal stimulation studies suggest that temperature regulation is controlled by a hierarchy of neural structures. Effector areas for specific thermoregulatory responses are located throughout the brain stem and spinal cord. The preoptic region, in and near the rostral hypothalamus, acts as a coordinating center and strongly influences each of the lower effector areas. The preoptic area contains neurons that are sensitive to subtle changes in hypothalamic or core temperature. Preoptic thermosensitive neurons also receive a wealth of somatosensory input from skin and spinal thermoreceptors. In this way, preoptic neurons compare and integrate central and peripheral thermal information. As a result of this sensory integration and its control over lower effector areas, the preoptic region elicits the thermoregulatory responses that are the most appropriate for both internal and environmental thermal conditions. Thermosensitive preoptic neurons are also affected by endogenous substances, such as pyrogens. By reducing the activity of warm-sensitive neurons and increasing the activity of cold-sensitive neurons, pyrogens cause fever, a state in which all thermoregulatory responses have elevated set-point temperatures.

Body Temperature Regulation↗
PubMed1998

Synaptic inhibition: its role in suprachiasmatic nucleus neuronal thermosensitivity and temperature compensation in the rat.

1. Whole-cell patch clamp recordings of neurones in the suprachiasmatic nucleus (SCN) from rat brain slices were analysed for changes in spontaneous synaptic activity during changes in temperature. While recent studies have identified temperature-sensitive responses in some SCN neurones, it is not known whether or how thermal information can be communicated through SCN neural networks, particularly since biological clocks such as the SCN are assumed to be temperature compensated. 2. Synaptic activity was predominantly inhibitory and mediated through GABAA receptor activation. Spontaneous inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) were usually blocked with perifusion of 10-50 microM bicuculline methiodide (BMI). BMI was used to test hypotheses that inhibitory synapses are capable of either enhancing or suppressing the thermosensitivity of SCN neurones. 3. Temperature had opposite effects on the amplitude of IPSPs and IPSCs. Warming decreased IPSP amplitude but increased IPSC amplitude. This suggests that thermally induced changes in IPSP amplitude are primarily influenced by resistance changes in the postsynaptic membrane. The thermal effect on IPSP amplitude contributed to an enhancement of thermosensitivity in some neurones. 4. In many SCN neurones, temperature affected the frequency of IPSPs and IPSCs. An increase in IPSP frequency with warming and a decrease in frequency during cooling made several SCN neurones temperature insensitive, allowing these neurones to maintain a relatively constant firing rate during changes in temperature. This temperature-adjusted change in synaptic frequency provides a mechanism of temperature compensation in the rat SCN.

Animals↗
PubMed1998

Hypothalamic neurons. Mechanisms of sensitivity to temperature.

Rostral hypothalamic neurons are influenced by endogenous factors that affect thermoregulation and fever. Intracellular recordings reveal the synaptic and intrinsic mechanisms responsible for neuronal thermosensitivity. Many temperature-sensitive and temperature-insensitive neurons display a depolarizing prepotential that precedes action potentials. Temperature has little effect on the prepotential of insensitive neurons; however, in warm-sensitive neurons, the prepotential's depolarization is elevated by warming, and this increases the firing rate. Intracellular cAMP can increase neuronal thermosensitivity by enhancing the thermal response of the prepotential, most likely by thermosensitive ionic conductances. Warm-sensitive neurons also receive inhibitory synaptic input (IPSPs) from temperature-insensitive neurons, enhancing the thermosensitivity of some neurons, because cooling increases IPSP amplitude and duration. Therefore, even though IPSP frequencies do not change, cooling can decrease firing rates by increasing IPSP amplitudes. Because endogenous factors change neuronal firing rate and thermosensitivity, these changes likely occur both post- and presynaptically as well as by ionic conductances that determine the time interval between action potentials.

Animals↗
PubMed1997

Neuronal thermosensitivity and survival of rat hypothalamic slices in recording chambers.

Several studies have examined the activity of neurons in hypothalamic tissue slices. The present experiments studied relationships between neuronal activity (firing rate and thermosensitivity) and tissue survival as a function of time and slice thickness. Rat hypothalamic tissue slices were sectioned at different thicknesses (350, 450, and 600 microm) and maintained in an oxygenated interface chamber which was perfused with artificial cerebrospinal fluid (ACSF). Electron and light microscopy were used to examine tissue morphology at different depths from the slice surfaces, and extracellular recordings were used to measure each cell's spontaneous activity and response to changes in temperature. Tissue damage was most evident at tissue layers nearest the gas-exposed surface. At 9 h in the chamber, 350 microm thick slices showed subtle changes in morphology with little difference between the gas-exposed and ACSF-exposed surfaces. In the 450 and 600 microm thick slices, tissue degeneration became more evident with increased damage at the gas-exposed surface. This damage extended fully into the tissue of the 600 microm section. There were no differences in firing rate or thermosensitivity between 350 and 450 microm slices; but in 600 microm slices, there were fewer spontaneously active neurons, although these neurons had a higher mean thermosensitivity. Based on the incidence of spontaneous activity and morphological integrity, the results suggest that electrophysiological experiments using 350 microm slices are preferable to experiments using thicker slices.

Action Potentials↗
PubMed1996

Cellular mechanisms for neuronal thermosensitivity in the rat hypothalamus.

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.

Action Potentials↗
PubMed1996

Fever's glass ceiling.

The importance of an upper limit of the febrile response has been recognized since the time of Hippocrates. Although the precise temperature defining this limit varies according to the site at which body temperature is measured, human core temperature is almost never permitted to rise above 41 degrees C-42 degrees C during fever. There are compelling physiological reasons for such an upper limit of regulated body temperature. The mechanisms by which the limit is maintained are most likely complex and involve special properties of thermoregulatory neurons themselves, circulating endogenous antipyretics (such as arginine vasopressin and alpha-melanocyte-stimulating hormone), and soluble receptors for the (pyrogenic) cytokine mediators of the febrile response.

Animals↗
PubMed1995

Temperature effects on membrane potential and input resistance in rat hypothalamic neurones.

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.

Action Potentials↗
PubMed1994

Circadian thermosensitive characteristics of suprachiasmatic neurons in vitro.

The circadian pacemaker in the hypothalamic suprachiasmatic nucleus (SCN) affects several regulatory systems, including body temperature. To study circadian changes in the firing rate and thermosensitivity of SCN neurons, single-unit activity was recorded from the dorsomedial and ventrolateral SCN in frontal slices of rat hypothalamus during changes in tissue temperature. When analyzed according to circadian time (CT), 305 neurons were characterized by firing rate and 208 neurons were characterized by thermosensitivity. Circadian firing-rate changes were evident only in the dorsomedial SCN, with peak firing rates occurring during the subjective day. Circadian changes in SCN neuronal thermosensitivity also were observed, but the greatest thermosensitivity occurred during the subjective night. Increased thermosensitivity was most dramatic in the ventrolateral SCN, where > 40% of the neurons were warm sensitive in the CT 16- to 20-h period. These changes in neuronal thermosensitivity may reflect interactions between body temperature and circadian rhythms.

Animals↗
PubMed1992

Regional interactions between thermosensitive neurons in diencephalic slices.

Rat brain slices were used to investigate regional interactions between thermosensitive neurons in different diencephalic regions. Horizontal tissue slices rested over three thermodes. This permitted independent thermal stimulation of rostral, middle, and caudal regions. Thermocouples measured tissue temperatures in these three locations, and extracellular recordings measured neuronal responses to temperature changes both locally (at the site of the recorded neuron) and in remote regions of the slice. Many of the neurons that were sensitive to remote temperatures were located near the lateral border of the diencephalic nuclei, especially in the perifornical area. All neurons displaying remote thermosensitivity also displayed local thermosensitivity. These neurons usually showed opposite responses to remote and local temperatures; i.e., most of these neurons were locally warm sensitive but showed cold sensitivity to remote temperatures. These findings indicate that thermosensitive synaptic networks extend throughout the diencephalon and may explain the effect of temperature on a variety of homeostatic systems.

Animals↗
PubMed1992

Delayed firing rate responses to temperature in diencephalic slices.

Thermoregulatory responses may be delayed in onset and offset by several minutes after changes in hypothalamic temperature. Our preceding study found neurons that displayed delayed firing rate responses during clamped thermal stimulation in remote regions of rat diencephalic tissue slices. The present study looked for similar delayed firing rate responses during clamped (1.5-10 min) changes in each neuron's local temperature. Of 26 neurons tested with clamped thermal stimulation, six (i.e., 23%) showed delayed responses, with on-latencies of 1.0-7.8 min. These neurons rarely showed off-latencies, and the delayed response was not eliminated by synaptic blockade. The on-latencies and ranges of local thermosensitivity were similar to delayed neuronal responses to remote temperature; however, remote-sensitive neurons displayed off-latencies, higher firing rates at 37 degrees C, and greater sensitivity to thermal stimulation. Our findings suggest that delayed thermosensitivity is an intrinsic property of certain neurons and may initiate more elaborate or prolonged delayed responses in synaptically connected diencephalic networks. These networks could explain the delayed thermoregulatory responses observed during hypothalamic thermal stimulation.

Animals↗
PubMed1991

Intracellular analysis of inherent and synaptic activity in hypothalamic thermosensitive neurones in the rat.

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.

Action Potentials↗
PubMed1990

In vitro osmosensitive hypothalamic neurons from hypertensive and normotensive rats.

Single-unit activity was recorded in hypothalamic tissue slices from spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats to identify differences in neuronal osmosensitivity between these two strains. Neurons were characterized according to location, firing rate, temperature sensitivity, and response to hyposmotic (280 mosmol/kgH2O) and hyperosmotic (320 mosmol/kgH2O) media. More than half of the thermosensitive neurons were also osmosensitive. Three groups of osmosensitive neurons were identified: 1) low-firing neurons excited by hyposmolality and inhibited by hyperosmolality, 2) high-firing neurons excited by hyposmolality, and 3) high-firing neurons excited by hyperosmolality. There were no differences between strains in terms of the proportions of osmosensitive neurons. Compared with WKY neurons, however, SH osmosensitive neurons displayed reduced sensitivity to hyperosmotic media. Also, SH osmotically insensitive neurons displayed lower spontaneous firing rates. These differences in osmosensitivity and spontaneous activity may provide a neuronal basis to explain some of the differences in water and sodium regulation observed in hypertensive rats.

Animals↗
PubMed1989

In vitro diencephalic neuronal thermosensitivity in normotensive and hypertensive rats.

Because morphological differences exist in hypothalamic neurons from spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats, the present study recorded neuronal spontaneous activity and thermosensitivity from diencephalic tissue slices of these two strains. With the use of extracellular recordings from horizontal tissue slices, neurons were characterized according to location, firing rate at 37 degrees C, and firing rate response to changes in local tissue temperature. Compared with WKY neurons, SH neurons had higher firing rates in the preoptic-anterior hypothalamus and lower firing rates in the dorsomedial hypothalamus. In addition, SH warm-sensitive neurons were less thermosensitive over the hyperthermic range (37-40 degrees C), and SH temperature-insensitive neurons had higher spontaneous firing rates. These differences in spontaneous activity and thermosensitivity provide a neuronal basis to explain the elevation of core temperature observed in SH rats.

Acclimatization↗