Temperature-sensitive properties of rat suprachiasmatic nucleus neurons

2001 ◽  
Vol 281 (3) ◽  
pp. R706-R715 ◽  
Author(s):  
Penny W. Burgoon ◽  
Jack A. Boulant
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Suprachiasmatic Nucleus ◽  
Interspike Interval ◽  
Slow Component ◽  
Resting Membrane Potential ◽  
Temperature Sensitive ◽  
Tissue Slices ◽  
Hypothalamic Tissue ◽  
Potential Threshold

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.

Effects of ouabain on neuronal thermosensitivity in hypothalamic tissue slices

1989 ◽  
Vol 257 (1) ◽  
pp. R21-R28
Author(s):  
M. C. Curras ◽  
J. A. Boulant
Keyword(s):  
Firing Rate ◽  
Neuronal Activity ◽  
Unit Activity ◽  
Single Unit ◽  
Single Unit Activity ◽  
Tissue Slices ◽  
Temperature Changes ◽  
Cold Sensitive ◽  
Hypothalamic Tissue

To determine the role of the electrogenic Na+-K+ pump in neuronal thermosensitivity, single-unit activity was recorded in rat hypothalamic tissue slices before, during, and after perfusions containing 10(-5) or 10(-6) M ouabain, a specific pump inhibitor. Most neurons were recorded in the preoptic-anterior hypothalamus. Some neurons were also tested with high magnesium-low calcium perfusions to determine ouabain's effects on neuronal activity during synaptic blockade. When the neurons were characterized according to thermosensitivity, 24% were warm sensitive, 8% were cold sensitive, and 68% were temperature insensitive. Ouabain increased the firing rate of 60% of all neurons. Ouabain did not reduce the thermosensitivity of cold-sensitive and warm-sensitive neurons; however, temperature-insensitive neurons became more warm sensitive during ouabain perfusion. This increase in warm sensitivity did not occur with ouabain plus high Mg2+-low Ca2+ perfusion, suggesting that Ca2+ is important in this response. These results indicate that the Na-K pump is not responsible for the thermosensitivity of hypothalamic cold-sensitive or warm-sensitive neurons; however, this pump may be actively employed by many neurons that remain insensitive to temperature changes.

Persistent α1-adrenergic receptor function in the nucleus locus coeruleus causes hyperexcitability in AD/HD model rats

2014 ◽  
Vol 111 (4) ◽  
pp. 777-786 ◽  
Author(s):  
Sachiyo Igata ◽  
Tokumasa Hayashi ◽  
Masayuki Itoh ◽  
Takashi Akasu ◽  
Makoto Takano ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Locus Coeruleus ◽  
Adrenergic Receptor ◽  
Wistar Rats ◽  
Developmental Disorders ◽  
Resting Membrane Potential ◽  
Spontaneous Firing ◽  
Inward Current ◽  
Spontaneous Firing Rate

Spontaneously hypertensive rats (SHR) are widely used as a model of attention deficit hyperactivity disorder (ADHD) as their ADHD-like behaviors are restored by methylphenidate. However, a postnatal neural development in SHR is unknown. We performed whole cell patch clamp recordings from locus coeruleus (LC) neurons in neonatal [postnatal day (P) 3–5], juvenile (P21–28), and adult (P 49–56) SHR and age-matched Wistar rats to evaluate α1- and α2-adrenergic receptor (ARs) activities at each developmental period. LC neurons in neonatal Wistar rats and SHR showed no difference in resting membrane potential and spontaneous firing rate, while juvenile and adult SHR LC neurons showed depolarized resting membrane potential and faster spontaneous firing rate than in Wistar rats. Blockade of α1-AR activity by prazosin hyperpolarized the membrane and abolished spontaneous firings in all developmental periods in SHR LC neurons, but not in juvenile and adult Wistar rats. α1-AR stimulation by phenylephrine evoked an inward current in juvenile LC neurons in SHR, but not in juvenile Wistar rats. This phenylephrine-induced inward current was abolished by nonselective cation channel blockers. By contrast, α2-AR stimulation-induced outward currents in the presence of an α1-AR antagonist were equivalent in SHR and Wistar LC neurons. These data suggest that Wistar LC neurons lose α1-AR function during development, whereas α1-ARs remain functional in SHR LC neurons. Thus persistent intrinsic activity of α1-ARs may be a neural mechanism contributing to developmental disorders in juvenile SHRs.

Cyclic GMP alters the firing rate and thermosensitivity of hypothalamic neurons

2008 ◽  
Vol 294 (5) ◽  
pp. R1704-R1715 ◽  
Author(s):  
Chadwick L. Wright ◽  
Penny W. Burgoon ◽  
Georgia A. Bishop ◽  
Jack A. Boulant
Keyword(s):  
Firing Rate ◽  
Cyclic Nucleotide ◽  
Temperature Sensitive ◽  
Tissue Slices ◽  
Hypothalamic Neurons ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Gated Channel ◽  
Cgmp Analog ◽  
Rostral Hypothalamus

The rostral hypothalamus, especially the preoptic-anterior hypothalamus (POAH), contains temperature-sensitive and -insensitive neurons that form synaptic networks to control thermoregulatory responses. Previous studies suggest that the cyclic nucleotide cGMP is an important mediator in this neuronal network, since hypothalamic microinjections of cGMP analogs produce hypothermia in several species. In the present study, immunohistochemisty showed that rostral hypothalamic neurons contain cGMP, guanylate cyclase (necessary for cGMP synthesis), and CNG A2 (an important cyclic nucleotide-gated channel). Extracellular electrophysiological activity was recorded from different types of neurons in rat hypothalamic tissue slices. Each recorded neuron was classified according to its thermosensitivity as well as its firing rate response to 2–100 μM 8-bromo-cGMP (a membrane-permeable cGMP analog). cGMP has specific effects on different neurons in the rostral hypothalamus. In the POAH, the cGMP analog decreased the spontaneous firing rate in 45% of temperature-sensitive and -insensitive neurons, an effect that is likely due to cGMP-enhanced hyperpolarizing K+ currents. This decreased POAH activity could attenuate thermoregulatory responses and produce hypothermia during exposures to cool or neutral ambient temperatures. Although 8-bromo-cGMP did not affect the thermosensitivity of most POAH neurons, it did increase the warm sensitivity of neurons in other hypothalamic regions located dorsal, lateral, and posterior to the POAH. This increased thermosensitivity may be due to pacemaker currents that are facilitated by cyclic nucleotides. If some of these non-POAH thermosensitive neurons promote heat loss or inhibit heat production, then their increased thermosensitivity could contribute to cGMP-induced decreases in body temperature.

scholarly journals Suppression of spikes during posttetanic hyperpolarization in auditory neurons: the role of temperature, Ih currents, and the Na+-K+-ATPase pump

2012 ◽  
Vol 108 (7) ◽  
pp. 1924-1932 ◽  
Author(s):  
Jun Hee Kim ◽  
Henrique von Gersdorff
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Atpase Activity ◽  
Brain Stem ◽  
High Frequency ◽  
Afferent Fiber ◽  
Resting Potential ◽  
Effect Of Temperature ◽  
Resting Membrane Potential ◽  
Temperature Sensitive

In vivo recordings from postsynaptic neurons in the medial nucleus of the trapezoid body (MNTB), an auditory brain stem nucleus, show that acoustic stimulation produces a burst of spikes followed by a period of hyperpolarization and suppressed spiking activity. The underlying mechanism for this hyperpolarization and reduced spiking is unknown. Furthermore, the mechanisms that control excitability and resting membrane potential are not fully determined for these MNTB neurons. In this study we investigated the excitability of principal neurons from the MNTB after high-frequency afferent fiber stimulation, using whole cell recordings from postnatal day 15–17 rat brain stem slices. We found that Na+-K+-ATPase activity mediates a progressive hyperpolarization during a prolonged tetanic train and a posttetanic hyperpolarization (PTH) at the end of the train, when postsynaptic action potentials failed to fire. Raising the temperature to more physiological levels (from 22 to 35°C) depolarized the resting membrane potential of both presynaptic and postsynaptic cells and decreased the latency of action potential firing during PTH. Higher temperatures also reduced the presynaptic calyx action potential failure rates by 50% during presynaptic PTH, thus increasing the safety-factor for presynaptic spiking. The effect of temperature on hyperpolarization-activated cation current ( Ih) is reflected in the resting potential at both pre- and postsynaptic neurons. We thus propose that temperature-sensitive Na+-K+-ATPase activity and Ih contribute to set the resting membrane potential and produce a brief period of suppressed spiking (or action potential failures) after a prolonged high-frequency afferent tetanus.

scholarly journals A Ba2+-Sensitive K+ Current Contributes to the Resting Membrane Potential of Neurons in Rat Suprachiasmatic Nucleus

2002 ◽  
Vol 88 (2) ◽  
pp. 869-878 ◽  
Author(s):  
Marcel de Jeu ◽  
Alwin Geurtsen ◽  
Cyriel Pennartz
Keyword(s):  
Membrane Potential ◽  
Suprachiasmatic Nucleus ◽  
Voltage Dependence ◽  
Brain Slices ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
M Current ◽  
Whole Cell Patch Clamp

A Ba2+-sensitive K+ current was studied in neurons of the suprachiasmatic nucleus (SCN) using the whole cell patch-clamp technique in acutely prepared brain slices. This Ba2+-sensitive K+ current was found in approximately 90% of the SCN neurons and was uniformly distributed across the SCN. Current-clamp studies revealed that Ba2+ (500 μM) reversibly depolarized the membrane potential by 6.7 ± 1.3 mV ( n = 22) and concomitantly Ba2+ induced an increase in the spontaneous firing rate of 0.8 ± 0.2 Hz ( n = 12). The Ba2+-evoked depolarizations did not depend on firing activity or spike dependent synaptic transmission. No significant day/night difference in the hyperpolarizing contribution to the resting membrane potential of the present Ba2+-sensitive current was observed. Voltage-clamp experiments showed that Ba2+ (500 μM) reduced a fast-activating, voltage-dependent K+ current. This current was activated at levels below firing threshold and exhibited outward rectification. The Ba2+-sensitive K+ current was strongly reduced by tetraethylammonium (TEA; 20 and 60 mM) but was insensitive to 4-aminopyridine (4-AP; 5 mM) and quinine (100 μM). A component of Ba2+-sensitive K+ current remaining in the presence of TEA exhibited no clear voltage dependence and is less likely to contribute to the resting membrane potential. The voltage dependence, kinetics and pharmacological properties of the Ba2+- and TEA-sensitive K+ current make it unlikely that this current is a delayed rectifier, Ca2+-activated K+ current, ATP-sensitive K+ current, M-current or K+ inward rectifier. Our data are consistent with the Ba2+- and TEA-sensitive K+ current in SCN neurons being an outward rectifying K+ current of a novel identity or belonging to a known family of K+ channels with related properties. Regardless of its precise molecular identity, the current appears to exert a significant hyperpolarizing effect on the resting potential of SCN neurons.

Effective synaptic current and motoneuron firing rate modulation

1995 ◽  
Vol 74 (2) ◽  
pp. 793-801 ◽  
Author(s):  
R. K. Powers ◽  
M. D. Binder
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Firing Rate ◽  
Discharge Rate ◽  
Reversal Potential ◽  
Repetitive Firing ◽  
Resting Membrane Potential ◽  
Synaptic Inputs ◽  
Rate Modulation ◽  
Repetitive Discharge

1. We used a modified voltage-clamp technique to measure the steady-state effective synaptic currents (I(N)) produced by activating four different input systems to cat hindlimb motoneurons: Ia afferent fibers, Ia-inhibitory interneurons, Renshaw interneurons, and contralateral rubrospinal neurons. In the same motoneurons, we measured the slope of the firing rate-injected current (f-I) relation in the primary range. We then reactivated these synaptic inputs during steady, repetitive firing to assess their effects on motoneuron discharge rate. 2. Our measurements of I(N) were derived from recordings made near the resting membrane potential, whereas the effects of the synaptic inputs on repetitive discharge were evaluated at more depolarized membrane potentials. Thus we adjusted the I(N) values for these changes in driving force based on estimates of the synaptic reversal potential and the mean membrane potential during repetitive discharge. 3. We found that changes in the steady-state discharge rate of a motoneuron produced by these synaptic inputs could be reasonably well predicted by the product of the estimated value of I(N) during repetitive firing and the slope of the motoneuron's f-I relation. Although there was a high correlation between predicted and observed changes in firing rate for our entire sample of motoneurons (r = 0.93; P < 0.001), the slope of the relation between predicted and observed firing rate modulation was significantly greater than 1. 4. The systematic difference between predicted and observed firing rate modulation observed in the overall sample was primarily due to the fact that our predictions underestimated the changes in firing rate produced by Ia excitation and Ia inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of the Negative After-Potential in Frog Single Nerve Fibers

1958 ◽  
Vol 193 (1) ◽  
pp. 195-202 ◽  
Author(s):  
Gordon M. Schoepfle ◽  
Floyd E. Bloom ◽  
Duane Hellam
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Slow Component ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Nerve Fibers ◽  
Resting Membrane Potential ◽  
Terminal Phase ◽  
Single Nerve ◽  
The Difference

The time course of the negative after-potential from an isolated single nerve fiber is adequately described by the sum of two exponential terms. Conductance changes are confined to the relatively brief initial phase. The difference between active and resting membrane potential bears a relation to over-all membrane resistance which is consistent with the view that the first phase of the negative after-potential is dependent on a change in potassium conductance. The prolonged terminal phase of the after-potential is characterized by an exponential time constant identical with that of the slow drift in membrane potential (slow component of electrotonus) associated with the break of an anodal pulse. Both magnitude and time parameter of this terminal phase vary with pre-existent membrane potential. The differential changes in magnitude of spike and after-potential resulting from changes in pre-existent membrane potential suggest that the effects of anoxia on the after-potential/spike ratio are dependent only on the change in membrane potential.

scholarly journals Muscarinic Modulation of Recruitment Threshold and Firing Rate in Rat Oculomotor Nucleus Motoneurons

2009 ◽  
Vol 101 (1) ◽  
pp. 100-111 ◽  
Author(s):  
Jose Luis Nieto-Gonzalez ◽  
Livia Carrascal ◽  
Pedro Nunez-Abades ◽  
Blas Torres
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Acetylcholine Receptors ◽  
Muscarinic Acetylcholine Receptors ◽  
Resting Membrane Potential ◽  
Oculomotor Nucleus ◽  
Recruitment Threshold ◽  
Bath Application ◽  
Lower Amplitude

Above recruitment threshold, ocular motoneurons (Mns) show a firing rate linearly related with eye position. Current hypothesis suggests that synaptic inputs are determinant for establishing the recruitment threshold and firing rate gain in these Mns. We investigated this proposal by studying the cholinergic modulation in oculomotor nucleus Mns by intracellular recordings in rat brain slice preparation. All recorded Mns were silent at their resting membrane potential. Bath application of carbachol (10 μm) produced a depolarization and a sustained firing that was not silenced on returning membrane potential to the precarbachol value via DC injection. In response to similar membrane depolarization or equal-current steps, carbachol-exposed Mns produced a higher firing rate and a shorter spike afterhyperpolarization phase with lower amplitude. The relationship between injected current and firing rate ( I– F) was linear in control and carbachol-exposed Mns. The slope of these relationships ( I– F gain) decreased with carbachol exposure. Bath application of agonist and antagonist of nicotinic and muscarinic acetylcholine receptors in addition to immunohistochemical studies support the notion that muscarinic receptors are primarily involved in the preceding responses. We conclude that muscarinic inputs play an important role in determining the recruitment threshold and firing rate gain observed in oculomotor Mns in vivo.

Carbon dioxide and pH effects on temperature-sensitive and -insensitive hypothalamic neurons

2007 ◽  
Vol 102 (4) ◽  
pp. 1357-1366 ◽  
Author(s):  
Chadwick L. Wright ◽  
Jack A. Boulant
Keyword(s):  
Heat Stroke ◽  
Ph Effects ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Tissue Slices ◽  
Hypothalamic Neurons ◽  
Electrophysiological Recordings ◽  
Sprague Dawley Rats ◽  
Hypothalamic Tissue ◽  
Solution Bathing

The preoptic-anterior hypothalamus (POAH) controls body temperature, and thermoregulatory responses are impaired during hypercapnia. If increased CO2 or its accompanying acidosis inhibits warm-sensitive POAH neurons, this could provide an explanation for thermoregulatory impairment during hypercapnia. To test this possibility, extracellular electrophysiological recordings determined the effects of CO2 and pH on the firing rates of both temperature-sensitive and -insensitive neurons in hypothalamic tissue slices from 89 male Sprague-Dawley rats. Firing rate activity was recorded in 121 hypothalamic neurons before, during, and after changing the CO2 concentration aerating the tissue slice chamber or changing the pH of the solution bathing the tissue slices. Increasing the aeration CO2 concentration from 5% (control) to 10% (hypercapnic) had no effect on most (i.e., 69%) POAH temperature-insensitive neurons; however, this hypercapnia inhibited the majority (i.e., 59%) of warm-sensitive neurons. CO2 affected similar proportions of (non-POAH) neurons in other hypothalamic regions. These CO2 effects appear to be due to changes in pH since the CO2-affected neurons responded similarly to isocapnic acidosis (i.e., normal CO2 and decreased pH) but were not responsive to isohydric hypercapnia (i.e., increased CO2 and normal pH). These findings may offer a neural explanation for some heat-related illnesses (e.g., exertional heat stroke) where impaired heat loss is associated with acidosis.

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