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Zablocki Department of Veterans Affairs Medical Center and Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53295
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Evidence suggests that
transmission of barosensitive input from arterial baroreceptors and
cardiac mechanoreceptors at nucleus tractus solitarius (NTS) neurons
involves non-N-methyl-D-aspartate (NMDA)
glutamate receptors, but there is a possibility that the contribution
of NMDA receptors might increase during periods of increased afferent
input, when enhanced neuronal depolarization could increase the
activation of NMDA receptors by removal of a Mg2+ block.
Thus the effects of NMDA on cardiac mechanoreceptor-modulated NTS
neuronal discharges were examined at different levels of arterial pressure used to change cardiac mechanoreceptor afferent input. To
determine whether the response was specific to NMDA,
(±)-
-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) was
also administered at different levels of neuronal discharge. In
anesthetized dogs, neuronal activity was recorded from the NTS while
NMDA or AMPA was picoejected at high versus low arterial stimulating
pressures. NMDA, but not AMPA, produced a significantly greater
discharge of mechanoreceptor-driven NTS neurons at higher versus lower
levels of stimulating pressure. These data suggest that the role played
by NMDA receptors is greater during periods of enhanced neuronal
depolarization, which could be produced by increases in afferent
barosensitive input.
medulla; nucleus tractus solitarius; AMPA; baroreceptors
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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MANY STUDIES have pointed to glutamate as the primary neurotransmitter for cardiovascular receptor inputs, including baroreceptor (2, 10, 21, 23) and cardiac receptor (19, 23) afferent input to neurons in the nucleus tractus solitarius (NTS), but the contribution of glutamate receptor subtypes to the transmission of this afferent input has not been conclusively determined. Evidence indicates that non-N-methyl-D-aspartate (NMDA) receptors may be the primary ionotropic receptor subtype involved in transmission to neurons that directly receive afferent baroreceptor activity (22), although additional evidence also supports a role for NMDA receptors (5, 6, 21). Studies from this laboratory have found that both NMDA and non-NMDA receptor antagonists alter discharges of both baroreceptor-modulated (16, 18) and cardiac mechanoreceptor-modulated (17) NTS neurons, suggesting that each type of ionotropic glutamate receptor may contribute to excitation of "baroreceptive" neurons, or neurons that receive barosensitive, pressure-related information from peripheral receptors. Whereas both glutamate receptor subtypes were found to be involved in the activation of these neurons, blockade of non-NMDA receptors eliminated activity in the majority of neurons, suggesting a greater role for this glutamate receptor subtype. However, the possibility exists that increased excitation of NTS baroreceptive neurons, induced by increases in afferent input from peripheral barosensitive receptors, will enhance the central contribution of NMDA receptors due to removal of a Mg2+ block of the channels with neuronal depolarization. This role for NMDA receptors has been described for other neural pathways (4, 20). Thus the role of NMDA receptors may be greater during periods of increased afferent input, as would occur during increases in blood pressure (BP), because some degree of neuronal depolarization could increase the availability of NMDA receptors. Therefore, the present study was conducted to examine whether the amount of NMDA-induced excitation of cardiac mechanoreceptor-modulated NTS neurons, activated by pressure-sensitive input from cardiac mechanoreceptors, was dependent on the level of afferent mechanoreceptor input. Results from this study suggest that NMDA receptors contribute more to the discharge of cardiac mechanoreceptor-modulated neurons during periods of increased pressure, suggesting that there is an activity-dependent role for NMDA receptors in the transmission of mechanosensitive input.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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General preparation.
The discharge of cardiac mechanoreceptor-modulated neurons in the NTS
was studied in anesthetized 12- to 15-kg mongrel dogs (initial dose of
50 mg/kg -chloralose and 500 mg/kg urethane, supplemental continuous
infusion of 250 mg -chloralose + 2.5 g urethane/h iv). All
experimental procedures followed were approved by the Animal Care and
Use Committees of the Medical College of Wisconsin and the Zablocki
Department of Veterans Affairs Medical Center. The left femoral artery
and vein were cannulated to permit measurement of arterial BP and
infusion of anesthetic, respectively. Arterial blood gases were
measured using an ABL 30 Radiometer Blood Gas Analyzer (Copenhagen,
Denmark) and kept within normal ranges (PCO2
35-45 mmHg, PO2 > 100 mmHg, pH
7.37-7.42) by adjustment of ventilation and infusion of
bicarbonate. Arterial BP was measured via the catheter in the left
femoral artery, which was connected to a Statham pressure transducer
and a Grass model 7D polygraph (Quincy, MA). The carotid sinus and
aortic depressor nerves were sectioned bilaterally to eliminate
arterial baroreceptor afferent input, because the study was focused on
examination of the responses of a specific population of neurons that
received cardiac mechanoreceptor inputs.
Experimental protocol. To regulate and alter BP, animals were given hexamethonium (20 mg/kg iv), followed by a slow infusion of phenylephrine (1.0 mg/100 ml iv) to maintain BP at a mean pressure of 135-145 mmHg to provide an adequate level of stimulation of cardiopulmonary receptors at physiological levels of pressure. In addition, small increases in the phenylephrine infusion rate were used to elevate BP slightly to test for pressure-sensitive modulation of recorded neurons. The presence of hexamethonium prevented any baroreflex-induced changes in heart rate that would normally occur with changes in BP. With the pressure controlled, the NTS was randomly explored using the multibarrel electrode until activity from a single dorsal medullary neuron that displayed a distinct cardiac rhythm was obtained. The pulse-synchronous nature of the discharge was determined by comparing neuronal discharge with the BP pulse. Small changes in BP were produced by changes in the infusion rate of phenylephrine to confirm the pressure-related sensitivity of the afferent-evoked discharge of the NTS neuron. Pressures were reestablished at control levels, and, after a control period of recording, 15 nl aCSF was picoejected onto the neuron to test for vehicle and ejection movement effects on the discharge of the NTS neuron. If any vehicle effects were noted, the experiment was stopped until a new vehicle with no effects was made and tested. The drugs were then remixed in the new vehicle, which had no effects on neuronal activity.
The following protocol was utilized to determine whether the role of NMDA receptors was a function of the level of ongoing activity of single NTS neurons receiving cardiac mechanoreceptor input. BP was set randomly at a low (80-90 mmHg) or high (135-145 mmHg) mean BP, and baseline neuronal discharge at this level of afferent stimulation was recorded over a 20-s period. NMDA (NMDA receptor agonist, 100 µM) was then picoejected (7-15 nl total volume) until a plateau in the increased discharge produced in response to activation of NMDA receptors on the recorded neuron was obtained and recorded. After recovery from the picoejection, the stimulating pressure was set to the remaining high or low level, after which baseline activity at this new pressure was recorded. Picoejection of NMDA was then repeated at the same rate and dose to establish the plateau firing rate at the new pressure, which was recorded for later analysis. In eight of the neurons tested for NMDA, the effects of the non-NMDA receptor agonist [(±)--amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA)] were also examined at the two levels of neuronal activation. AMPA (3.75 µM, 7-15 nl total volume) was picoejected onto the neuron in a
manner similar to NMDA, with the order of administration of glutamate
agonists randomized. Care was taken to allow the neuron to return to
the baseline level of discharge before the second agonist was tested.
Baseline neuronal activity and peak levels of activity induced by NMDA
or AMPA administration were determined for the two different levels of
arterial-stimulating BP.
To ensure that any enhanced responses of the neurons to administration
of NMDA was due to increased availability of the NMDA receptors versus
altered release of glutamate or other modulators at the higher
pressure, a limited additional protocol was performed on three
pulse-synchronous neurons. As described for the pressure stimulation
protocols, a baroreceptive neuron that responded to pressure activation
of cardiac receptors was identified. The stimulation pressure was then
lowered to a level below the threshold pressure needed to activate the
neuron to prevent physiological changes in peripheral receptor input.
AMPA (3.75 µM) was then picoejected at a slow constant rate
(20-40 fmol/min) to establish a steady-state level of neuronal
excitation via activation of non-NMDA receptors. Once activity had
plateaued, NMDA (100 µM) was simultaneously picoejected at 1.2 pmol/min, a rate shown to be effective in activation of NMDA receptors.
This slow rate of ejection was continued until a new plateau level for
nerve activity was established. Frequency of picoejection of AMPA
was then increased (40-60 fmol/min) to establish a new, higher
steady-state of neuronal excitation. NMDA was again simultaneously
picoejected onto the neuron at the same rate and dose as the first
trial to examine the effects of excitation of NMDA receptors at this
new level of neuronal activation. Because AMPA only activates non-NMDA
receptors, any response to activation of the NMDA receptors at a higher
level of AMPA administration should be due to increased availability of
NMDA receptors and not to changes in glutamate or neuromodulator release.
Data analysis. Analysis of recorded unit neuronal activity was accomplished off-line from recorded data using a Hewlett-Packard 310 computer equipped with a 16-channel Infotek 12-bit analog-to-digital converter. Unit activity was directed through a window discriminator whose output was then fed into a digital counter/timer that was sampled at a frequency of 20 Hz. Averaged spikes per second were obtained for a 20-s baseline control period before each picoejection administration of NMDA or AMPA. Peak unit discharge rates in response to administration of either NMDA or AMPA were determined for both high and low levels of stimulating BP. Given the change in baseline discharge that occurred with a change in arterial pressure, a key measure of the effects of either glutamate agonist was the magnitude of the agonist-evoked activity, or the difference in neuronal discharge from baseline to peak response to NMDA or AMPA administration at each pressure. This magnitude of evoked activity as well as baseline and peak levels of activity for AMPA or NMDA administration were compared for high versus low arterial pressures using a one-way ANOVA, with significance set at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Eighteen neurons identified as cardiac mechanoreceptor modulated
by their pulse-synchronous and pressure-sensitive discharges were
examined to determine the response to picoejection of NMDA at high
versus low stimulation pressures. The summed data show that increases
in arterial pressure were found to produce significant increases in
baseline discharge rates of the cardiac mechanoreceptor-modulated NTS
neurons, verifying the pressure sensitivity of the afferent input and
ensuring that there was increased afferent input and thus greater NTS
neuronal activation at the higher pressures (baseline, Fig.
1). Picoejection of NMDA induced a
significantly greater increase in peak discharge at the high versus low
BP (peak NMDA, Fig. 1). The magnitude of the NMDA-evoked difference in
firing rate from baseline to peak discharge rate was also significantly greater at the higher versus lower pressure (
NMDA, Fig. 1). However, there was a range of both pressure sensitivities and responses to
administration of NMDA. An increase in the magnitude of the NMDA-evoked
response at the high stimulating BP was obtained in 14 of 18 neurons
studied. Two of the neurons did not have any differential response to
NMDA, and two neurons actually had a decrease in the magnitude of the
NMDA-evoked activity at the higher stimulating pressure. The raw
discharge and averaged activity of a neuron in response to picoejection
of NMDA at high (A) versus low BP (B) is shown in
Fig. 2. The traces reflect the increase in the baseline neuronal discharge rate at the higher pressure and the
enhanced response to picoejection of NMDA at this level of neuronal
activation. Some variation in spike amplitude due to respiration is
evident in the raw activity traces. The complete averaged discharge
response of this neuron that had an increase in baseline activity, and
a significantly greater evoked activity in response to NMDA in response
to the higher BP is shown in Fig. 2C. The increase in
baseline discharge was associated with an increased peak discharge rate
and a greater magnitude in the NMDA-evoked activity at the higher
stimulating BP. Figure 3 demonstrates the pulse-synchronous and pressure-sensitive nature of the discharge of
this neuron (B) and the stable shape of the action potential at different stimulating BP (A) before and after
administration of NMDA, necessary to ensure accurate analysis of
neuronal firing rates. Figure 4 shows raw
and averaged neuronal activity for a neuron that had a small increase
in baseline discharge but no difference in the NMDA-evoked response at
the high versus low stimulating pressures.
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To determine whether there was a relationship between the amount of
change in the baseline firing rate and the magnitude of the response to
NMDA administration at low versus high stimulating BP, the values for
the change in baseline firing rate from low to high pressure for each
neuron were plotted versus the change in the magnitude of the
NMDA-evoked responses for low to high BP (Fig.
5). Linear regression was used to examine
the relationship between these parameters. As can be seen, there was a
correlation between the baseline firing rate and the peak increase in
response to NMDA picoejection (R = 0.69). This suggests
that there is a direct relationship between the change in baseline
firing, or ongoing discharge, with the magnitude of the response to
administration of NMDA. Thus greater increases in the baseline
discharge rate will result in greater increases in discharge in
response to NMDA, and vice versa.
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Unlike NMDA, there was no significant difference in the peak rates of
firing in response to AMPA administration (peak AMPA, Fig. 1), and thus
no significant difference in the magnitude of the evoked discharge
between high and low stimulation pressures (AMPA, Fig. 1). For four
of eight neurons tested, AMPA induced a slightly greater magnitude of
evoked activity at the high versus low BP. No difference in AMPA-evoked
activity was seen in the remaining four neurons. An example of a neuron
that had an increase in baseline activity in response to the higher
stimulating pressure, an increase in peak discharge to AMPA
administration, but no difference in the magnitude of the response to
AMPA administration (peak minus baseline activity) is shown in Fig.
6. The raw neuronal activity rates in
Fig. 6, A and B, demonstrate the increase in baseline discharge of the neuron to high versus low stimulating pressures (BP) as well as a respiratory-modulated component in the
discharge of this neuron. Administration of AMPA produced a significant
increase in firing at both stimulating BP, as reflected in the averaged
neuronal traces shown in Fig 6C, top. The
elevation in baseline resulted in the elevated peak discharge rate, but the magnitude of the AMPA-evoked discharge was not different for low
versus high stimulating pressures. This is demonstrated by the traces
shown in Fig. 6C, bottom, where the difference in
baseline activity between that at high stimulating BP versus low BP was added to the curve for the low BP response. As can be seen, this resulted in complete overlap of both curves, demonstrating that AMPA
evoked the same amount of activity at the two stimulating pressures.
This type of response is different from that seen for most responses to
NMDA (Fig. 2), where, despite an increase in baseline activity, the
magnitude of the change of NMDA-evoked activity was greater at the high
versus low stimulating BP.
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In a limited study in three cardiac mechanoreceptor-modulated neurons,
baseline activity was increased via picoejection of AMPA rather than by
increasing BP. BP was held constant at a low level to eliminate changes
in glutamate or neuromodulator release as a variable in these studies.
The evoked response of each neuron to picoejection of NMDA was greater
at the higher level of AMPA administration than at the lower level. An
example of this response is shown in Fig.
7. Administration of AMPA at a low rate
(AMPA1) increased baseline activity slightly, but there was no response to subsequent administration of NMDA. However, increasing the rate of
AMPA administration (AMPA2) produced a greater increase in firing and
subsequent administration of NMDA at the same rate and amount now
increased discharge of the neuron. These data suggest that there is an
increased availability of NMDA receptors, because identical amounts of
NMDA were administered during each trial, eliminating differential
availability of neurotransmitter as a possible confounding influence.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The results from this study suggest that NMDA receptors play a greater role in central transmission of barosensitive afferent input during periods of elevated BP, when rates of discharge of peripheral barosensitive receptors are greater. This increased level of afferent input produces a greater activation of NTS neurons, which could result in depolarization and loss of the Mg2+ blockade of NMDA receptors. Because similar responses to NMDA administration were obtained regardless of whether the NTS neuron was activated by increasing levels of afferent input or by increasing amounts of picoejected AMPA to directly activate the non-NMDA receptors, it suggests that the response is due primarily to increased activation of NMDA receptors and not to increased release of neurotransmitters/modulators. Whereas there was some tendency for an activity-dependent increase in neuronal discharge in response to administration of AMPA as well in a few neurons, there was no significant effect in response to AMPA as a group. It is possible that the trend seen for increased discharge to AMPA at high stimulating pressures may be due to greater availability of NMDA receptors at the higher BP, which could have been activated by endogenous release of glutamate. The order of the neurons was not determined in these studies, and, therefore, it is not known whether second- or higher-order neurons were studied. This factor may also be important, based on earlier studies.
The roles of different glutamate receptors in the transmission of afferent input from barosensitive arterial baroreceptors and cardiac mechanoreceptors are not completely understood. There is evidence from whole animal studies (6, 14, 19, 21, 22) that different types of glutamate receptors activate baroreceptive NTS neurons, although there is some controversy as to the extent of these individual contributions. Other studies from brain slices, which have examined neuronal responses to solitary tract stimulation, have also shown evidence for roles for NMDA receptors, non-NMDA receptors, or both in the activation of NTS neurons by sensory inputs (1-3, 13). These studies have not been able to assign a baroreceptor role for the neurons, because the generalized stimulation of the solitary tract was used to activate the neurons. However, a recent study by Bonham and Chen (5) has found a role for NMDA receptors in the transmission of baroreceptor input to second-order NTS neurons. Studies from this laboratory have found that both NMDA and non-NMDA receptor antagonists alter discharge of both baroreceptor-modulated (16, 18) and cardiac mechanoreceptor-modulated (17) NTS neuronal discharge, suggesting that each type of glutamate ionotropic receptor may contribute to excitation of the neurons. However, in most neurons, blockade of non-NMDA receptors had the greatest attenuating effect on neuronal activity, suggesting a greater role for non-NMDA receptors. Results from the current study suggest that increased excitation of cardiac mechanoreceptor-modulated NTS neurons, which could occur during periods of transient hypertension, could enhance the central contribution of NMDA receptors, a possibility not examined in our earlier studies. The recent study of Bonham and Chen (5) also suggests that the role for NMDA receptors in the transmission of baroreceptive information increases as the neurons become depolarized.
The effect of neuronal depolarization on enhancing the activation of NMDA receptors has been described in other systems. In the hippocampus, high-frequency stimulation has been found to lead to depolarization of the postsynaptic membrane, which removes the Mg2+ block for NMDA channels, allowing Ca2+ influx. This calcium, acting as a second messenger, is thought to lead to long-term potentiation of discharge of the neuron (4, 20). Conversely, some studies have found a desensitization or adaptation to the continued administration of either NMDA or AMPA (15). Long-term depression via NMDA receptors has been reported after low-frequency stimulation in the hippocampus (8). It is proposed that high-frequency stimulation may lead to higher intracellular Ca2+, which induces potentiation, whereas low intracellular Ca2+, resulting from low-frequency stimulation, may lead to depression. It is therefore possible that the phosphorylation state of the NMDA receptor influences whether hippocampal synapses, and thus NTS synapses, are potentiated or depressed (9).
The possibility that variable levels of neuronal activation may result in activity-dependent excitation of NMDA receptors was the focus of this study. Long-term potentiation, long-term depression, accommodation, and other nonlinear responses to depolarization have been reported for NTS neurons thought to receive barosensitive inputs (7, 11, 12). The role of NMDA receptors in initiation of these responses has not been well defined, and the extracellular responses of the neurons to different levels of physiological activation by pressure stimulation of afferent inputs has not been described. We did not observe any decaying responses or adaptation to administration of either NMDA or AMPA in this study. However, our administration of either agent was restricted to ~3 min, which might not be sufficient to induce the short-term depression reported for some of these neurons. We did see a potentiation of firing to the administration of NMDA in neurons with enhanced degrees of excitation at the high stimulating BP or level of AMPA administration, suggesting that activation of these receptors may contribute to the short-term potentiation reported by others. In conclusion, we found evidence for an activity-dependent role for NMDA receptors in the excitation of cardiac mechanoreceptor-modulated NTS neurons. The importance of the role of this finding during physiological regulation of BP, particularly during hypertension, remains to be determined.
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ACKNOWLEDGEMENTS |
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The authors acknowledge the excellent technical and histological assistance of Claudia A. Hermes and Angela R. Cowan.
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FOOTNOTES |
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This research was supported by Veterans Affairs Medical Research Funds, National Heart, Lung, and Blood Institute Grant HL-55490, and American Heart Association Grant-In-Aid 0150518.
Address for reprint requests and other correspondence: J. L. Seagard, Research Service 151, Zablocki VA Medical Center, 5000 W. National Ave., Milwaukee, WI 53295 (E-mail: jseagard{at}mcw.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/ajpheart.00601.2002
Received 15 July 2002; accepted in final form 12 November 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
Andresen, MC,
and
Yang M.
Non-NMDA receptors mediate sensory afferent synaptic transmission in medial nucleus tractus solitarius.
Am J Physiol Heart Circ Physiol
259:
H1307-H1311,
1990
2.
Andresen, MC,
and
Yang M.
Excitatory amino acid receptors and afferent synaptic transmission in the nucleus tractus solitarius.
In: Nucleus of the Solitary Tract, edited by Barraco IRA. Boca Raton, FL: CRC, 1993, p. 187-192.
3.
Aylwin, ML,
Horowitz JM,
and
Bonham AC.
NMDA receptors contribute to primary visceral afferent transmission in the nucleus of the solitary tract.
J Neurophysiol
77:
2539-2548,
1997
4.
Bashir, Z,
Alford S,
Davies S,
Randall A,
and
Collingridge G.
Long-term potentiation of NMDA receptor-mediated synaptic transmission in the hippocampus.
Nature
349:
156-158,
1991[Medline].
5.
Bonham, AC,
and
Chen CY.
Glutamatergic neural transmission in the nucleus tractus solitarius: N-methyl-D-asparate receptors.
Clin Exp Pharmacol Physiol
29:
497-502,
2002[Web of Science][Medline].
6.
Chen, CY,
and
Bonham AC.
Non-NMDA and NMDA receptors transmit area postrema input to aortic baroreceptor neurons in NTS.
Am J Physiol Heart Circ Physiol
275:
H1695-H1702,
1998
7.
Felder, RB,
and
Mifflin SW.
Baroreceptor and chemoreceptor afferent processing in the solitary tract nucleus.
In: Nucleus of the Solitary Tract, edited by Barraco IRA. Boca Raton, FL: CRC, 1993, p. 169-186.
8.
Kirkwood, A,
Dudek S,
Gold J,
Aizenman C,
and
Bear M.
Common forms of synaptic plasticity in the hippocampus and neocortex in vitro.
Science
260:
1518-1521,
1993
9.
Mammen, AT,
and
Huganir RL.
Regulation of NMDA receptors by protein phosphorylation.
In: The Inotropic Glutamate Receptors, edited by Monaghan DT,
and Wenthold RJ.. Totowa, NJ: Humana, 1997, p. 135-148.
10.
Meeley, MP,
Underwood MD,
Talman WT,
and
Reis DJ.
Content and in vitro release of endogenous amino acids in the area of the nucleus of the solitary tract of the rat.
J Neurochem
53:
1807-1817,
1989[Web of Science][Medline].
11.
Mifflin, SW.
Short-term potentiation of carotid sinus nerve inputs to neurons in the nucleus of the solitary tract.
Respir Physiol
110:
229-236,
1997[Web of Science][Medline].
12.
Mifflin, SW,
and
Felder RB.
Synaptic mechanisms regulating cardiovascular afferent inputs to solitary tract nucleus.
Am J Physiol Heart Circ Physiol
259:
H653-H661,
1990
13.
Miller, BD,
and
Felder RD.
Excitatory amino acid receptors intrinsic to synaptic transmission in nucleus tractus solitarii.
Brain Res
456:
333-343,
1988[Web of Science][Medline].
14.
Ohta, H,
and
Talman WT.
Both NMDA and non-NMDA receptors in the NTS participate in the baroreceptor reflex in rats.
Am J Physiol Regul Integr Comp Physiol
267:
R1065-R1070,
1994
15.
Otis, TS,
Zhang S,
and
Trussel LO.
Direct measurement of AMPA receptor desensitization induced by glutamatergic synaptic transmission.
J Neurosci
16:
7496-7504,
1996
16.
Seagard, JL,
Dean C,
and
Hopp FA.
Glutamate receptor subtypes involved in transmission of baroreceptor input to NTS neurons.
Soc Neurosci Abstr
23:
722,
1997.
17.
Seagard, JL,
Dean C,
and
Hopp FA.
Role of glutamate receptors in transmission of vagal cardiac input to neurons in the nucleus tractus solitarius.
J Physiol
520:
243-253,
1999
18.
Seagard, JL,
Dean C,
and
Hopp FA.
Neurochemical transmission of baroreceptor input in the NTS.
Brain Res Bull
51:
111-118,
2000[Web of Science][Medline].
19.
Wilson, CG,
Zhang Z,
and
Bonham AC.
Non-NMDA receptors transmit cardiopulmonary C fibre input in nucleus tractus solitarii in rats.
J Physiol
493:
773-785,
1996.
20.
Xie, X,
Berger T,
and
Barrionuevo G.
Isolated NMDA receptor-mediated synaptic responses express both LTP and LTD.
J Neurophysiol
67:
1009-1013,
1992
21.
Zhang, J,
and
Mifflin SW.
Influences of excitatory amino acid receptor agonists on nucleus of the solitary tract neurons receiving aortic depressor nerve inputs.
J Pharmacol Exp Ther
282:
639-647,
1997
22.
Zhang, J,
and
Mifflin SW.
Differential roles for NMDA and non-NMDA receptor subtypes in baroreceptor afferent integration in the nucleus of the solitary tract of the rat.
J Physiol
511:
733-745,
1998
23.
Zhang, W,
and
Mifflin SW.
Excitatory amino-acid receptors contribute to carotid sinus and vagus nerve evoked excitation of neurons in the nucleus of the tractus solitarius.
J Auton Nerv Syst
55:
50-56,
1995[Web of Science][Medline].
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baseline activity) at high versus low BP.
Unlike NMDA, the peak response (peak AMPA) and magnitude of evoked
activity (
).
Regression analysis yielded a R value of 0.69 and a
slope of 0.93, indicating a direct relationship between the change
obtained in baseline firing rate and the magnitude of the response to
administration NMDA. This suggests that increases in baseline firing
induced by higher stimulating arterial pressure (increased
barosensitive afferent input) results in increased responses to
activation of NMDA receptors. Conversely, decreases in baseline
pressure also result in decreases in magnitude of the response to NMDA
administration. Thin lines represent 95% confidence intervals
for the regression.
