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Department of Anatomy and Cell Biology and Physiology, University of Western Ontario, London, Ontario N6A 5C1, Canada
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Neurotransmitters relaying ascending
visceral information were examined by comparing the response of neurons
in the insular cortex to vagal stimulation (0.8 Hz, 2 mA) before and
after neurotransmitter antagonist injections (200 nl) in the
ventroposterior parvocellular nucleus of the thalamus (VPpc). Cobalt
(10 mM; presynaptic blocker) and kynurenate (100 µM; nonspecific
excitatory amino acid antagonist) injections in the VPpc resulted in an
attenuation (73-100 and 38-98%, respectively) of the evoked
cortical response. Injections of the specific
N-methyl-D-aspartate (NMDA) antagonist
DL-2-amino-5-phosphonopentanoic acid (200 µM and 2 mM)
did not affect the vagally evoked response, whereas the nonspecific
non-NMDA antagonist L-glutamic acid diethylester (200 µM)
attenuated the vagally evoked response by 66-100%. Three concentrations of the
DL-
-amino-3-hydroxy-5-methylisoxazole-propionic acid
(AMPA)-specific antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 and
200 µM and 2 mM) attenuated the vagally evoked cortical response
by 29 ± 9, 31 ± 10, and 59 ± 8%, respectively. The
more selective AMPA antagonist
6-nitro-7-sulphamoylbenzo(f)quinoxaline-2,3-dione (200 µM and 2 mM)
inhibited the vagally evoked cortical response by 53 ± 8 and
52 ± 3%, respectively. Phentolamine (0.1 and 1.0 µM), a
general -adrenergic antagonist, and picrotoxin (0.1 and 1.0 µM), a
GABAA antagonist, did not affect the vagally evoked response. Atropine, a muscarinic cholinergic antagonist, decreased the
vagally evoked response by 40 ± 2% at a concentration of 0.1 µM, but a higher concentration of 1.0 µM had no effect. These results indicate that the non-NMDA excitatory amino acid receptor is
necessary for the relay of visceral information in the VPpc. Muscarinic
receptors may modulate visceral neuronal excitability in the VPpc,
although the exact interaction between the inhibitory (m2) and
excitatory (m3 or m5) muscarinic receptor types found in the thalamus
is not known.
autonomic; vagus; cholinergic
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE AUTONOMIC NERVOUS SYSTEM has been traditionally regarded as a motor system responsible for regulating the internal environment. The vagus nerve plays a major role in autonomic control by conveying visceral sensory information through a variety of afferents contained within it. The modalities conveyed by these afferents include sensory information from the viscera of the neck (laryngeal, tracheal, and esophageal), thorax (including cardiac and pulmonary), and abdomen (including gastric and intestinal). That this visceral input ascends to the cerebral cortex was demonstrated as early as 1938 when Bailey and Bermer (1) showed that stimulation of the cephalic end of several cervical vagus nerves resulted in an increase in the rate and amplitude of cortical electrical activity in the orbitoinsular region. These results were later confirmed in 1951 by Dell and Olson (9), who stimulated the cervical vagus and recorded evoked potentials throughout the forebrain and cortex.
Anatomic tracing studies have elucidated the central pathways carrying vagal afferent information. It has been shown that visceral information from the nucleus of the solitary tract (NTS), the primary site of termination of general visceral afferents, projects ipsilaterally to the parabrachial nucleus (PB) and then contralaterally to the ventral basal thalamus where it is relayed to the insular cortex (IC) (6). More specifically, there is evidence that the general visceral afferents from the PB are relayed to the granular IC through the ventroposterior parvocellular nucleus of the thalamus (VPpc) (8).
Previously, electrophysiological investigations have been carried out
to identify the neurotransmitters used in the visceral sensory pathway.
An investigation by Jhamandas and Harris (13) showed
that both N-methyl- D-aspartate (NMDA)
and non-NMDA receptors mediate the excitatory inputs from the NTS to
the PB. However, it has been shown that only NMDA receptors mediate the
aortic baroreceptor reflex in the NTS (6). In a recent
study, the neurotransmitters mediating visceral input from the PB to
the VPpc were investigated. It was determined that the visceral
afferent sensory information through the PB is mediated by NMDA
receptors and that 2-adrenergic and GABA receptors
contribute to the tonic activity of ventral basal thalamic neurons
receiving visceral input (26).
This study was conducted to determine the neurotransmitters involved in the relay of visceral information in the ventrobasal thalamus to the cortex. Vagally evoked single and multiunit recordings were recorded in the granular IC. Antagonists to glutamate, acetylcholine, catecholamines, and GABA were pressure injected into the VPpc, and the effect on the evoked cortical response was observed.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Surgical preparation.
Thirty-three male Wistar rats (250-300 g) were anesthetized with a
combination of 3% -chloralose (150 mg/kg ip) and 40% urethane (0.4 g/kg ip) and were supplemented with 3% -chloralose (30 mg/kg iv) as
needed. Catheters were inserted into the right femoral artery for the
purpose of monitoring blood pressure and heart rate and into the right
femoral vein for the administration of drugs. Arterial blood pressure
was measured using a pressure transducer (Gould P23 ID) connected to a
Grass model 7E polygraph, and heart rate was determined from the pulse
pressure using a Grass model 7P 44C tachograph. An endotracheal tube
was inserted, and the animals were allowed to breathe room air. The
left vagus nerve, including the aortic depressor nerve, was located
through a midline cervical incision, isolated, and placed on stainless
steel electrodes fixed in place with dental impression material
(Perfourm, Miles Laboratories). The vagus nerve was crushed distal to
the electrode. The animal was placed in a stereotaxic frame (David
Kopf), and small burr holes were made in the parietal and temporal
bones for micropipette (thalamus) or microelectrode (IC) insertion. A
heating blanket connected to a temperature controller was used to
maintain body temperature at 37.0 ± 1°C throughout the experiment.
Vagal stimulation and insular recordings. Peristimulus-time histograms were compiled by the summation of 100 single pulses (2-ms duration) of vagal stimulation delivered at a rate of 0.8 Hz. This rate of stimulation did not elicit reflex changes in blood pressure or heart rate. The appropriate intensity of vagal stimulation was determined to be the stimulation intensity that caused an ~40-mmHg depressor response at 50 Hz.
Extracellular single and multiunit recordings of IC neurons were obtained using 3.0 M NaCl-filled glass recording microelectrodes. Extracellular neuronal activity was recorded in the IC in response to single-pulse vagal stimulation. The search routine comprised recording evoked neuronal activity from the upper region of the IC in response to vagal stimulation and then moving ventrally by 10 µm until a responsive site was found. In some rats, more than one track was explored. After testing a given neuron, the recording micropipette was moved ventrally to obtain further responsive sites. Signals were amplified, displayed on an oscilloscope, and fed into a window discriminator connected to a computer to monitor spontaneous frequency of firing and to compile peristimulus-time histograms in response to vagal stimulation. Before the death of the animal, an electrolytic lesion (3.5 µA, 0.5 Hz, 1-s duration, 15 min) was made in the last recording site in the IC to mark it.Microinjections.
Thalamic injections of antagonists or vehicle (10 mM PBS, pH 7.4) were
made using a glass micropipette (tip diameter 
20 µm). All
injections into the VPpc were 200 nl. Antagonists (Sigma, St. Louis,
MO) were dissolved in PBS at the following concentrations: 10 mM cobalt
(presynaptic blocker), 100 mM kynurenate (general excitatory amino acid
antagonist), 0.1 and 1.0 µM atropine (general muscarinic cholinergic
antagonist), 0.1 and 1.0 µM phentolamine (general -adrenergic
antagonist), and 0.1 and 1.0 µM picrotoxin (general GABA antagonist).
DL-2-Amino-5-phosphonopentanoic acid (AP-5; NMDA-specific
antagonist), L-glutamic acid diethylester (GDE;
non-NMDA-specific antagonist),
6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; non-NMDA-specific
antagonist), and
6-nitro-7-sulphamoylbenzo(f)quinoxaline-2,3-dione [NBQX;
DL--amino-3-hydroxy-5-methylisoxazole-propionic acid
(AMPA)-specific antagonist] were dissolved in PBS at the following
concentrations: 20 and 200 µM and 2 mM for CNQX and NBQX; 200 µM
and 2 mM for AP-5; and 200 µM for GDE (all obtained from Tocris
Neuramin in Essex, UK).
Data analysis. Analysis of data obtained from peristimulus-time histograms of cortical neuronal activity was performed using a computer program (IPEE, Yim Software). The program calculates the significant responses as activity occurring after the stimulus artifact in which five consecutive bins (2 ms each) are one standard deviation above or below the prestimulus baseline. Absolute response was determined by calculating the total number of spikes minus baseline and then multiplying this value by the response duration. For each neuronal recording, the data were normalized by representing the absolute response after antagonist injection as a percentage of the absolute response before antagonist injection. This was done to account for the variability in absolute neuronal activity both within and between the animals. A t-test was used to test significance of changes in responses before and after antagonist injections (P < 0.05). A total of 92 neurons in 33 rats was recorded in the experiment. Some neurons were tested with more than one drug.
Histology. At the end of each experiment, under deep anesthesia, the animals were perfused transcardially with 0.9% saline followed by 10% Formalin. The location of the micropipette and microelectrode tracks in the thalamus and IC were verified histologically in 50-µm-thick thionin-stained coronal sections.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Neuron characteristics. In this study, only excitatory neuronal responses to vagal stimulation were searched for and tested. Peristimulus-time histograms represent evoked cortical responses to 100 vagal stimuli summed over a period of 2 min. Vagal stimulation elicited an increase in cortical neuronal activity with an average latency of the response of 42 ± 2 ms and a range of 6-90 ms. The average duration of the responses was 46 ± 2 ms with a range of 8-146 ms.
PBS and cobalt injections.
Injections of PBS into the thalamus did not significantly change the
vagally evoked neuronal response in the IC (n = 45 neurons in 33 rats). Injection of cobalt (10 mM) into the VPpc resulted in an 87.1% attenuation (72.8-100%) of the cortical response to vagal stimulation (n = 6 neurons in 4 rats). The
vagally evoked response recovered after ~30 min. The spontaneous
baseline activity was not significantly altered. Examples of typical
peristimulus-time histograms and average responses for PBS and cobalt
are shown in Fig. 1.
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Excitatory amino acid antagonist injections.
Kynurenate (100 mM) injections into the VPpc decreased (65.3%; range
38.2-97.9%) the response of units in the IC to vagal stimulation
(n = 6 neurons in 5 rats; Fig.
2). A similar significant attenuation
(80.2%; range 65.8-100%) of the evoked response of neuronal activity in the IC was observed following the injection of the
non-NMDA antagonist GDE (200 µM, n = 7 neurons in 5 rats); however, neuronal activity was unaltered following the injection of the NMDA-specific antagonist AP-5 (200 µM, n = 6 neurons in 6 rats; 2 mM, n = 9 neurons in 3 rats) into
the VPpc (Fig. 2). In addition, the vagally evoked response in the
cortex was attenuated with the injection of the nonspecific non-NMDA
antagonist CNQX (20 µM, 29.2 ± 9.3%, n = 10 neurons in 3 rats; 200 µM, 30.86 ± 10.4%, n = 9 neurons in 5 rats; and 2 mM, 59.0 ± 7.6%, n = 11 neurons in 8 rats) and was also attenuated with the AMPA-specific antagonist NBQX (200 µM, 53.3 ± 7.8%, n = 8 neurons in 4 rats; 2 mM, 51.7 ± 2.8%, n = 8 neurons in 4 rats; Fig. 3). For the
higher dose of CNQX and NBQX, the inhibition range of the vagally
evoked response in the cortex was 29.0-84.4 and 38.6-60.3%,
respectively.
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Cholinergic antagonist injection.
Atropine, a muscarinic cholinergic antagonist, decreased the vagally
evoked response by 39.7 ± 2.1% at a concentration of 0.1 µM
(n = 4 neurons in 3 rats), but a higher concentration
of 1.0 µM (n = 8 neurons in 3 rats) had no
significant effect (Fig. 4). There were
no changes in baseline firing with either dose of atropine.
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Catecholamine and GABA antagonist injection.
Phentolamine and picrotoxin, a general -adrenergic and a
GABAA antagonist, respectively, had no effect on the
vagally evoked neuronal response at both 0.1 and 1.0 µM
concentrations (phentolamine: 0.1 µM, n = 5 neurons
in 3 rats; 1.0 µM, n = 5 neurons in 3 rats; picrotoxin: 0.1 µM, n = 11 neurons in 3 rats; 1.0 µM, n = 11 neurons in 3 rats; Fig.
5). No baseline changes were noted with
either antagonist.
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Recording and injection sites.
The recording sites in the IC are shown in Fig.
6. The vagally evoked neuronal responses
were within or near the granular IC. Nonresponsive neurons were not
included in this study. All effective injections of cobalt and
antagonists were within the VPpc (Fig.
7). Ineffective injection sites are also
shown in Fig. 7. Note that effective injection sites were the ones that
were only in the VPpc and not in the surrounding areas. There were no
apparent differences in the response of single or multiunit cortical
recordings within or between animals.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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These results show that the injection of cobalt in the VPpc attenuates the vagally evoked neuronal response in the IC. It is possible that this stimulation of the vagus may not stimulate all classes of vagal afferents. Thus there may be only certain types of vagal afferents that are being shown to be relayed through the thalamus. In addition, the classes of afferents that are not represented by the vagal stimulation may have alternate neurotransmitter receptors that mediate their relay through this region.
Anatomic tracing and physiological studies have indicated that visceral information enters the NTS and is relayed to the PB, where it is contralaterally sent to the VPpc and finally to the IC (6, 7). It is interesting to note, however, that the PB also has a direct projection to the IC (6, 7). The results in this study indicate that for the relay of visceral information, the VPpc is a mandatory relay site from the PB to the IC, because by blocking the synaptic output in the VPpc with cobalt, vagally evoked neuronal activity in the cortex was also blocked despite the direct projection from the PB to the IC. The direct projection from the PB to the IC may serve as a modulator or may not be involved at all in the relay of visceral afferent information to higher brain centers.
In this study, it is also reported that the injection of kynurenate and the specific non-NMDA receptor antagonists GDE, CNQX, and NBQX in the VPpc attenuate the vagally evoked neuronal response in the IC. Evidence that the antagonists were only affecting neurons restricted in the VPpc and not in areas surrounding the nucleus comes from the control injection sites. Only injections directly into the VPpc were effective at antagonizing the vagally evoked response in the IC. This dismisses the probability that the effects seen were due to the injected drugs spreading to other areas of the brain.
Excitatory amino acids, such as glutamate and aspartate, are well established as neurotransmitters in the central nervous system. There are at least four types of receptors characterized for these substances: NMDA receptor, the two non-NMDA receptors kainate and AMPA, and the metabotropic receptors (14). Cortical neuronal activity in response to vagal stimulation was completely attenuated following the administration of kynurenate in the VPpc, indicating that the relay of this visceral information requires an excitatory amino acid, most likely glutamate. Furthermore, the specific non-NMDA receptor antagonist GDE inhibited the vagally evoked cortical response, whereas the specific NMDA receptor antagonist AP-5 had no effect, indicating that the visceral information must be relayed via a non-NMDA receptor in the VPpc. The possible contribution of excitatory amino acids in afferent transmission to the thalamus has been investigated in vivo in the ventrobasal thalamus by Salt and Eaton (27). Their investigations demonstrated that both NMDA and non-NMDA receptors are involved in the transmission of natural somatosensory stimuli, although they appear to be differentially recruited in accordance with the duration of the sensory input. The thalamic response to short-duration (10-20 ms) or prolonged (>1 s) stimulation of hair vibrissa follicle sensory afferents is selectively attenuated by the antagonism of the non-NMDA receptor. In contrast, antagonism of NMDA receptors results in a selective inhibition of thalamic neuronal response to prolonged (>1 s) sensory stimulation only (27). In our investigation, the vagus was stimulated with low frequency (<1 Hz) for a long period of time (>2 min), and the evoked cortical response was also attenuated by the antagonism of the non-NMDA receptor in the thalamus.
In addition, another study showed that the descending pathway for visceral information is relayed by NMDA receptors in the lateral hypothalamus (5) and by non-NMDA receptors in the ventrolateral medulla (4). Perhaps the excitatory amino acid receptor type reflects the type of integration of visceral information at each relay nucleus. Presumably, at the resting membrane potential, NMDA receptor channels do not open unless they are first depolarized by other means (17). Often, the non-NMDA receptor provides the initial depolarization adequate to allow for the NMDA receptor channel to open (17). In the PB, however, the depolarization needed to open the NMDA channel may occur by other means, possibly the opening of channels linked to other neurotransmitters, including neuropeptides. This involvement of other neurotransmitters could allow for integration of other inputs and could essentially modulate the transmission of visceral information. It may be significant that the PB appears to be the main gateway for receiving visceral information, from the NTS and the spinal cord, and then distributes this information to many regions of the forebrain as well as receiving extensive supraspinal input from these areas (7). In the VPpc, however, the non-NMDA receptor may be primarily involved in relaying visceral sensory information to the cortex without allowing for extensive modulation of the signal.
In our study, we also attempted to determine which specific non-NMDA receptor, kainate or AMPA, was relaying the visceral afferent information to the IC. The vagally evoked response in the cortex was attenuated with both CNQX and NBQX. Previous experiments showed that both CNQX and NBQX have a higher affinity for the AMPA receptor over the kainate receptor in vivo, although CNQX is more potent than NBQX at antagonizing the kainate receptor (11, 28). Hence, for the purpose of this study, NBQX can be considered to be AMPA specific and CNQX to be kainate specific when comparing the two antagonists. Because CNQX was effective at attenuating the cortical response at the 20 µM concentration, this may suggest that visceral information may be relayed through a kainate receptor in the VPpc. However, it is likely that both kainate and AMPA contribute to transmission, because at a very high concentration of CNQX (2 mM), the evoked response is antagonized by a further 25%.
In this study, we also attempted to examine the role of acetylcholine in the transmission of visceral information in the VPpc. Injection of the general muscarinic cholinergic antagonist atropine in the VPpc only decreased the vagally evoked cortical response when administered at a low dose (0.1 µM), whereas at a higher dose (1.0 µM), it had no effect. Cholinergic neurons appear to play a part in areas involved in central autonomic regulation, including the ventrolateral medulla, dorsal vagal nucleus, nucleus ambiguus, and NTS (24). Cholinergic afferents in the thalamus arise from the pontomesencephalic reticular formation (21). The PB innervates several thalamic nuclei in the rat, and there are numerous cholinergic neurons scattered in and around the PB (10). It is possible that these cholinergic neurons projecting to the VPpc modulate visceral neuronal excitability via M currents whose presence has been shown in the thalamus (3, 18, 19). The administration of atropine, a muscarinic cholinergic antagonist, decreased the vagally evoked response by ~40% at a concentration of 0.1 µM, but at a higher concentration of 1.0 µM, it had no effect. This differential response to increasing atropine concentrations may be explained by the presence of more than one muscarinic receptor in the thalamus.
Five muscarinic receptor genes (m1-m5) that encode distinct muscarinic cholinergic receptors have been cloned (2, 15, 20, 25). The m1, m3, and m5 subtypes are thought to mediate primarily excitatory synaptic transmissions, whereas the m2 and m4 mediate primarily inhibitory synaptic transmission (20). The m3 and m5 subtypes are abundant in the thalamus, and there may be more m3 and m5 excitatory receptor subtypes than m2 subtypes in the VPpc (30). A low (0.1 µM) concentration of receptor antagonist would elicit an inhibition of neuronal excitation, whereas with a higher (1.0 µM) concentration, m2 receptors would also be attenuated, canceling out any response. To test this hypothesis, additional experiments are required using muscarinic cholinergic receptor antagonists specific for the three subtypes found in the ventrobasal thalamus.
-Adrenergic antagonist and a GABAA antagonist injected
into the VPpc had no significant effect on the vagally evoked response in the IC. These two neurotransmitter systems were investigated because
both of these are found in the thalamus.
GABA is widely distributed in the nervous system of vertebrates as well as invertebrates. The inhibitory transmitter GABA and its synthesizing enzyme have been identified within terminals in the ventrobasal thalamus as well as other thalamic nuclei (12, 22, 23). Histochemical and biochemical studies have shown that catecholamines are also present in almost all brain areas. Catecholamine-containing neurons in the brain have widespread efferent trajectories, abundant axon collaterals, and a particularly large number of nerve terminals (29).
From our results, it appears that these two neurotransmitter systems are not involved in the relay of visceral information to the IC. The possibility that the lack of effect on the relay of visceral information in the VPpc reflects a low dose of phentolamine or picrotoxin can be ruled out based on the following. First, the 0.1-µM dose of each antagonist was used to report the effects of the catecholaminergic and GABAergic systems for the relay of visceral information in the PB (26). Second, in this study, a precautionary 10-fold dose of inhibitor (1.0 µM) was also used, with no effect.
Perspectives
This study indicates that afferent visceral information is relayed through the VPpc to the IC via a non-NMDA excitatory amino acid receptor, most likely the kainate receptor. In contrast, visceral sensory information is relayed by an NMDA receptor in the PB (26) and in the lateral hypothalamus (5). This difference in excitatory amino acid receptor type may reflect the integration of visceral information at each relay nucleus, with the VPpc serving primarily as a necessary relay station of information with few modulatory effects.The muscarinic cholinergic receptors seem to be involved in modulating the visceral neuronal excitability in the VPpc through a mixture of inhibitory (m2) and excitatory (m3 and m5) receptor subtypes.
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ACKNOWLEDGEMENTS |
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This study was supported by the Heart and Stroke Foundation of Ontario, Canada. D. F. Cechetto is a Career Investigator of the Heart and Stroke Foundation of Canada. F. Barnabi is an Ontario Graduate Scholar.
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FOOTNOTES |
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Address for reprint requests and other correspondence: D. F. Cechetto, Univ. of Western Ontario, Dept. of Anatomy & Cell Biology, Medical Science Bldg., Rm. M 438, London, ON N6A 5C1, Canada (E-mail: cechetto{at}uwo.ca).
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.
Received 6 September 2000; accepted in final form 24 July 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Time of
application of 100 single pulses (2 ms) of electrical stimulation to
the cervical vagus nerve. B: bar graphs showing the average
cortical neuronal response before and after injection of cobalt
(n = 6 neurons in 4 rats) and PBS (n = 45 neurons in 33 rats) into the VPpc. *Significant change
(P < 0.05).
, More than 1 neuron in each rat. There was a total of 92 neurons recorded in 33 rats. AI, agranular insular cortex; Cc, corpus callosum; Cpu, caudate
putamen; DI, dysgranular insular cortex; LV, lateral ventricle; and
Pir, piriform cortex.
,
injection sites that caused no change in evoked cortical activity. For
atropine injections,