Medulla Of Cat Research Articles

Renal alterations in cats (Felis catus) housed in shelters and affected by systemic AA-amyloidosis: Clinicopathological data, histopathology, and ultrastructural features.

AA-amyloidosis is frequent in shelter cats, and chronic kidney disease is the foremost cause of death. The aims were to describe kidney laboratory and microscopic findings in shelter cats with AA-amyloidosis. Cats were included if kidney specimens were collected post-mortem and laboratory data were available within 6 months before death. Renal lesions were evaluated with optical and electron microscopy. Mass spectrometry was used to characterize amyloid. Nine domestic short-hair cats were included; 4 females and 5 males with a median age of 8 years (range = 2-13). All cats had blood analyses and urinalyses available. Serum creatinine concentrations were increased in 6 cats and symmetric dimethylarginine was increased in all of the cats. All of the cats had proteinuria. Eight of 9 cats had amyloid in the medulla, and 9 had amyloid in the cortex (glomeruli). All cats had amyloid in the interstitium. Six cats had concurrent interstitial nephritis and 1 had membranoproliferative glomerulonephritis. All cats had extrarenal amyloid deposits. Amyloid was AA in each case. In conclusion, renal deposition of amyloid occurs in both cortex and medulla in shelter cats and is associated with azotemia and proteinuria. Renal involvement of systemic AA-amyloidosis should be considered in shelter cats with chronic kidney disease. The cat represents a natural model of renal AA-amyloidosis.

Responses of neurons in the rostral ventrolateral medulla of conscious cats to anticipated and passive movements.

The vestibular system contributes to regulating sympathetic nerve activity and blood pressure. Initial studies in decerebrate animals showed that neurons in the rostral ventrolateral medulla (RVLM) respond to small-amplitude (<10°) rotations of the body, as in other brain areas that process vestibular signals, although such movements do not affect blood distribution in the body. However, a subsequent experiment in conscious animals showed that few RVLM neurons respond to small-amplitude movements. This study tested the hypothesis that RVLM neurons in conscious animals respond to signals from the vestibular otolith organs elicited by large-amplitude static tilts. The activity of approximately one-third of RVLM neurons whose firing rate was related to the cardiac cycle, and thus likely received baroreceptor inputs, was modulated by vestibular inputs elicited by 40° head-up tilts in conscious cats, but not during 10° sinusoidal rotations in the pitch plane that affected the activity of neurons in brain regions providing inputs to the RVLM. These data suggest the existence of brain circuitry that suppresses vestibular influences on the activity of RVLM neurons and the sympathetic nervous system unless these inputs are physiologically warranted. We also determined that RVLM neurons failed to respond to a light cue signaling the movement, suggesting that feedforward cardiovascular responses do not occur before passive movements that require cardiovascular adjustments.

MicroRNA expression profiling of cat and dog kidneys

MicroRNAs (miRNAs) play a role in the pathogenesis of certain diseases and may serve as biomarkers. Here, we present the first analysis of miRNA expression in the kidneys of healthy cats and dogs. Kidneys were divided into renal cortex (CO) and medulla (MD), and RNA sequence analysis was performed using the mouse genome as a reference. A total of 277, 276, 295, and 297 miRNAs were detected in cat CO, cat MD, dog CO, and dog MD, respectively. By comparing the expression ratio of CO to MD, we identified highly expressed miRNAs in each tissue as follows: 41 miRNAs including miR-192-5p in cat CO; 45 miRNAs including miR-323-3p in dog CO; 78 miRNAs including miR-20a-5p in cat MD; and 11 miRNAs including miR-132-5p in dog MD. Further, the target mRNAs of these miRNAs were identified. These data provide veterinary medicine critical information regarding renal miRNA expression.

Rhythmic activity of neurons in the rostral ventrolateral medulla of conscious cats: effect of removal of vestibular inputs.

Although it is well established that bulbospinal neurons located in the rostral ventrolateral medulla (RVLM) play a pivotal role in regulating sympathetic nerve activity and blood pressure, virtually all neurophysiological studies of this region have been conducted in anesthetized or decerebrate animals. In the present study, we used time- and frequency-domain analyses to characterize the naturally occurring discharges of RVLM neurons in conscious cats. Specifically, we compared their activity to fluctuations in carotid artery blood flow to identify neurons with cardiac-related (CR) activity; we then considered whether neurons with CR activity also had a higher-frequency rhythmic firing pattern. In addition, we ascertained whether the surgical removal of vestibular inputs altered the rhythmic discharge properties of RVLM neurons. Less than 10% of RVLM neurons expressed CR activity, although the likelihood of observing a neuron with CR activity in the RVLM varied between recording sessions, even when tracking occurred in a very limited area and was higher after vestibular inputs were surgically removed. Either a 10-Hz or a 20- to 30-Hz rhythmic discharge pattern coexisted with the CR discharges in some of the RVLM neurons. Additionally, the firing rate of RVLM neurons, including those with CR activity, decreased after vestibular lesions. These findings raise the prospect that RVLM neurons may or may not express rhythmic firing patterns at a particular time due to a variety of influences, including descending projections from higher brain centers and sensory inputs, such as those from the vestibular system.

Cardiac‐related and other rhythmic activity of neurons in the rostral ventrolateral medulla (RVLM) of conscious cats: effects of vestibular lesions

Recordings were made from neurons in the RVLM in conscious cats before and after removal of vestibular input through a bilateral vestibular neurectomy. Blood flow through the carotid artery was also measured so we could determine whether a unit had cardiac-related activity (CRA). Only a small fraction of RVLM neurons exhibited CRA, but the fraction increased from 4% to 9% following vestibular lesions. CRA neurons were often clustered: multiunit recordings revealed that when a CRA unit was present, another was in the same field approximately 50% of the time. In 32% of the instances where pairs of RVLM neurons with CRA were examined at the same location, short time scale interactions between their discharges were demonstrated. Frequency-domain analysis revealed that a small fraction of RVLM neurons with CRA displayed higher-frequency components (10–30 Hz) as well, most often after vestibular lesion. These data suggest that rhythmic firing of RVLM neurons including CRA may be ‘state dependent,’ and is masked until the animal is alerted or agitated.

Activity of Neurons in the Rostral Ventrolateral Medulla (RVLM) of Conscious Cats

Although numerous studies in decerebrate or anesthetized animals of several species have considered the activity of neurons in the RVLM, to date no neurophysiological studies of this region have been conducted in conscious animals. The goal of the present study was to determine the firing patterns of RVLM neurons in conscious cats, and to compare the neuronal activity in this preparation to that previously documented in anesthetized animals. Recovery surgery was performed to implant a recording chamber on the caudal aspect of the skull, as well as a telemetric blood pressure recording device (Data Sciences Intl.) and probes to measure blood flow from the carotid artery (Transonic Systems). Blood pressure and blood flow measurements were used to establish whether units displayed cardiac‐related activity. Few (&lt;25%) RVLM neurons exhibited robust cardiac‐related firing, but the mean coherence value relating unit activity to the arterial pulse (0.45±0.07) was higher than in anesthetized animals. Moreover, the mean spontaneous firing rate of RVLM neurons with cardiac‐related activity was over 6 times higher in awake cats than in anesthetized animals. Many RVLM neurons that lacked cardiac‐related firing displayed multifaceted patterns of rhythmic activity. These data suggest that the activity of RVLM neurons is highly complex in awake felines.

Are the Thalamic Projections of Nucleus Z of the Medulla Oblongata Reorganized after Partial Deafferentation of the Ventrolateral Nucleus of the Thalamus?

The possible plastic reorganization of projections from the somatosensory relay nucleus Z of the cat medulla oblongata to the partially deafferented ventrolateral nucleus of the thalamus was studied by retrograde labeling with horseradish peroxidase. Partial deafferentation of the ventrolateral nucleus of the thalamus was produced by prior (three months) electrolytic destruction of the contralateral cerebellar interpositus nucleus or the lateral vestibular nucleus of Deiters. The results demonstrated local intense labeling of a group of neurons in nucleus Z, and there was a small group of labeled neurons in cell group x of the vestibular complex projecting to the ventrolateral nucleus of the thalamus, where these projections were found to overlap with those from the cerebellar nuclei. After lesioning of the cerebellar interpositus nucleus or lateral vestibular nucleus of Deiters, ipsilateral projections in the monosynaptic circuit consisting of nucleus Z and the ventrolateral nucleus of the thalamus did not form. The absence of reorganization of projections from nucleus Z to the ventrolateral nucleus of the thalamus in terms of the formation of ipsilateral projections may be associated with its being part of the somatosensory relay nucleus, which is specialized for relaying and transmitting information strictly of the specific proprioceptive modality.

Regulation of common carotid arterial blood flow by nitrergic neurons in the medulla of cats

Glutamate stimulation of the dorsal facial area, an area located dorsal to the facial nucleus, increases common carotid arterial blood flow. Nitrergic neurons are important in cardiovascular regulatory areas. We investigated whether the nitrergic neurons might be present and play a role in the dorsal facial area to regulate the arterial blood flow. Injections of l-arginine (an NO precursor) and sodium nitroprusside (an NO donor) into the area caused dose-dependent increases in the arterial blood flow. Injection of N G-nitro-arginine methyl ester ( l-NAME, an NO synthase inhibitor) or methylene blue (a guanylate cyclase inhibitor) decreased the arterial blood flow. Nitrergic neurons and fibers were found in the dorsal facial area by histochemical staining of nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase, a maker of NO synthase. In conclusion, nitrergic neurons are present in the dorsal facial area and appear to release NO tonically in stimulating the area to cause increase in common carotid arterial blood flow.

Regulation of the common carotid arterial blood flow by nicotinic receptors in the medulla of cats

Actions of glutamate and serotonin on their respective receptors in the dorsal facial area (DFA) of the medulla are known to regulate common carotid arterial (CCA) blood flow in cats. Less is known about acetylcholine action on its nicotinic receptor (nAChR) subtypes in the DFA for regulation of CCA blood flow and this aspect was investigated. Nicotinic and muscarinic agonists and antagonists were microinjected into the DFA through a three-barrel tubing in anesthetized cats. CCA blood flow was dose-dependently increased by nicotine (a non-selective nAChR agonist) and choline (a selective alpha7-nAChR agonist). These effects of nicotine were attenuated by alpha-bungarotoxin (an alpha7-nAChR antagonist), methyllycaconitine (an alpha7-nAChR antagonist), mecamylamine (a relatively selective alpha3beta4-nAChR antagonist) and dihydro-beta-erythroidine (a relatively selective alpha4beta2-nAChR antagonist). The choline-induced flow increase was attenuated by alpha-bungarotoxin and mecamylamine, but not by dihydro-beta-erythroidine. Muscarinic agonists (muscarine and methacholine) and antagonist (atropine) affected neither the basal nor the nicotine-induced increase in the CCA blood flow. Functional alpha7, alpha4beta2, and alpha3beta4 subunits of the nAChR appear to be present on the DFA neurons. Activations of these receptors increase the CCA blood flow. The present findings do not preclude the presence of other nAChRs subunits. Muscarinic receptors, if any, on the DFA are not involved in regulation of the CCA blood flow. Various subtypes of nAChRs in the DFA may mediate regulation of the CCA and cerebral blood flows.

Role of glutamate in a visceral sympathoexcitatory reflex in rostral ventrolateral medulla of cats

The rostral ventrolateral medulla (rVLM) is involved in processing visceral sympathetic reflexes. However, there is little information on specific neurotransmitters in this brain stem region involved in this reflex. The present study investigated the importance of glutamate and glutamatergic receptors in the rVLM during gallbladder stimulation with bradykinin (BK), because glutamate is thought to function as an excitatory neurotransmitter in this region. Stimulation of visceral afferents activated glutamatergic neurons in the rVLM, as noted by double-labeling with c-Fos and the cellular vesicular glutamate transporter 3 (VGLUT3). Visceral reflex activation significantly increased arterial blood pressure as well as extracellular glutamate concentrations in the rVLM as determined by microdialysis. Barodenervation did not alter the release of glutamate in the rVLM evoked by visceral reflex stimulation. Iontophoresis of glutamate into the rVLM enhanced the activity of sympathetic premotor cardiovascular rVLM neurons. Also, the responses of these neurons to visceral afferent stimulation with BK were attenuated significantly (70%) by blockade of glutamatergic receptors with kynurenic acid. Microinjection of either an N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonopentanate (25 mM, 30 nl) or an dl-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (2 mM, 30 nl) into the rVLM significantly attenuated the visceral sympathoexcitatory reflex responses. These results suggest that glutamate in the rVLM serves as an excitatory neurotransmitter through a baroreflex-independent mechanism and that both NMDA and AMPA receptors mediate the visceral sympathoexcitatory reflex responses.

Responses of neurons containing VGLUT3/nNOS-cGMP in the rVLM to cardiac stimulation

Responses of glutamatergic neurons in the rostral ventrolateral medulla to stimulation of cardiac sympathetic afferents have not been defined. Nitric oxide influences neural function of glutamate. We evaluated the relationship between vesicular glutamate transporter 3, c-Fos and neuronal nitric oxide synthase/soluble guanylyl cyclase in the rostral ventrolateral medulla following cardiac stimulation. In anesthetized cats with barodenervation and vagotomy, epicardial application of bradykinin, but not its vehicle, caused pressor responses. More vesicular glutamate transporter 3-containing neurons colocalized with c-Fos or c-Fos and neuronal nitric oxide synthase in the rostral ventrolateral medulla in bradykinin-treated cats (n = 6; P < 0.05) than in control animals (n = 4). Colocalization of neuronal nitric oxide synthase, soluble guanylyl cyclase and c-Fos or vesicular glutamate transporter 3 was noted following bradykinin stimulation. Findings indicate activation of rostral ventrolateral medulla glutamatergic neurons by cardiac stimulation, which may be influenced by nitric oxide via cGMP.

Electroacupuncture induces c-Fos expression in the rostral ventrolateral medulla and periaqueductal gray in cats: relation to opioid containing neurons

Our previous studies have shown that electroacupuncture (EA) at the Neiguan–Jianshi (P5–P6) acupoints inhibits sympathetic outflow and attenuates excitatory visceral cardiovascular reflexes through enkephalin- or β-endorphin-related opioid receptors in the rostral ventrolateral medulla (rVLM). It is not known whether EA at these acupoints activates neurons containing enkephalin or β-endorphin in the rVLM as well as in the periaqueductal gray (PAG) that are involved in EA-mediated central neural regulation of sympathetic activity. The present study evaluated activated neurons in the rVLM and PAG by detecting c-Fos immunoreactivity, and identified the relationship between c-Fos nuclei and neuronal structures containing enkephalin or β-endorphin in these regions. To enhance the detection of cell bodies containing enkephalin or β-endorphin, colchicine (90–100 μg/kg) was injected into the subarachnoid space in anesthetized cats 28–30 h prior to EA or the sham-operated control for EA. Following bilateral barodenervation and cervical vagotomy, EA (1–4 mA, 2 Hz, 0.5 ms) was performed at the P5–P6 acupoints (overlying median nerve; n=7) for 30 min. Identical procedures, with the exception of electrical stimulation, were carried out in five control animals. EA decreased blood pressure (BP) in four of seven cats (5–15 mm Hg) while the sham procedure for EA produced no responses. Perikarya containing enkephalin were found in the rVLM and rarely in the PAG, while no cell bodies labeled with β-endorphin were identified in either region. Compared to animals in the control group, more c-Fos immunoreactivity, located principally in close proximity to fibers containing enkephalin or β-endorphin, was observed in the rVLM and ventrolateral PAG (vlPAG) in EA-treated cats. Moreover, neurons double-labeled with c-Fos and enkephalin in the rVLM were significantly increased in cats following EA stimulation ( P<0.05). These data indicate that EA at the P5–P6 acupoints activates neurons in the rVLM and vlPAG. These activated neurons contain enkephalin in the rVLM, and most likely interact with nerve fibers containing enkephalin or β-endorphin in both the rVLM and vlPAG. The results from this study provide the first anatomical evidence showing that EA at the P5–P6 acupoints has the potential to influence neuronal structures (perikarya, axons and/or dendrites) containing enkephalin or β-endorphin in specific regions of the brain stem. These neurons likely form the substrate for EA's influence on sympathoexcitatory cardiovascular reflexes.

Dexamethasone has a central antiemetic mechanism in decerebrated cats.

Dexamethasone is an effective antiemetic drug, but its mechanism of action is unclear. We designed this study to investigate the direct antiemetic action of dexamethasone in the medulla of cats. By using an oscillographic vomiting model, decerebrated cats received microinjections of dexamethasone 100 nL (1 microg, n = 7; 0.1 microg, n = 7) into the bilateral nuclei tractus solitarii, which led to a significant prolongation of the latency (1 microg, 6.4 +/- 1.1 min versus 28.2 +/- 4.9 min, P < 0.05; 0.1 microg, 6.7 +/- 1.1 min versus 27.1 +/- 5.0 min, P < 0.05) of the first emetic episode and significantly decreased the frequency of emetic episodes (1 microg, 2.7 +/- 0.8 versus 0.1 +/- 0.4, P < 0.05; 0.1 microg, 2.9 +/- 0.9 versus 0.3 +/- 0.5, P < 0.05) induced by xylazine. Pretreatment with mifepristone, a glucocorticoid receptor antagonist, blocked the antiemetic effect of dexamethasone in the bilateral nuclei tractus solitarii. However, microinjection of dexamethasone into the unilateral nucleus tractus solitarius alone did not alter the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. Local application of dexamethasone into the area postrema had no effect on the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. These results suggest that dexamethasone exerts its central antiemetic action through an activation of the glucocorticoid receptors in the bilateral nuclei tractus solitarii in the medulla.

Involvement of N-methyl- d-aspartate receptors in post-hypoxic depression of the dorsomedial medulla in cats

Pressor and sympathoexcitatory responses induced by microinjection of glutamate (Glu) into the dorsomedial medulla (DM) were depressed after hypoxia in anesthetized cats. This study was undertaken to investigate which Glu receptor subtypes would be involved in the post-hypoxic depression. Hypoxia was induced by inhalation of a 5% O 2 and 95% N 2 gas mixture. The pressor and sympathoexcitatory responses to microinjections of N-methyl- d-aspartic acid (NMDA) or α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) into the DM were significantly depressed after hypoxia, suggesting the involvement of both NMDA and AMPA receptors. However, pretreatment with kynurenic acid or dl-2-amino-5-phosphonopentanoic acid, but not 6-cyano-7-nitroquinoxaline-2,3-dione, 5 min before hypoxia could effectively prevent the post-hypoxic depression of Glu-induced responses. These results further suggest that post-hypoxic depression of Glu-induced responses in the DM was predominately mediated by NMDA receptors.

Central sympathetic chemosensitivity and Kir1 potassium channels in the cat

The possible involvement of potassium channels in central chemosensitivity, with special reference to the Kir1.1 potassium channel, was investigated by studying the CO 2 response of presympathetic neurons in the rostroventrolateral medulla (RVLM) in the absence or presence of various K + channel inhibitors. Synaptic input to RVLM neurons was blocked by local injection of ω-agatoxin and ω-conotoxin. Activity of RVLM neurons was measured by recording the electrical activity in preganglionic (WR-T 3) or postganglionic (renal) sympathetic nerves after perfusion of the lower brainstem via the left vertebral artery with CO 2-enriched saline solution. Unspecific K + channel blockade by BaCl 2 reduced the excitatory response of sympathetic activity after CO 2-perfusion to 56% of control. A quantitatively similar inhibition of the central CO 2 response was obtained after administration of 9-fluorenylmethylchloroformate (FMOC-Cl) which eliminates pH sensitivity of Kir1 and Kir4.1. Furthermore, two structurally different Kir1 inhibiting toxins, tertiapin and Lq2, also reduced the central CO 2 response to ∼50% of control. In contrast, charybdotoxin (CTX) had no effect on the CO 2 response. Using RT-PCR the expression of mRNA homologous to rat Kir1 mRNA was identified in the cat medulla oblongata. These data suggest that a modulation of potassium channel activity possibly via Kir1 may contribute to central chemosensitivity.

Synergism between cocaine and atropine at the caudal ventrolateral medulla of cats

We have previously reported that the anticholinergic properties of cocaine may be important in cocaine induced apneusis. We have studied the effects of the cholinergic muscarinic antagonist atropine (ATR) on cocaine induced apneusis at the caudal chemosensitive areas of the ventrolateral medulla oblongata (CVLM). Experiments were performed in urethane anesthetized and tracheotomized cats with the CVLM surgically exposed. Topical application of ATR (44 mM ) to the CVLM produced significant decrements in minute ventilation (V E ) and mean arterial blood pressure (MABP) (P<0.05) but the effects on tidal volume (V T ), respiratory frequency (f) and heart rate (HR) were not significant. Administration of cocaine (37 mM) to ATR pretreated animals increased the incidence of cocaine induced respiratory arrest to more than twofold greater than when cocaine was administered in the absence of pretreatment. The ATR pretreated animals that did not experience inspiratory arrest after cocaine were shown to exhibit significant decrements in f and V E as a consequence of prolonged inspiratory pauses. The reduction in MABP after cocaine in ATR pretreated animals was also significant. These results suggest that ATR enhances the central respiratory toxicity of cocaine by acting synergistically at CVLM chemosensitive sites.

The nNOS/cGMP signal transducing system is involved in the cardiovascular responses induced by activation of NMDA receptors in the rostral ventrolateral medulla of cats

Nitric oxide (NO) is synthesized from l-arginine by NO synthase (NOS). NO stimulates the soluble form of guanylyl cyclase (sGC) and induces accumulation of cyclic guanosine monophosphate (cGMP). The purpose of this study was to examine whether the cardiovascular responses induced by N-methyl- d-aspartate (NMDA) in the rostral ventrolateral medulla (RVLM) depend on the actions of NOS and sGC. In anesthetized cats, the extracellular NO level was measured by in vivo voltammetry using a nafion/porphyrine/o-phenylenediamine-coated carbon-fiber electrode. Microinjection of NMDA into the RVLM produced hypertension and bradycardia associated with NO formation. These NMDA-induced responses were attenuated by prior injections of 7-nitroindazole, a neuronal NO synthase (nNOS) inhibitor, and 1H- [1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a sGC inhibitor. These findings suggest that NO is involved in the NMDA-induced cardiovascular responses in the RVLM.

Activation of noradrenergic mechanism attenuates glutamate-induced vasopressor responses in the pons and medulla of cats in vivo

1. Using anesthetized cats, the authors examined the noradrenergic modulation of the glutamate induced pressor and depressor responses in various brainstem areas, including pontine gigantocellular tegmental field (FTG), dorsomedial medulla (DM), rostral ventrolateral medulla (RVLM), and caudal ventrolateral medulla (CVLM). 2. Unilateral microinjection of L-glutamate (Glu, 3 nmol in 30 nL saline) into FTG, DM and RVLM produced an increased in systemic arterial presure (SAP) and a decrease in heart rate (HR), while into CVLM produced decreases of SAP and HR. 3. Application of norepinephrine (NE) into the pressor areas (005 to 5 nmol) did not alter the resting SAP and HR, but significantly attenauted the Glu-induced pressor response with an order of potency: FTG > DM > RVLM. In the depressor CVLM, NE alone produced a dose-dependent decrease of resting SAP and HR, but did not affect the Glu-induced depressor responses. 4. The involvement of different adrenoceptor subtypes was further investigated by application of selective adrenoceptor agonists including phenylephrine (α1), clonidine (α2), and isoproterenol (β). Responses to these agonists are similar to those elicited by NE, except that only α-adrenoceptor agonists could antagonize the Glu-induced pressor responses of the RVLM. 5. Our observations indicate that NE not only inhibits the pressor mechanisms in various brainstem areas but also elicits a direct depressor response in CVLM. These findings also suggest that NE acts more likely a neurotransmitter, rather than a modulator, in the CVLM.

Correlation of vasomotor- and respiratory-controlling mechanisms around the caudal ventrolateral medulla in cats

We examined the involvement of caudal ventrolateral medulla (CVLM) in respiratory control. Microinjection of glutamate (Glu) into CVLM decreased systemic arterial blood pressure (SAP) and altered phrenic nerve activities (PNA). Among 143 depressor sites, 55% (78/143) increased respiratory frequency (Rf), while 72% altered PNA amplitude (36% increased and 36% decreased). A small but significant positive correlation was observed between the magnitudes of depressor responses and inhibition of PNA amplitude (r=0.1718, n=143), indicating a substantial cross-talk between depressor and PNA inhibitory neurons. Furthermore, microinjections of acetylcholine (ACh) mimicked the Glu-induced depressor responses. However, ACh did not alter Rf, but still reduced PNA amplitude. Our findings suggest that Rf-regulating and depressor neurons are two separate neuronal populations, coexisting in CVLM. The PNA inhibitory and depressor neurons, in contrast, could have stronger correlation.

Dorsal facial area of cat medulla; 5-HT 2 action on glutamate release in regulating common carotid blood flow

Serotonin (5-HT) may inhibit glutamate release in the dorsal facial area (DFA) of the medulla and decrease common carotid arterial (CCA) blood flow. We attempted to clarify which subtype(s) of 5-HT receptor was involved. A microdialysis probe was inserted in DFA. The concentration of glutamate in dialysates were determined by chromatography. Glutamate concentration was dose-dependently decreased by perfusion of 5-HT or DOI, a 5-HT 2 agonist, but not by 5-CT, a 5-HT 1 agonist. The 5-HT-induced decrease in glutamate was reversed by co-perfusion of ketanserin, a 5-HT 2 antagonist, but not by propranolol, a 5-HT 1 antagonist. CCA blood flow was decreased when 5-HT or DOI was perfused, and was reversed by co-perfusing ketanserin. In conclusion, 5-HT may inhibit glutamate release via 5-HT 2 receptor in DFA, resulting in the reduction of CCA blood flow.