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D F Cechetto

Publications and source records attributed to D F Cechetto.

At least 55 records · Page 3Linked to original sources

Effect of age on autonomic and cardiac responses in a rat stroke model.

The cardiovascular system and its responses change with increasing age. This has seldom been considered in experimental models of stroke, although most strokes occur in the elderly. We studied 57 male Wistar rats in three age groups: 47 to 70 days old (juvenile), 110 to 152 days old (young adult), and 186 to 245 days old (mature adult), each group being subdivided into experimental and sham operation groups. All rats underwent occlusion or sham occlusion of the left middle cerebral artery and monitoring of the mean arterial blood pressure, heart rate, sympathetic nerve activity, plasma catecholamine levels, and electrocardiogram. Eight of the 12 rats in the oldest group died within 6 hours of the middle cerebral artery occlusion; of these, the youngest was 186 days old. The mature adult rats that died before completion of the experiment showed the highest level of sympathetic nerve activity and the only significant increase in the QT interval of the electrocardiogram. Following middle cerebral artery occlusion, sympathetic nerve activity increased in the young adult rats but most strikingly in the mature adult rats that died before the end of the 6-hour experiments. Plasma norepinephrine levels were significantly elevated at 4 and 6 hours after middle cerebral artery occlusion in the oldest group and only at 6 hours in the juvenile rats. The results of this study are consistent with impaired sympathetic and cardiovascular regulation in the mature adult rat. High sympathetic activity may represent one mechanism leading to fatal cardiac arrhythmias. Age-related impairment of sympathetic regulation may contribute to the higher mortality seen among elderly patients with stroke.

Aging↗

Asymmetry of sympathetic consequences of experimental stroke.

Asymmetries of sympathetic regulation at the level of the inferior cervical ganglia have long been recognized. Lateralization of autonomic representation may also occur in the brain, since inactivation of the left and right hemispheres by intracarotid amobarbital produces an increase and decrease in heart rate, respectively. However, this conclusion has remained tentative, since the differential effect of lateralized brain lesions on sympathetic activity has not been studied systematically. Forty-eight urethan-anesthetized Wistar rats were divided into three groups: a group given left middle cerebral artery occlusion, and a group given sham operation. Heart rate, mean arterial blood pressure, renal sympathetic nerve discharge, and electrocardiogram were monitored throughout the 4-hour experiments. Plasma epinephrine and norepinephrine levels were measured at baseline and 1 and 4 hours after occlusion or sham occlusion. The mean arterial pressure decreased in the group given sham operation and to lesser extent in the group given left middle cerebral artery occlusion. By contrast, mean arterial pressure did not fall in the group given right middle cerebral artery occlusion and at 4 hours was significantly higher than control values in the sham-occluded rats. Renal sympathetic nerve discharge was decreased in the sham-occluded group, increased significantly from 20 minutes to 2 hours in the group given left middle cerebral artery occlusion, and increased from about 20 minutes to the end of the experiment in the group given right middle cerebral artery occlusion. The plasma norepinephrine level was significantly elevated at 1 hour (93%) and 4 hours (44%) only in the group given right middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Hypothalamic and cortical sympathetic responses relay in the medulla of the rat.

Previously, investigations have indicated that the efferent pathway for sympathetic responses originating in the insular cortex (IC) must initially synapse in the lateral hypothalamic area (LHA). The LHA projects to both the ventrolateral medulla (VLM) and directly to the thoracic spinal cord. To determine the role of the VLM in mediating sympathetic responses from the IC and the LHA, in alpha-chloralose-anesthetized rats, renal nerve responses were recorded following electrical stimulation of these two forebrain sites before and after bilateral injection (300 nl) of cobalt (a synaptic blocking agent) into the VLM. The results demonstrated that a complete block of the increase in sympathetic nerve activity following stimulation of the IC or the LHA could be obtained with cobalt injections into the VLM. The most effective injection sites were located in the rostral ventrolateral medulla at the rostrocaudal middle and posterior regions of the C1 group of neurons. Chemical stimulation with DL-homocysteic acid, in the LHA, to activate cell bodies only evoked a decrease in arterial blood pressure and sympathetic nerve activity. These responses were also blocked by cobalt injection into the VLM. Injections of cobalt into the nucleus of the solitary tract did not block sympathetic responses elicited from the LHA. These results indicate that the efferent pathway for sympathetic responses from the IC through the LHA goes to the preganglionic region of the spinal cord via a mandatory synapse in the VLM.

Animals↗

Organization of visceral and limbic connections in the insular cortex of the rat.

The anterograde and retrograde transport of horseradish peroxidase was used to study the anatomical organization of visceral and limbic terminal fields in the insular cortex. Following injections into the ventroposterolateral parvicellular (VPLpc) and ventroposteromedial parvicellular (VPMpc) visceral relay nuclei of the thalamus, dense anterograde and retrograde labeling was present in the posterior granular and dysgranular insular cortices, respectively. The parabrachial nucleus had extensive connections with the posterior dysgranular cortex and to a lesser degree with the anterior dysgranular and granular cortices. In contrast, injections into the medial prefrontal cortex and mediodorsal nucleus of the thalamus resulted in dense anterograde and retrograde labeling primarily in the anterior agranular cortex, whereas injections in the amygdala resulted in axonal labeling in the agranular and dysgranular insular cortices. Injections into the lateral hypothalamic area resulted in dense anterograde and retrograde labeling mainly in the agranular and dysgranular cortices and moderate to light labeling in the granular cortex. Our results indicate that ascending visceral afferents, VPLpc, VPMpc, and parabrachial nuclei, are topographically organized in the granular and dysgranular fields of the insular cortex, whereas the agranular cortex appears to receive highly integrated limbic afferents from the infralimbic cortex and the mediodorsal nucleus of the thalamus. Although these visceral and limbic inputs to the insular cortex are segregated for the most part into different longitudinally oriented strips of cortex, limbic input from the lateral hypothalamic area and the amygdala, which have extensive autonomic as well as limbic connections, are more diffusely distributed over the different regions of the insular cortex. This organization may subserve a role for the insular cortex in integration of autonomic response with ongoing behaviour and emotion.

Afferent Pathways↗

Calcitonin gene-related peptide (CGRP) immunoreactive projections from the thalamus to the striatum and amygdala in the rat.

The organization of calcitonin gene-related peptide-like immunoreactive (CGRPir) innervation of the amygdala and caudate-putamen in the rat was examined by using immunohistochemistry for CGRP combined with retrograde transport of the fluorescent dye fluoro-gold, as well as anterograde transport of Phaseoleus vulgaris leucoagglutinin (PHA-L). The lateral part of the central nucleus of the amygdala and the amygdalostriatal transition zone was densely innervated by CGRPir terminals at all anterior-posterior levels. More caudally, the lateral part of the caudate-putamen also had large numbers of CGRPir terminals. Injections of fluoro-gold into the amygdala and amygdalostriatal transition area followed by immunohistochemistry for CGRP revealed double-labeled neurons in the subparafascicular, lateral subparafascicular, and posterior intralaminar nuclei of the thalamus and peripeduncular nucleus. Injections into the caudate-putamen demonstrated double-labeled neurons in the more lateral parts of this same nuclear complex. PHA-L injections into the posterior thalamic nuclei from which the CGRPir projections arise confirmed the medial-to-lateral organization of the projections to the amygdala and striatum. The subparafascicular nucleus and the rostral portion of the lateral subparafascicular nucleus primarily projected to the medial amygdala and the amygdalostriatal transition area, while the more lateral cell groups, including the caudal part of the lateral parafascicular, posterior intralaminar, and peripeduncular nuclei projected to the lateral amygdala and the caudate-putamen. These CGRPir projections may be involved in mediating conditioned autonomic and behavioral responses to acoustic stimuli or somatosensory stimuli.

Amygdala↗

Insular cortex stimulation produces lethal cardiac arrhythmias: a mechanism of sudden death?

The rat posterior insular cortex has recently been shown to possess cardiac chronotropic organization and therefore may be involved in cortical mechanisms of sudden death. In order to assess the potential of this region for cardiac arrhythmogenicity, phasic microstimulation of tachycardia zones was undertaken in the urethane-anesthetized rat. The insular stimulus was triggered by the R wave of the electrocardiogram (ECG) and delayed so that resultant putative cardiac sympathetic nerve activity would be synchronous with the T wave of the ECG. This resulted in increasing degrees of heart block leading to escape rhythms, ventricular ectopics and ultimately death in asystole. Heart block was associated with elevated plasma norepinephrine levels and myocardial damage. Such effects have not been previously demonstrated for a cortical site. These data suggest that pathophysiological activation of the insular cortex by stroke, epileptic seizure, or under conditions of severe emotional stress could predispose to ECG changes, cardiac arrhythmias and sudden death.

Animals↗

Autonomic responses and efferent pathways from the insular cortex in the rat.

The anatomical distribution of autonomic, particularly cardiovascular, responses originating in the insular cortex was examined by using systematic electrical microstimulation. The localization of these responses to cell bodies in the insular cortex was demonstrated by using microinjection of the excitatory amino acid, D,L-homocysteic acid. The efferents from the cardiovascular responsive sites were traced by iontophoretic injection of the anterograde axonal tracer Phaseoleus vulgaris leucoagglutinin (PHA-L). Two distinct patterns of cardiovascular response were elicited from the insular cortex: an increase in arterial pressure accompanied by tachycardia or a decrease in arterial pressure with bradycardia. The pressor responses were obtained by stimulation of the rostral half of the posterior insular cortex while depressor sites were located in the caudal part of the posterior insular area. Both types of site were primarily located in the dysgranular and agranular insular cortex. Gastric motility changes originated from a separate but adjacent region immediately rostral to the cardiovascular responsive sites in the anterior insular cortex. Tracing of efferents with PHA-L indicated a number of differences in connectivity between the pressor and depressor sites. Pressor sites had substantially more intense connections with other limbic regions including the infralimbic cortex, the amygdala, the bed nucleus of the stria terminalis and the medial dorsal and intralaminar nuclei of the thalamus. Alternatively, the depressor region of the insular cortex more heavily innervated sensory areas of the brain including layer I of the primary somatosensory cortex, a peripheral region of the sensory relay nuclei of the thalamus and the caudal spinal trigeminal nucleus. In addition, there were topographical differences in the projection to the lateral hypothalamic area, the primary site of autonomic outflow for these responses from the insular cortex. These differences in connectivity may provide the anatomic substrate for the specific cardiovascular responses and behaviors integrated in the insular cortex.

Animals↗

Cardiac chronotropic organization of the rat insular cortex.

Clinical evidence implicates the cerebral cortex in the genesis of ECG changes and cardiac arrhythmias. Such findings are not infrequent following acute cortical stroke and during partial seizures. Electrical stimulation of the cerebral cortex, however, only rarely and inconsistently results in cardiac changes. When encountered, attendant alterations in blood pressure and respiration occur; consequently, it is unclear whether the cardiac effects are primary or secondary to these. Phasic insular cortex microstimulation linked to the ECG cycle, a new technique, elicits only heart rate effects, eliminating confounding variables. The insular cortex was chosen for study because of its profuse autonomic and limbic connectivity. Cardiac chronotropic sites were demonstrated in 37 chloralose-anesthetized rats, with tachycardia represented in the rostral posterior insula, and bradycardia in the caudal posterior insula. Both effects were abolished by atenolol but not by atropine, implying their mediation by respective increases or decreases in sympathetic activity. This is the first report of the demonstration of a cortical region wherein stimulation affects heart rate and no other parameter.

Animals↗

Evidence for a cholinergic projection from the pedunculopontine tegmental nucleus to the rostral ventrolateral medulla in the rat.

Recent studies indicate that cholinergic innervation of the rostral ventrolateral medulla (RVL) may play an important role in regulation of blood pressure, but the origin of this input is not known. Using retrograde fluorescent tracing combined with immunohistochemistry for choline acetyltransferase, we found that as many as 10% of the cholinergic neurons in the pedunculopontine tegmental nucleus (PPT) can be retrogradely labeled from the RVL. Anterograde tracing of this pathway with PHA-L demonstrated that descending fibers from the region of the PPT ramify and give off terminal boutons in the RVL. These studies indicate that PPT may be a major source of cholinergic afferents to the RVL.

Animals↗

Cerebrogenic cardiac arrhythmias. Cerebral electrocardiographic influences and their role in sudden death.

Electrocardiographic repolarization changes, comprising QT prolongation, T-wave flattening or inversion, and ST-segment alterations, are most commonly seen after subarachnoid and intracerebral hemorrhage, but may occur in other neurologic conditions. They may presage arrhythmias. The effects likely are mediated by the sympathetic nervous system. Cerebral arrhythmogenesis may underlie sudden death in both normal and epileptic populations. Experimental evidence suggests that the insula has a cardiac chronotropic organization, and may be involved in the genesis of arrhythmias seen in epilepsy or after cerebral hemorrhage or stroke.

Animals↗

Subcortical sites mediating sympathetic responses from insular cortex in rats.

Stimulation of the insular cortex elicits a number of autonomic responses. The insular cortex projects directly to the lateral hypothalamic area, the parabrachial nucleus, and the nucleus of the solitary tract, which in turn project directly to sympathetic preganglionic areas. To determine which of these subcortical sites mediates sympathetic responses evoked from the insular cortex, changes in renal nerve activity were recorded before and after injection of the synaptic blocking agent cobalt into each of these regions. Blood pressure, heart rate, and renal nerve activity were continuously monitored in chloralose or urethan-anesthetized rats. Single-pulse electrical stimulation (200 microA, 1 ms) elicited either an early increase or decrease in renal nerve activity from pressor and depressor sites, respectively, in the insular cortex. Cobalt injections (500 nl) into the lateral hypothalamic area attenuated the nerve response 10-100%. Cobalt injections into the nucleus of the solitary tract significantly enhanced the initial increase in the nerve response obtained from pressor sites in the insular cortex. Injections into the parabrachial nucleus did not affect the nerve responses. These results suggest that there is a mandatory synapse in the lateral hypothalamic area in the pathway from the insular cortex to the sympathetic nervous system.

Animals↗

Calcitonin gene-related peptide immunoreactivity in the visceral sensory cortex, thalamus, and related pathways in the rat.

It has been proposed that calcitonin gene-related peptide (CGRP) may serve as a major neuromodulator in visceral sensory pathways, but its exact role in the visceral sensory thalamus and cortex has not been determined. We therefore examined the distribution of CGRP-like immunoreactive (CGRPir) innervation of the insular cortex and the parvicellular division of the ventroposterior nucleus of the thalamus (VPpc) in the rat by using immunohistochemistry for CGRP combined with retrograde transport of the fluorescent dye fluoro-gold. Modest numbers of CGRPir fibers were distributed in the dysgranular and agranular insular cortex, but few were observed in the granular insular cortex. The density of CGRPir innervation increased caudally along the rhinal fissue and was considerably greater in the perirhinal cortex. When fluoro-gold was injected into the insular cortex numerous retrogradely labeled neurons were seen in the VPpc, but few of these were CGRPir. Retrogradely labeled CGRPir neurons were, however, seen in the ventral lateral and medial parabrachial (PB) subnuclei. Injection of fluoro-gold into the perirhinal cortex (which is just caudal to the insular cortex along the rhinal fissure) resulted in many retrogradely labeled CGRPir neurons in the posterior thalamic region, including the subparafascicular, the lateral subparafascicular, and the posterior intralaminar nuclei. The VPpc was heavily innervated by CGRPir fibers but contained few CGRPir cell bodies. Injection of fluoro-gold into the VPpc resulted in many retrogradely labeled CGRPir neurons in the external medial PB subnucleus bilaterally, but with a contralateral predominance. Smaller numbers of retrogradely labeled CGRPir neurons were also observed in the ventrolateral PB subnucleus, bilaterally with an ipsilateral predominance. These results suggest that CGRP may be a neuromodulator in the ascending visceral sensory pathways from the PB to the VPpc and the insular cortex, but not between the latter two structures.

Animals↗

Autonomic and myocardial changes in middle cerebral artery occlusion: stroke models in the rat.

Stroke models in larger animals such as the cat, dog and monkey are becoming increasingly more expensive and less readily available. However, the rat is an excellent model for focal cerebral ischemia. Rats are readily available, inexpensive and their neuroanatomy and brain function have been studied extensively. Increases in plasma catecholamines and myocardial damage have been observed in clinical stroke. We examined autonomic and myocardial changes in two rat stroke models. In one model only the middle cerebral artery was occluded (MCAO) while the other model involved occlusion of both the MCA and the common carotid artery (MCAO/CCAO). Arterial blood pressure and heart rate were monitored continuously in 25 male rats (326-430 g) that underwent one of the following procedures: (1) MCAO only; (2) MCAO/CCAO; (3) CCAO only; and (4) sham occlusions (SHAM). Arterial blood samples (0.5 ml) for radioenzymatic assay of norepinephrine (NE) and epinephrine (E) were taken twice before the occlusions and at 90 and 180 min after the occlusions. The animals were perfused at the end of the experiment and the heart removed and examined histologically. Tetrazolium salts were reacted with oxidative enzymes to delineate the region of inadequate perfusion. The mean blood pressure and pulse pressure of the SHAM, MCAO/CCAO and CCAO groups significantly declined from initial values (from an average of 78 to 53 mm Hg) during the course of the experiment. However, the mean blood pressure and pulse pressure of the MCAO rats did not change during the experiment, so that the final mean blood pressure and pulse pressure were significantly higher than in the other 3 groups. The levels of both NE and E increased significantly (NE, 1443 +/- 285.9 to 4095 +/- 929 pg/ml; E, 2402 +/- 623 to 3741 +/- 1166 pg/ml) following occlusion in the MCAO group only while the other 3 groups did not change. Four of 6 hearts in the MCAO group were abnormal, showing evidence of subendocardial hemorrhage, ischemic damage or subendocardial congestion. MCAO also resulted in a consistent region of the brain with inadequate perfusion including the insular cortex. These autonomic and myocardial changes appear to mimic some of the changes seen clinically in stroke patients and provide the first acute stroke model for studying autonomic dysfunction in the rat.

Animals↗

Neurochemical organization of the hypothalamic projection to the spinal cord in the rat.

The hypothalamus provides a major projection to the spinal cord that innervates primarily lamina I of the dorsal horn and the sympathetic and parasympathetic preganglionic cell columns. We have examined the chemical organization of the neurons that contribute to this pathway by using combined retrograde transport of fluorescent dyes and immunohistochemistry for 15 different putative neurotransmitters or their synthetic enzymes. Our results demonstrate that 5 cytoarchitectonically distinct cell groups in the hypothalamus contribute to the spinal projection and that each has its own predominant chemical types. In the paraventricular nucleus, substantial numbers of hypothalamo-spinal neurons stain with antisera against arginine vasopressin (25-35%), oxytocin (20-25%), and met-enkephalin (10%). About 25% of the neurons with spinal projections in the retrochiasmatic area stain with an antiserum against alpha-melanocyte-stimulating hormone. Nearly 100% of the hypothalamo-spinal neurons in the tuberal lateral hypothalamic area stain with this same antiserum, but these cells do not stain for other proopiomelanocortin-derived peptides, and so probably contain a cross-reacting peptide. This population must be distinguished from an adjacent cell group, in the perifornical region, where many spinal projection neurons stain with antisera against dynorphin (25%) or atrial natriuretic peptide (20%). Finally, in the dorsal hypothalamic area as many as 55-75% of the neurons with spinal projections are dopaminergic, on the basis of their staining with an antiserum against tyrosine hydroxylase. These 5 neurochemically distinct projections from the hypothalamus to the spinal cord are discussed in the context of their possible functional significance.

Animals↗

Evidence for a viscerotopic sensory representation in the cortex and thalamus in the rat.

The functional organization of the insular cortex was studied by recording neuronal responses to visceral sensory stimuli. Horseradish peroxidase (HRP) was then iontophoresed at the recording sites to identify afferents from the ventrobasal thalamus to specific visceroceptive sites in the insular cortex. The relationship of the ventrobasal thalamus to the insular cortex and to brainstem relay nuclei for the ascending visceral projections was then examined by using the axonal transport of HRP, wheat germ agglutinin conjugated to HRP (WGA-HRP), and fluorescent dyes. Of a total of 55 neurons that were tested for responses to visceral sensory stimuli, 33 units responded to at least one visceral sensory modality: 6 received gastric mechanoreceptor input, 8 responded to taste inputs, 13 were activated by arterial chemoreceptors and/or showed respiratory related activity, and 6 responded to cardiovascular baroreceptor stimulation. On the basis of its cytoarchitecture and connections with the thalamus, the insular cortex was divided into a dorsal granular area, an intermediate dysgranular region, and a ventral agranular strip. Taste-responsive neurons were located anteriorly, primarily in the dysgranular region, whereas unit responses to general visceral modalities were distributed dorsally and posteriorly in the granular insular cortex. Gastric mechanoreceptor-responsive units were situated more dorsally and anteriorly in the granular insular cortex, while cardiopulmonary inputs were located more ventrally and posteriorly. Injections of HRP into the gustatory insular cortex resulted in retrograde labeling of neurons in the parvicellular part of the ventroposterior medial thalamic nucleus (VPMpc). Injections into the general visceral insular cortex retrogradely labeled neurons lateral to VPMpc in the ventroposterior lateral parvicellular thalamic nucleus (VPLpc). Injections of HRP, WGA-HRP, and fluorescent dyes into VPMpc and VPLpc verified that their projection to the insular cortex is topographically organized. In the same experiments, retrogradely labeled neurons in the parabrachial nucleus identified the likely subnuclei within this nucleus for relay of visceral sensory information to the thalamus. Injections of WGA-HRP into the parabrachial nucleus demonstrated that its projection to the ventrobasal thalamus is also topographically organized. These results demonstrate the relationship of general visceral and special visceral (taste) representations in the insular cortex. The ascending pathway for visceral sensory information appears to be viscerotopically organized at all levels of the neuraxis, including the insular cortex.

Action Potentials↗

Central representation of visceral function.

Recent studies of the visceral sensory system, using both electrophysiological and neuroanatomical methods, indicate that there is representation of multiple visceral modalities at all levels of the central nervous system. In the nucleus of the solitary tract gustatory afferents are represented rostrally, and general visceral afferents caudally. At the pontine relay, the parabrachial nucleus, the gustatory afferents are represented medially, and the general visceral afferents laterally. Although the evidence for anatomical separation of visceral projections is incomplete for the hypothalamus and amygdala, the visceral sensory thalamus and cortex are viscerotopically organized. The results indicate that the ascending visceral sensory system is viscerotopically organized at all levels of the brain, and that this information is important for the integration of autonomic responses at all levels of the neuroaxis.

Afferent Pathways↗

Spinal and trigeminal dorsal horn projections to the parabrachial nucleus in the rat.

We studied afferents to the parabrachial nucleus (PB) from the spinal cord and the spinal trigeminal nucleus pars caudalis (SNVc) in the rat by using the anterograde and retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Injections of WGA-HRP into medial PB retrogradely labeled neurons in the promontorium and in lamina I of the dorsal rostral SNVc, while injections into lateral PB and the Kölliker-Fuse nucleus retrogradely labeled neurons in these areas as well as in lamina I throughout the caudal SNVc and spinal dorsal horn. Injections of WGA-HRP into the caudal SNVc and dorsal horn of the spinal cord resulted in terminal labeling in the dorsal, central, and external lateral subnuclei of PB and the Kölliker-Fuse nucleus, all of which are known to receive cardiovascular and respiratory afferent information. Injections of WGA-HRP into the promontorium and dorsal rostral SNVc resulted in terminal labeling in the same PB subnuclei, as well as in the medial and the ventral lateral PB subnuclei, which are sites of relay for gustatory information ascending from the medulla to the forebrain. The spinal and trigeminal projection to PB may mediate the convergence of pain, chemosensory, and temperature sensibilities with gustatory and cardiorespiratory systems in PB.

Afferent Pathways↗

Central pathways relaying cardiovascular afferent information to amygdala.

It has been suggested that cardiovascular information to the amygdala is relayed through the paraventricular nucleus of the hypothalamus (PVH) and the parabrachial nucleus (PB;7). To test this possibility spontaneously firing units in the amygdala of 12 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of PVH and PB and for their responsiveness to baroreceptor (BA) and chemoreceptor (CA) activation. In the ipsilateral amygdala 27 of 140 units responded to PVH stimulation, 9 of which also responded to CA and none to BA, whereas 46 of 150 units responded to PB stimulation, 11 of which also responded to CA and 2 to BA. To demonstrate the relative contribution of the PVH and PB in relaying cardiovascular information to the amygdala, in an additional six cats, the effect of neuronal block and lesions of these two nuclei on potentials evoked in the amygdala by stimulation of the buffer nerves was tested. Reversible neuronal block with injections of procaine in the PB significantly attenuated these evoked potentials. Electrolytic and chemical (kainic acid) lesions in the same PB sites also were effective in attenuating the responses. The potentials were unaltered by injection of procaine in the PVH. These results indicate that the PB is a site of relay of chemoreceptor and of some baroreceptor information from the medulla to the amygdala.

Afferent Pathways↗