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At least 19 recordsLinked to original sources
PubMed1989

Direct projections from the central amygdaloid nucleus to the hypothalamic paraventricular nucleus: possible role in stress-induced adrenocorticotropin release.

The amygdala, particularly the central amygdaloid nucleus, is important for the expression of adrenocorticotropin and corticosterone responses during stress. The aim of the present study was to determine if the central amygdaloid nucleus directly innervated the hypothalamic paraventricular nucleus. To accomplish this aim, the Phaseolus vulgaris leucoagglutinin lectin anterograde tracing method was used. Injections of the tracer into the medial central amygdaloid nucleus resulted in axonal and terminal labeling within the medial and lateral parvocellular parts of the caudal paraventricular nucleus. A dense patch of labeling was observed within the lateral wing of the lateral part of the parvocellular paraventricular nucleus. Only a few labeled axons were observed within the paraventricular nucleus of animals that had lectin injections localized to the lateral part of the central nucleus. Tracer injections localized to the medial amygdaloid nucleus resulted in axonal and terminal labeling primarily within the anterior parvocellular and periventricular regions of the paraventricular hypothalamic nucleus. Sparse to moderate axonal and terminal labeling was observed within the magnocellular parts of the paraventricular nucleus in animals that had injections of tracer into either the medial central nucleus or the medial nucleus. No labeling was observed within the paraventricular nucleus of animals that had injections of lectin within other amygdaloid nuclei or adjacent regions of the striatum. The results demonstrated a topographically organized projection from the amygdala to the hypothalamic paraventricular nucleus. The central nucleus mainly innervates the caudal lateral and medial parvocellular paraventricular nucleus. The medial nucleus innervates the rostral parvocellular parts of the paraventricular nucleus. These pathways could form the anatomical substrates of amygdaloid modulation of neuroendocrine responses to stressors.

Adrenocorticotropic Hormone↗
PubMed1988

Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus.

The hypothalamic paraventricular nucleus (PVN) has been implicated in a remarkable number of functions including control of pituitary-adrenocortical activity in response to stress, body fluid homeostasis, milk ejection reflex, prolactin secretion, thyroid hormone secretion, analgesia, food intake, gastrointestinal functions, cardiovascular functions, and control of pineal melatonin synthesis. Paraventricular neurons produce hormones of key importance in neuroendocrine regulation such as vasopressin (VP), oxytocin (OX), 41-residue corticotropin releasing factor (CRF), thyrotropin releasing hormone (TRH), somatostatin (SOM) and the putative prolactin releasing factor vasoactive intestinal polypeptide (VIP). Three recent advances pertinent to the organization of the PVN include: (1) the evidence that the structure of the PVN is compartmental in nature, topographically segregated cellular units seem to carry out different functions; (2) the discovery that paraventricular neurons are capable of expressing a multitude of neuromediators simultaneously, thus cellular units can be best specified by a certain combination of neuromediators; (3) evidence that the composition of the neuromediator "cocktail" in individual neurons is variable and depends on the physiological status of the animal. Hence, the PVN may be best considered as a dynamic mosaic of chemically specified subgroups of neurons. The flexibility of neurotransmitter status in paraventricular neurons may play a central role of a functional plasticity of fixed anatomical circuits.

Animals↗
PubMed1994

Reduced febrile responses to pyrogens after lesions of the hypothalamic paraventricular nucleus.

The hypothalamic paraventricular nucleus (PVN) is recognized as a major site of autonomic control, but the role of this nucleus in thermoregulation is unclear. Therefore the role of the PVN in the febrile response and in the maintenance of normal body temperature was investigated. Conscious, unrestrained rats with chronic lesions of the PVN received intracerebroventricular injections of several doses of prostaglandin (PG) E2 or intraperitoneal applications of Escherichia coli lipopolysaccharide. The body temperatures of both lesioned and sham-operated animals, monitored via radio telemetry, were compared. Intracerebroventricular PGE2 at doses of 10, 25, and 50 ng caused dose-dependent fevers in both PVN-lesioned and sham-operated animals, which at lower doses were smaller in the lesioned animals than in the sham-operated animals. Intraperitoneal lipopolysaccharide application, 50 micrograms/kg body wt, evoked a significantly lower febrile response in PVN-lesioned animals than in controls. The body temperature of PVN-lesioned animals and controls showed no difference during 300 min of exposure to heat (32 degrees C) or cold (7 degrees C). These results suggest that the PVN contributes to the complex regulation of temperature during the febrile response but not during the maintenance of normal body temperature.

Animals↗
PubMed1996

GABA and glutamate mediate rapid neurotransmission from suprachiasmatic nucleus to hypothalamic paraventricular nucleus in rat.

1. Intracellular sharp electrode and whole-cell patch-clamp recording from characterized paraventricular nucleus (PVN) neurones in rat hypothalamic slices were used to study the synaptic mechanism and associated neurotransmitters that mediate their response to suprachiasmatic nucleus (SCN) stimulation. 2. Electrical stimulation restricted to SCN evoked short-latency inhibitory postsynaptic potentials (IPSPs) or combinations of IPSPs and excitatory postsynaptic potentials (EPSPs) in all (n = 59) PVN neurones tested. Type I neurones (n = 18) were magnocellular and a majority (13/18) demonstrated monosynaptic IPSPs that reversed polarity at the chloride equilibrium potential and were sensitive to bicuculline. 3. Type II (n = 10) and III parvocellular (n = 13), and unclassifiable neurones (n = 18) displayed combinations of IPSPs and EPSPs following similar stimuli applied to SCN. IPSP blockade with bicuculline uncovered SCN-evoked monosynaptic dual-component EPSPs that were sensitive to N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists. In addition, chemical microstimulation within SCN was associated with transient increases in spontaneous EPSPs recorded from these PVN neurones. 4. These data imply that the amino acids GABA and glutamate are important mediators of fast monosynaptic transmission from SCN to defined neurones in PVN, and are candidates for conveying circadian rhythmicity to PVN regulation of neuroendocrine and autonomic processes.

Animals↗
PubMed1986

In vivo voltammetric monitoring of noradrenaline release and catecholamine metabolism in the hypothalamic paraventricular nucleus.

The paraventricular hypothalamic nucleus receives a dense noradrenergic innervation. Electrochemically treated carbon fibre electrodes were implanted in the paraventricular nucleus of anaesthetized rats and their locations were histologically controlled after each experiment. Differential normal pulse voltammograms showed an oxidation peak at +50 mV. This peak was mainly due to 3,4-dihydroxyphenylacetic acid synthesized by noradrenergic terminals since: it appeared at the same oxidation potential as 3,4-dihydroxyphenylacetic acid in vitro; it was rapidly suppressed after inhibition of tyrosine hydroxylase by alpha-methyl-p-tyrosine or monoamine oxidase by pargyline; blockade of dopamine-beta-hydroxylase by FLA 63 induced a marked increase in this signal, whereas this drug was without effect in dopaminergic terminals fields (striatum, zona incerta); stimulation of alpha 2 noradrenergic receptors by clonidine (50 micrograms/kg) decreased the peak height and this effect was reversed by piperoxane (30 mg/kg). This oxidation peak corresponded to a 3,4-dihydroxyphenylacetic acid concentration of 2 microM. On the other hand, when recorded from rats which were treated with pargyline 3 h before recording, a small peak appeared at +100 mV. This signal was attributed to the oxidation of extracellular noradrenaline on the basis of the following arguments: it appeared at the same potential as noradrenaline in vitro; desipramine (25 mg/kg) induced a 4-fold increase in this peak height; piperoxan (2 mg/kg) enhanced this signal and reversed the decrease induced by clonidine (50 micrograms/kg); electrical stimulations (bipolar electrode, square pulses, 0.3 ms, 200 microA, 15 Hz for 40 s) in the rostral part of the A1 group were followed by an immediate, short-lasting 4-fold increase in the signal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Rapid stress-induced elevations in corticotropin-releasing hormone mRNA in rat central amygdala nucleus and hypothalamic paraventricular nucleus: an in situ hybridization analysis.

High densities of nerve cells containing corticotropin-releasing hormone (CRH) are located in the central nucleus of the amygdala (CeA) and paraventricular nucleus (PVN) of the hypothalamus. These brain regions play an important role in activating autonomic, behavioral, and endocrine responses to stress. This study was conducted to provide needed information concerning the acute effects of stress on CeA and PVN CRH mRNA expression. Rats were exposed to restraint stress for 1 h and brains collected after a 1-h post-stress interval. CRH mRNA expression occurring in the CeA and PVN was examined using in situ hybridization techniques. Densitometric analysis revealed that acute restraint stress produced significant increases in CRH mRNA levels in the PVN and in the rostral CeA region. In addition, the area in the rostral CeA encompassing high CRH mRNA signals increased significantly after stress. Results provide clear evidence that CRH neurons in the CeA and PVN exhibit rapid increases in CRH mRNA expression after exposure to stress.

Amygdala↗
PubMed1998

Anatomical interactions between the central amygdaloid nucleus and the hypothalamic paraventricular nucleus of the rat: a dual tract-tracing analysis.

Axonal connections between the amygdala and the hypothalamic paraventricular nucleus were examined by combined anterograde-retrograde tract tracing. Iontophoretic injections of the retrograde tracer Fluorogold were placed in the paraventricular nucleus, and the anterograde tracer PHA-L in the ipsilateral central or medial amygdaloid nuclei. Single and double-label immunohistochemistry were used to detect tracers. Single label anterograde and retrograde tracing suggest limited evidence for direct connections between the central or medial amygdala and the paraventricular nucleus. In general, scattered PHA-L-positive terminals were seen in autonomic subdivisions of the paraventricular nucleus (lateral parvocellular, dorsal parvocellular and ventral medial parvocellular subnuclei) following central or medial amygdaloid nucleus injection. Double-label studies indicate that central and medial amygdaloid nucleus efferents contact paraventricular nucleus-projecting cells in several forebrain nuclei. In the case of central nucleus injections, PHA-L positive fibers occasionally contacted Fluorogold-labeled neurons in the anteromedial, ventromedial and preoptic subnuclei of the bed nucleus of the stria terminalis. Overall, such contacts were quite rare, and did not occur in the bed nucleus of the stria terminalis regions showing greatest innervation by the central amygdaloid nucleus. In contrast, medial amygdala injections resulted in a significantly greater overlap of PHA-L labeling and Fluorogold-labeled neurons, with axosomatic appositions observed in medial divisions of the bed nucleus of the stria terminalis, anterior hypothalamic area and preoptic area. The results provide anatomical evidence that a substantial proportion of amygdaloid connections with hypophysiotrophic paraventricular nucleus neurons are likely multisynaptic, relaying in different subregions of the bed nucleus of the stria terminalis and hypothalamus.

Amygdala↗
PubMed2003

Pre- and postsynaptic GABA(B) receptors modulate rapid neurotransmission from suprachiasmatic nucleus to parvocellular hypothalamic paraventricular nucleus neurons.

The suprachiasmatic nucleus (SCN), the dominant circadian pacemaker in mammalian brain, sends axonal projections to the hypothalamic paraventricular nucleus (PVN), a composite of magno- and parvocellular neurons. This neural network likely offers SCN output neurons a means to entrain diurnal rhythmicity in various autonomic and neuroendocrine functions. Earlier investigations using patch-clamp recordings in slice preparations have suggested differential innervation by SCN efferents to magnocellular versus parvocellular PVN cells. In magnocellular PVN, cells respond to focal electrical stimulation in SCN with a GABA(A) receptor-mediated postsynaptic inhibition whose magnitude can be modulated by presynaptic GABA(B) receptors. By contrast, SCN-evoked responses in parvocellular PVN neurons typically involve both GABA(A)- and glutamate-receptor-mediated components. In the present patch-clamp study, 69/85 periventricular parvocellular PVN cells displayed SCN-evoked inhibitory and/or excitatory postsynaptic currents (IPSCs; EPSCs). In the presence of selective receptor antagonists, we sought evidence for their modulation by GABA acting at pre- and/or postsynaptic GABA(B) receptors. Cells responded to bath-applied baclofen (5-10 microM) with a tetrodotoxin-resistant membrane hyperpolarization associated with a reduction in input resistance and/or outward current, due to increase in a potassium conductance, blockable with 2-hydroxysaclofen (300 microM). At 1 microM where baclofen had no significant postsynaptic effect, evidence of activation of presynaptic GABA(B) receptors included reduction in SCN-evoked IPSCs and EPSCs with no change in their kinetics, and paired-pulse depression that was sensitive to both baclofen and saclofen. Baclofen also induced significant reductions in frequency but not amplitudes of miniature IPSCs and EPSCs. These observations suggest that levels of synaptically released GABA from the terminals of SCN output neurons can influence the relative contribution of pre- versus postsynaptic GABA(B) receptors in modulating both excitatory and inhibitory SCN innervation to parvocellular PVN neurons.

Animals↗
PubMed2001

Lesion of central part of the dorsomedial nucleus alters vasopressin but not corticotropin releasing hormone mRNA levels in rat hypothalamic paraventricular nucleus.

Functional significance of neural projections from the hypothalamic dorsomedial nucleus (DMN) to the paraventricular nucleus (PVN) was investigated using surgical lesion of the central part of the DMN. Under basal conditions, DMN lesion resulted in a decrease in magnocellular vasopressin (AVP) mRNA levels in the PVN, rise in pituitary proopiomelancortin (POMC) mRNA concentrations and elevated plasma corticosterone levels. Corticotropin-releasing hormone (CRH) mRNA levels remained unaffected. In sham operated animals, osmotic stress induced by hypertonic saline injection failed to modify AVP mRNA, but increased CRH and POMC mRNA levels and peripheral hormone release. The rise in CRH mRNA levels after osmotic stress was potentiated in DMN lesioned animals. Thus, the DMN participates in the control of hypothalamic peptide gene expression and pituitary adrenocorticotropic function.

Animals↗
PubMed1997

Plasticity in the stress-regulating circuit: decreased input from the bed nucleus of the stria terminalis to the hypothalamic paraventricular nucleus in Wistar rats following adrenalectomy.

The bed nucleus of the stria terminalis is involved in the stress-regulating circuit by funnelling limbic information to the hypothalamic paraventricular nucleus. Since adrenalectomy influences both limbic structures (by inducing cell death in the hippocampus) and the hypothalamic paraventricular nucleus (by increased corticotrophin-releasing hormone synthesis), we investigated whether the bed nucleus of the stria terminalis is also influenced by adrenalectomy. For this purpose, we analysed and compared the projections from the bed nucleus of the stria terminalis to the hypothalamic paraventricular nucleus in normal and adrenalectomized rats by anterograde tracer injections in the bed nucleus of the stria terminalis. Quantitative analysis of the fibre pattern in the hypothalamic paraventricular nucleus of normal rats revealed a homogeneous distribution of fibres of the bed nucleus of the stria terminalis over the different subdivisions of the hypothalamic paraventricular nucleus. In adrenalectomized rats, the absolute fibre density was significantly lower in the whole hypothalamic paraventricular nucleus (1.17 +/- 0.27 10(-3) microm/microm3 in adrenalectomized rats versus 2.59 +/- 0.24 10(-3) microm/microm3 in normal rats; P < 0.01) and all its subdivisions. The largest decrease of fibre density was found in the corticotrophin-releasing hormone-rich part of the hypothalamic paraventricular nucleus (relative fibre density; adrenalectomized rats: 0.602 +/- 0.106, versus 1.095 +/- 0.019 in normal rats, P < 0.01). These results show a loss of input from the bed nucleus of the stria terminalis to the hypothalamic paraventricular nucleus, and particularly to the corticotrophin-releasing hormone neurons, following adrenalectomy. The data suggest that this pathway within the stress-regulating circuit is functionally affected by corticosteroids in adult rats and may imply that human disorders associated with corticosteroid imbalance are allied to a changed circuitry in the brain.

Adrenalectomy↗
PubMed2001

PRL-releasing peptide inhibits food intake in male rats via the dorsomedial hypothalamic nucleus and not the paraventricular hypothalamic nucleus.

PRL-releasing peptide inhibits food intake after intracerebroventricular injection. PRL-releasing peptide immunoreactivity is found in several hypothalamic nuclei involved in feeding, with highest levels in the paraventricular and dorsomedial hypothalamic nuclei. The aim of this study was to examine the effect of PRL-releasing peptide on food intake after administration into these nuclei. Paraventricular nucleus injection of PRL-releasing peptide did not alter food intake. Dorsomedial hypothalamic nucleus injection of PRL-releasing peptide decreased 1 h food intake [PRL-releasing peptide (1 nmol) 83.4 +/- 6.1% saline all; P < 0.05]; and continued until 8 h postinjection [PRL-releasing peptide (1 nmol) 89.2 +/- 4.1% saline; P < 0.05]. To investigate the mechanism of this inhibition of food intake, we examined PRL-releasing peptide's effect on neuropeptide release from hypothalamic explants. alpha MSH release was increased [PRL-releasing peptide (100 nmol), 5.4 +/- 1.6 pmol/explant; change vs. basal, P < 0.01], whereas agouti-related protein release was unchanged. The release of cocaine- and amphetamine-regulated transcript was inhibited [PRL-releasing peptide (100 nmol), -33.5 +/- 12.6 pmol/explant; change vs. basal, P < 0.01]. PRL-releasing peptide dose-dependently increased neurotensin release [PRL-releasing peptide (1 nmol), 3.7 +/- 2.6 pmol/explant; change vs. basal, P = NS; PRL-releasing peptide (10 nmol), 7.2 +/- 2.7 pmol/explant; change vs. basal, P < 0.01; PRL-releasing peptide (100 nmol), 36.8 +/- 5.4 pmol/explant; change vs. basal, P < 0.001]. Our data suggest that the dorsomedial hypothalamic nucleus is important in the inhibitory effect of PRL-releasing peptide on food intake and that PRL-releasing peptide alters the release of several hypothalamic neuropeptides important in the control of food intake.

Animals↗
PubMed1995

Convergent influence of the central nucleus of the amygdala and the paraventricular hypothalamic nucleus upon brainstem autonomic neurons as revealed by c-fos expression and anatomical tracing.

Combinations of anatomical tracing with detection of Fos (the protein product of the immediate early gene c-fos) consequent to the stimulation of the central nucleus of the amygdala were used to explore the possibility that the hypothalamic paraventricular nucleus participates in the activation of brainstem neurons in the nucleus of the solitary tract and ventrolateral medulla. After injections of the anterograde tracer Phaseolus vulgaris leucoagglutinin in the paraventricular nucleus, labeled fibers and varicosities were found to impinge on catecholaminergic and non-catecholaminergic Fos-positive neurons in the brainstem. After injections of a retrograde tracer in the nucleus of the solitary tract or ventrolateral medulla, we observed that some of the Fos-positive neurons within the parvocellular paraventricular nucleus that project to the brainstem were catecholaminergic or oxytocinergic. The results indicate that direct and indirect inputs from the amygdala may influence the activity of autonomic neurons in the brainstem. The paraventricular nucleus, via its direct projections onto catecholaminergic and non-catecholaminergic neurons, may participate in activation of brainstem neurons. Activated catecholaminergic and oxytocinergic parvocellular neurons in the paraventricular nucleus may be involved in the transmission of autonomic signals from the amygdala toward the brainstem.

Amygdala↗
PubMed1988

Ether stress stimulates noradrenaline release in the hypothalamic paraventricular nucleus.

Differential normal-pulse voltammetry was combined with treated carbon fibre electrodes for monitoring in vivo extracellular catechols synthesized by noradrenergic terminals innervating the paraventricular hypothalamic nucleus. From urethane-anaesthetized rats, pretreated with a monoamine oxidase inhibitor, pargyline, we were able to monitor a catechol signal which unequivocally corresponded to extracellular noradrenaline, and we observed that ether inhalation for 2 min induced an immediate increase in this signal. Electrical stimulation of the ventral noradrenergic pathway (10 Hz for 40 s) induced a similar effect. On the other hand, from freely moving rats which were not treated with pargyline, we recorded a catechol peak which mainly corresponded to 3,4-dihydroxyphenylacetic acid which was synthesized by noradrenergic terminals. However, electrochemical and biochemical evidence strongly suggested that the increase in this signal induced by a 2-min ether stress does not correspond to 3,4-dihydroxyphenylacetic acid, but to an increase in the extracellular noradrenaline concentration. In both experimental situations the time course of the effects was identical: ether stress induced an immediate and pronounced increase in norepinephrine release, and this effect lasted as long as the stimulus duration. This effect appeared specific for noradrenergic terminals, since no effect on dopamine release was observed when recorded from the striatum or behind the paraventricular hypothalamic nucleus from the A13 dopaminergic group. In conclusion, our data are consistent with those which suggest a facilitatory action of norepinephrine on neurosecretory neurons whose cell bodies are located in the paraventricular hypothalamic nucleus and which play a major role in the hormonal response to stress.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Chemically defined collateral projections from the pons to the central nucleus of the amygdala and hypothalamic paraventricular nucleus in the rat.

Triple fluorescence labelling was employed to reveal the distribution of chemically identified neurons within the pontine laterodorsal tegmental nucleus and dorsal raphe nucleus which supply branching collateral input to the central nucleus of the amygdala and hypothalamic paraventricular nucleus. The chemical identity of neurons in the laterodorsal tegmental nucleus was revealed by immunocytochemical detection of choline-acetyltransferase or substance P; in the dorsal raphe nucleus, the chemical content of the neurons was revealed with antibody recognizing serotonin. The projections were defined by injections of two retrograde tracers, rhodamine- and fluorescein-labelled latex microspheres, in the central nucleus of the amygdala and paraventricular nucleus, respectively. Neurons projecting to both the central nucleus of the amygdala and the paraventricular nucleus were distributed primarily within the caudal extensions of the laterodorsal tegmental nucleus and dorsal raphe nucleus. Approximately 11% and 7% of the labelled cells in the laterodorsal tegmental nucleus and dorsal raphe nucleus projected via branching collaterals to the paraventricular nucleus and central nucleus of the amygdala. About half of these neurons in the laterodorsal tegmental nucleus were cholinergic, and one-third were substance-P-ergic; in the dorsal raphe nucleus, approximately half of the neurons containing both retrograde tracers were serotonergic. These results indicate that pontine neurons may simultaneously transmit signals to the central nucleus of the amygdala and paraventricular nucleus and that several different neuroactive substances are found in the neurons participating in these pathways. This coordinated signalling may lead to synchronized responses of the central nucleus of the amygdala and paraventricular nucleus for the maintenance of homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1996

Role of the hypothalamic paraventricular nucleus in cardiovascular regulation.

1. The paraventricular hypothalamic nucleus (PVH) is a complex structure with both neuroendocrine and autonomic functions. It is a major source of vasopressin and the primary source of corticotropin-releasing factor. In addition, parvicellular PVH neurons have reciprocal connections with brainstem autonomic centres and directly innervate sympathetic preganglionic neurons. Evidence is reviewed which indicates that in conscious rats PVH activation increases blood pressure, heart rate, renal nerve activity and plasma renin activity. 2. In conscious rats, a non-hypotensive haemorrhage (13 mL/kg blood loss over 24 min) results in increased numbers of Fos-immunoreactive cell nuclei within both magnocellular and parvicellular PVH neurons, including the ventral medial parvicellular regions known to contain neuronal projections to brainstem autonomic centres and spinal cord sympathetic preganglionic neurons. 3. Cell-selective ibotenate lesions of the parvicellular PVH significantly blunt the corticosterone response but do not alter blood pressure, heart rate or plasma renin concentration response to non-hypotensive or hypotensive haemorrhage. This and earlier studies indicate that, while the PVH is necessary for the corticosterone response and contributes to increased vasopressin release during blood loss, it does not play an important role in the sympathetic nervous system and renin-angiotensin responses to hypovolaemia and hypotension. 4. There is evidence to indicate that the parvicellular PVH serves as a necessary relay for cardiovascular and renin responses to certain behavioural stressors. We propose that cardiovascular information relayed to parvicellular PVH autonomic regions may be used to modulate behavioural, rather than homeostatic, effects on haemodynamics and renin release.

Animals↗
PubMed1985

Connections of neurons in the region of the nucleus tractus solitarius with the hypothalamic paraventricular nucleus: their possible involvement in neural control of the cardiovascular system in rats.

Extracellular recordings were made from 607 spontaneously firing neurons within the nucleus tractus solitarius (NTS) and its vicinity in urethane-anesthetized male rats. Following electrical stimulation of the hypothalamic paraventricular nucleus (PVN) area, 21% of the neurons were orthodromically excited, 6% were inhibited and 2.5% were antidromically activated. The antidromic spike latencies were 22-64 ms. Among those orthodromically responding neurons, 81 neurons were tested by pressure pulse stimulation of the isolated carotid sinus. The pressure stimulation produced excitation in 7 and inhibition in 13 neurons. Of the 8 tested neurons which were antidromically activated, one neuron was excited and another neuron inhibited by the pressure pulse stimulation. These results provide electrophysiological evidence for reciprocal connections between neurons in the NTS region and the PVN, and give support to the hypothesis that the PVN is involved in the neural control of the cardiovascular system.

Animals↗