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J Physiol. 1998 Dec 1; 513(Pt 2): 521–530.
PMCID: PMC2231294

Influence of the hypothalamic paraventricular nucleus on cardiovascular neurones in the rostral ventrolateral medulla of the rat


  1. The question of whether neurones in the paraventricular nucleus (PVN) of the hypothalamus have an excitatory influence on reticulo-spinal vasomotor neurones of the rostral ventrolateral medulla (RVL) has been addressed in this study using anaesthetized rats.
  2. Extracellular microelectrode recordings were made from sixty vasomotor neurones in the RVL, identified by their cardiac cycle-related probability of discharge, by the decrease in activity in response to an increase in arterial blood pressure produced by intravenous phenylephrine and by the increase in activity in response to a decrease in blood pressure produced by intravenous nitroprusside.
  3. More than 70 % of these RVL vasomotor neurones were identified as spinally projecting by antidromically activating their axons via a stimulating electrode in the lateral funiculus of the T2 or T10 segment of spinal cord.
  4. Activation of neurones at different sites in the PVN with a microinjection of d,l-homocysteic acid (DLH) elicited either pressor or depressor responses.
  5. At PVN pressor sites fifteen RVL vasomotor neurones were shown to be activated prior to the blood pressure change. A further twenty RVL vasomotor neurones were observed to decrease activity following the blood pressure rise. At PVN depressor sites twelve RVL neurones were inhibited prior to the blood pressure change whereas another thirteen identified RVL neurones increased their discharge following the fall in blood pressure.
  6. In three rats single shock electrical stimulation at a PVN pressor site, first identified with DLH, elicited a single or double action potential in thirteen RVL neurones with a latency of 27 ± 1 ms.
  7. It is concluded that PVN neurones may elicit increases in blood pressure via excitatory connections with RVL-spinal vasomotor neurones, and that other PVN neurones may elicit decreases in blood pressure via inhibitory connections with these RVL neurones.

Reticulo-spinal neurones in a circumscribed region of the rostral ventrolateral medulla (RVL) are considered to play an essential role in vasomotor control (Ross et al. 1984; Brown & Guyenet, 1985; Dampney, 1994). However evidence is accumulating which shows that another brain site, the paraventricular nucleus of the hypothalamus (PVN) may also have an important function in cardiovascular homeostasis (Porter & Brody, 1986; Jin & Rockhold, 1989; Martin & Haywood, 1993; Coote, 1995; Coote et al. 1997). Lesions of the PVN attenuate the development of hypertension in Dahl salt-sensitive rats (Goto et al. 1981) and in spontaneouly hypertensive rats (Ciriello et al. 1984) and reduce the renal vascular response to volume load (Lovick et al. 1993). Furthermore, neurally mediated changes in heart rate, blood pressure and renal sympathetic nerve activity can be elicited by chemical stimulation of neurones in PVN (Porter & Brody, 1986; Kannan et al. 1989; Martin & Haywood, 1992; Malpas & Coote, 1994; Gardner et al. 1995; Gardner & Coote, 1996). We have shown that some of these effects of stimulating the PVN are mediated by spinally projecting neurones from this nucleus that excite sympathetic cardiovascular neurones in the spinal cord (Malpas & Coote, 1994). This latter action was dependent on activating a PVN-spinal vasopressin pathway since the effect was selectively blocked by intrathecal application of a vasopressin V1a antagonist to the thoracic spinal cord (Malpas & Coote, 1994). In an earlier series of experiments, Porter & Brody (1986) failed to block a PVN-induced pressor response by similar spinal application of a V1a antagonist and therefore they suggested that PVN neurones may exert an action on vasomotor neurones in the RVL. However, there is no evidence that PVN neurones can directly influence the activity of RVL vasomotor neurones, although there is anatomical evidence showing that PVN neurones project into the ventrolateral medullary region (Luiten et al. 1985; Motawei et al. 1995). There is, though, one previous report by Caverson et al. (1983) showing that, in the cat, electrical stimulation of the PVN could activate neurones in the ventral medulla. However, these neurones had spinal axons conducting at 27 m s−1 which is somewhat high for reticulo-spinal axons projecting onto spinal sympathetic neurones (Coote & Macleod, 1984; Dampney et al. 1985). Furthermore, according to Barman & Gebber (1985) fast-conducting ventral medullary neurones in the cat project to the thoracic ventral horn and do not influence sympathetic neurones. The study by Caverson et al. (1983) also did not provide evidence that the ventral medullary neurones were vasomotor, although four neurones were excited by electrical stimulation of the ipsi-lateral carotid sinus nerve, a response that was interpreted as being due to chemoreceptor fibre activation.

Therefore this lack of clear-cut evidence for a PVN-RVL vasomotor neurone projection prompted the present electrophysiological study. The aim was to determine whether identified RVL cardiovascular neurones respond to activation of PVN neurones. For this purpose cardiovascular-like neurones in the ventrolateral medulla were identified by several electrophysiological criteria, as well as by their location and the characteristics of their response to chemical stimulation of neurones at various sites in the PVN using anaesthetized rats.


Animal preparation

The experiments were performed on twenty-five male rats (Sprague- Dawley) weighing 255–319 g (298.82 ± 1.65 g, mean ±s.e.m.), anaesthetized with a mixture of α-chloralose (50 mg kg−1) and urethane (650 mg kg−1) both given intravenously after initial induction with Enflurane (Zhang & Johns 1997). An adequate depth of anaesthesia was monitored by observing arterial blood pressure, heart rate and the disappearance of pedal reflexes and briskness of corneal reflexes, and was maintained by regular (every 60 min) administration of additional anaesthesia (0.05 ml equivalent to 5 % of initial dose, i.v.) or sooner if needed. The femoral artery was cannulated with a polyethylene catheter (PE-50 tubing) which was connected to a pressure transducer (S. E. Medic or Biotronix) and a multitrace chart recorder (Lectromed UK) for continuous recording of arterial blood pressure. A femoral vein was also cannulated for administration of drugs. Electrocardiogram (ECG) signals were obtained from an ECG monitor via two platinum electrodes inserted under the skin of the limbs. The trachea was cannulated and spontaneous respiration maintained throughout the experiment. The head of the rat was mounted in a stereotaxic instrument (Narishige). Body temperature was maintained at 37°C with a heating blanket. In experiments in which the spinal cord was stimulated, animals were paralysed with gallamine (Flaxedil, 4–5 mg kg−1i.v.). In these animals adequacy of anaesthesia was maintained by regular (1 h) doses of anaesthetic and checked by observing blood pressure and heart rate. During muscular paralysis ventilation was maintained with a positive pressure animal ventilator (Harvard; 60–80 beats min−1) to maintain arterial CO2 pressure around 40 mmHg. This was measured by an arterial blood sample (0.15 ml) taken once in each experiment using a stat profile 3 analyser (Nova).

Extracellular recording

For recording units in the rostral ventrolateral medulla (RVL), the occipital bone overlying the cerebellum was surgically removed to allow placement of a glass micropipette filled with 0.5 m sodium acetate containing 1 % Pontamine Sky Blue (PSB, pH 7.4, resistance, 3–5 MΩ). Using a micrometer the pipette was inserted vertically through the intact cerebellum and advanced dorsoventrally to the ventrolateral medulla on the right side using co-ordinates of the rat brain atlas of Paxinos & Watson (1986). Co-ordinates ranged from 11–13.6 mm caudal to the bregma, 1.8–2.2 mm lateral to mid-line and 7.1–7.7 mm from the surface of the vermal cerebellum. Extracellularly recorded neurone activity was amplified (Neurolog), displayed on an oscilloscope and recorded on tape (Racal store 4). Action potentials were discriminated (Neurolog) and counted in selected bins (1000 ms and 2 or 3 ms) using a pulse integrator and period generator (Neurolog). The output was then displayed continually via a Latch counter (Neurolog) on a pen recorder and also fed into a computer which generated post-event histograms. The effects of phenylephrine (i.v.) on blood pressure and of exciting PVN neurones on neuronal activity in the ventrolateral medulla were expressed quantitatively as the mean percentage change from control levels determined in periods of 1 min before and after a test. At the end of the recording period, the sites of the last recorded unit were marked by iontophoretic deposition of PSB dye from the recording electrode (6 mA for 10 min, negative current).

All recorded units in the ventrolateral medulla were tested for their response to an increase in arterial blood pressure following an intravenous injection of phenylephrine (4–6 μg) and some (see Results) were also tested for their response to a fall in blood pressure produced by injection of sodium nitroprusside (10 μg, i.v.).

Stimulation of PVN

For stimulation of neurones in the PVN, a small craniotomy was made on the right side immediately caudal to the bregma to allow vertical placement, under micrometer control, of a glass micropipette into the right PVN (co-ordinates: 1.3–2.2 mm caudal to the bregma, 0.3ndash0.6 mm lateral to mid-line and 7–8 mm below the surface of the cortex). The glass micropipettes had a tip size of 30–60 μm and were filled with d,l-homocysteic acid (DLH, 0.2 M, pH 7.4) dissolved in saline and containing 1 % PSB to mark the injection sites. To stimulate PVN neurones, 20 nmol DLH in a volume of 0.1 μl of 0.9 % NaCl solution was injected under micrometer control using a modified microlitre syringe (Hamilton).

In three experiments PVN neurones were also activated by electrical stimulation using a double barrelled micropipette, one barrel of which was a Woods metal filled barrel connected to a constant current stimulator driven by a stimulus generator (Digitimer). The other barrel of the micropipette was filled with DLH (0.2 M) as described above, for exciting cell bodies of PVN neurones. Monopolar electrical stimulation was performed using negative current square wave pulse (0.2 ms duration, < 100 μA).

The indifferent electrode was a crocodile clip attached to occipital muscle. In twenty rats the spinal cord was exposed at T2 or T10 (three rats) and a concentric bipolar electrode (SNE-100/50, Clark Electromedical Instruments) placed vertically into the lateral funiculus on the right side with the tip 500 μm below the dorsolateral sulcus. Single electrical square wave pulses (0.2 ms duration < 100 μA) were generated from a constant current stimulator (Grayden Electronics) in order to antidromically stimulate axons of spinally projecting neurones in the RVL.

Spontaneous and stimulus-evoked changes in neuronal activity were analysed either by ECG triggered histograms, or by post stimulus histograms using a computer. In addition, records of firing rate (Neurolog) and blood pressure were continually registered on a chart recorder. All raw data were captured on a tape recorder (4 channel Racal).

Histological verification of recording and injection sites

At the end of each experiment, the brain was removed and fixed in formalin. Frozen coronal serial sections (60 μm) through the hypothalamus and medulla were cut and mounted on gelatinized slides and air dried. Sections were stained in Cresyl Violet. The position of the recording and microinjection sites were determined by the location of PSB spots identified histologically using standard procedures. The serial sections and the locations of PSB spots were reconstructed according to the rat brain atlas of Paxinos & Watson (1986).

All data are expressed as means ±s.e.m.


The mean blood pressure after anaesthesia in twenty-five rats was 84.1 ± 1.5 mmHg.

Characteristics of the recorded activity of ventrolateral medullary neurones

The population of neurones we recorded could be divided into two types on the basis of the response to a rise or fall in blood pressure produced by phenylephrine (i.v.) or nitroprusside (i.v.), respectively, on the characteristic pattern of discharge related to the cardiac cycle, and on their location in the ventrolateral medulla. We report only those neurones which were inhibited by a rise in blood pressure or excited by a fall in blood pressure as illustrated in Fig. 1. Sixty neurones responded appropriately to the induced changes in arterial blood pressure and were determined to lie within a circumscribed region of the ventrolateral medulla (Fig. 2).

Figure 1
Characteristic reponse of an RVL spinal vasomotor neurone to a change in blood pressure
Figure 2
Location of vasomotor neurones recorded

All neurones displayed on-going activity (7 ± 0.4 spikes s−1). The majority (92 %) fired with a single spike separated by intervals greater than 50 ms (Fig. 3A) whilst the remainder fired with a burst of two successive spikes separated by an interval of less than 10 ms with longer intervals between each double discharge (Fig. 3B) as reported by others (Chan et al. 1991). These characteristics were unchanged even after 1 h of recording. All these neurones decreased action potential firing frequency by a mean of 74.6 ± 3.4 % co-incident with a rise in arterial blood pressure (72 ± 1 mmHg) produced by phenylephrine (i.v.). In the case of double discharging neurones, both action potentials disappeared and reappeared simultaneously following the change in blood pressure and the interburst frequency increased with deactivation of the baroreceptors, thus confirming the likelihood they were recorded from a single neurone. The responses of seven neurones were tested to a depressor response produced by nitroprusside (i.v.). Coincident with the fall in blood pressure (42.1 ± 2.9 mmHg), these neurones increased their firing rate by 109 ± 8.1 %. All these neurones displayed a decreased probability of firing rate following systole or the R wave of the ECG, in each cardiac cycle (Fig. 3C). Forty-two neurones were shown to have spinally projecting axons as evidenced by the constancy of the response to stimulation via the spinally placed electrode and its absence when the spinal stimulus was delivered within a critical period of a spontaneous spike (Fig. 4A, B and C). Antidromic response latencies had a mean of 49.2 ± 3.1 ms, and ranged from 24 to 100 ms with the longer latencies occurring in the three animals in which T10 stimulation was used. These latencies gave a mean conduction velocity of 1.6 ± 0.1 m s−1, based on the straight line conduction distance between stimulating (T2 or T10) and recording electrode.

Figure 3
Characteristics of the discharge pattern of RVL spinal vasomotor neurones
Figure 4
Responses of a reticulo-spinal vasomotor neurone

Location of the RVL neurones

Pontamine Sky Blue spots indicating recording sites were identified in histological material and mapped onto drawn outlines of coronal sections of the medulla (Fig. 2). The neurones that were inhibited by a rise in blood pressure were found in greater abundance at ventrolateral medullary sites between −11.6 to −12.8 mm caudal to bregma with a few distributed more caudally down to −13.8 mm caudal to bregma. Hereafter these neurones are referred to as rostral ventrolateral medullary (RVL) neurones.

Effect of PVN stimulation on the activity of RVL neurones

Chemical stimulation

Microinjection of DLH into PVN produced either an increase in arterial blood pressure (mean, 29 ± 3 mmHg) or a decrease (mean, 20 ± 1 mmHg) depending on the location of the micropipette (Fig. 5). At PVN pressor sites RVL neurones showed one of two responses: either an abrupt increase in firing rate (118 ± 19 %) preceding the pressor response (15 neurones; Fig. 5A, left panel), or a decrease in activity (85 ± 5 %) following the blood pressure rise (20 neurones; Fig. 5A, right panel). Seventy-one per cent of neurones giving either of these responses were antidromically activated from the spinal cord. At PVN depressor sites RVL neurones showed either a decrease in activity (78 ± 7 %) beginning prior to the fall in blood pressure (12 neurones; Fig. 5B, right panel) or an increase in discharge (185 ± 50 %) which followed the blood pressure fall (13 neurones; Fig. 5B, left panel). Seventy percent of both groups of neurones were antidromically activated on stimulating the spinal cord.

Figure 5
Effects of PVN stimulation on RVL spinal vasomotor neurones

Of the remaining 29 or 30 % of RVL neurones recorded when stimulating PVN pressor or depressor sites respectively, 20 % could not be shown to be antidromically activated by the spinal stimulus and the remainder were not tested.

Electrical stimulation

Single shock stimulation, via the Woods metal filled barrel of the micropipette assembly at pressor sites in the PVN at which DLH ejected from the other barrel evoked discharge in an identified RVL vasomotor neurone, elicited single (12 neurones) or double (1 neurone) action potential discharge in 13 neurones. A typical example of a post-stimulus histogram generated by the PVN stimulus is shown in Fig. 4D. In this example PVN stimulation (30 μA) led to a higher probability of synaptic activation of the RVL neurone after 27 ms. Cancellation by spontaneous activity was not observed. The range of latencies for the thirteen RVL neurones determined from such post-stimulus histograms was 27 ± 1 ms. We did not test the ability of the RVL neurones to follow a higher frequency of PVN stimulation than 1 Hz. However, the standard deviation of the latency of the evoked response shown in Fig. 4D was 2.1 ms and for the other thirteen neurones had a mean of 1.91 ms. The straight line distance between the PVN stimulating electrode and RVL recording site was estimated to be 10 mm, giving a conduction velocity of 0.3–0.4 m s−1.

All the stimulation sites were confirmed to lie within the PVN region, on histological location of spots of PSB ejected from the DLH-containing barrel, two examples of which are shown in coronal sections of the hypothalamus (Fig. 6) and all of which are plotted in the drawings from three levels of the hypothalamus (Fig. 7).

Figure 6
Position of positive sites in PVN
Figure 7
Location of negative sites in the hypothalamus

Microinjection of DLH (< 100 nl) at sites immediately outside the PVN did not result in any change in blood pressure, heart rate or RVL neurone activity. These negative sites are plotted for three representative levels of the hypothalamus in Fig. 7. For comparison, the location of PSB spots at which DLH (< 100 nl) elicited positive responses in the same six experiments are shown for clarity on the left of the sections although these relate to sites stimulated on the right side.


In this study vasomotor neurones in the ventrolateral medulla were distinguished by their characteristic responses to drug-induced blood pressure rises and falls, and the type of pulse modulation of their discharge. These effects of cardiovascular changes suggest that the neurones are sensitive to arterial baroreceptor activation. The majority of neurones were located in the rostral part of the ventrolateral medulla and correspond to those neurones observed by several laboratories and described as vasomotor reticulo-spinal neurones (Sun & Guyenet, 1987; Morrison et al. 1988; Haselton & Guyenet 1989; Chan et al. 1991; Sun & Spyer, 1991ac; Ermirio et al. 1993). The spontaneous firing rate of all these vasomotor neurones has a similar pattern to that reported in earlier studies (Morrison et al. 1988) with some neurones displaying a ‘beating’ activity consisting of two successive action potentials regularly repeated (Chan et al. 1991). However the mean firing rate for the population of vasomotor neurones was lower than previously reported, a feature which was most likely a consequence of the type and depth of anaesthesia (Sun & Spyer, 1991b,c). In the present study male Sprague-Dawley rats were deeply anaesthetized with chloralose and urethane. Most other studies have not used this combination of anaesthetics. For example either halothane (Sun & Guyenet, 1987), sodium pentobarbitone (Chan et al. 1991), urethane (Ermirio et al. 1993) or urethane and pentobarbitone (Sun & Spyer, 1991b,c) have been used. In addition, in several of these studies, animals were paralysed and artificially ventilated (Sun & Guyenet, 1987; Sun & Spyer, 1991ac; Ermirio et al. 1993), although this did not noticeably effect the firing rates we observed in the present experiments with Flaxedil.

The present series of experiments has shown for the first time that the discharge of RVL vasomotor type neurones including spinally projecting neurones can be altered by activation of neurones in the paraventricular nucleus. We believe these responses were due to activating PVN neurones, because injection of similar volumes of DLH just outside the boundary of PVN did not cause any change in blood pressure or in RVL neurone activity. Much of the observed influences of PVN neurones could be attributed to a primary effect on VLM neurones rather than secondary to blood pressure changes. Thus at several PVN sites activation or inhibition of RVL neurones occurred prior to a change in blood pressure. Furthermore, RVL neurones were shown to increase their activity following PVN stimulation despite an accompanying pressor response which, if produced by phenylephrine (i.v.) alone would have caused a profound reflex inhibition. Similarly, decreases in RVL neurone activity occurred at PVN sites which also caused depressor responses. Therefore, we conclude that the activity of RVL neurones can be altered independently of blood pressure changes. The present experiments did not address the possibility of whether this occurred because there was also a gating by the PVN of the baroreflex inputs prior to their arrival at the RVL. The answer to this interesting question will require alternative experimental approaches.

Since these RVL neurones are likely to be vasomotor neurones regulating blood pressure, their activation should also lead to an increase in blood pressure and vice versa. Hence PVN vasomotor effects could possibly be mediated via the RVL. This would explain the finding that some PVN pressor effects are not prevented by pharmacological antagonism of the PVN spinal pathway terminating on spinal vasomotor neurones (Riphagen & Pittman, 1985; Porter & Brody, 1986; Malpas & Coote, 1994).

The question of which pathways mediate the actions of PVN neurones on RVL neurones was addressed by electrically stimulating with a single shock at the same PVN site at which DLH injection gave an excitatory response. It was reasoned that the electrical stimulus and the DLH injection activated the same neurones although we cannot exclude the possibility that fibres of passage were also effected by the electrical pulse. The short latency and the low variability of the response in RVL neurones led us to believe that the connection between PVN and RVL neurones was fairly direct, possibly even monosynaptic, although intracellular recording is necessary to confirm this. A high proportion of the RVL neurones were shown to be spinally projecting so indicating that the PVN has a pathway to the spinal cord via RVL neurones, in addition to a direct PVN spinal projection to spinal vasomotor neurones (Strack et al. 1989; Hosoya et al. 1991; Ranson et al. 1995; Pyner & Coote, 1997).

There is anatomical evidence that PVN neurones project into the region where RVL neurones are located (Luiten et al. 1985) but so far no studies have examined connections with identified RVL spinal neurones. Such a confirmation of our electrophysiological data clearly is required. Nonetheless recent anatomical evidence published in a preliminary form shows that there are three separate routes by which PVN neurones may influence spinal neurones. One is a projection to RVL, another is a direct projection to the spinal cord, and a third is a small projection to both regions (Pyner & Coote, 1997).

Considerable evidence is now available indicating that the PVN has a significant role in cardiovascular regulation (Coote, 1995; Coote et al. 1997). Both excitatory and inhibitory effects have been reported (Porter & Brody, 1986; Kannan et al. 1987; Katafuchi et al. 1988; Malpas & Coote, 1994). The present study shows that part of these effects could be mediated via the RVL site, since both excitation and inhibition of RVL neurones was observed prior to PVN-induced pressor and depressor responses. How these actions are co-ordinated with the direct spinal ones reported previously by us (Malpas & Coote, 1994) remains to be determined. The latter actions are mediated via the release of vasopressin (Malpas & Coote, 1994) and it is conceivable that the peptide pathway plays a modulating role to co-ordinate and enhance the gain of PVN-RVL influences on spinal vasomotor neurones (Sermasi & Coote, 1994) in response to disturbances of homeostasis.

Hypothalamic excitatory inputs onto RVL neurones have been described by others. Only one study activated PVN neurones, but this failed to provide evidence that RVL spinal neurones were vasomotor (Caverson et al. 1983). In fact, in view of the fast conduction speed of the reticulo-spinal units and lack of other vasomotor characteristics of these neurones described by Caverson et al. (1983) it is more likely they were respiratory neurones located in the vicinity of RVL (Brown & Guyenet, 1985), which project to the thoracic ventral horn (Coote & Macleod, 1984; Barman & Gebber, 1985). In contrast, there is good evidence in the rat of a projection to RVL from the lateral hypothalamus (Sun & Guyenet, 1986) and from the defence area of the perifornical region (Hilton & Smith, 1984). The RVL therefore, is a convergent region for several hypothalamic inputs (Barman, 1990). Whether these inputs are uniformally distributed to all RVL spinal vasomotor neurones remains to be determined. It would be important to know the answer to this question since, at least as far as the PVN is concerned, the pattern of evoked cardiovascular changes is different from that occurring in the defence reaction (Coote, 1995; Badoer, 1996; Coote et al. 1997). It might therefore be expected that projecting neurones from the different hypothalamic sites are differentially distributed to RVL neurones as has also been suggested by Barman (1990). One might speculate that the pattern of distribution will depend on the neuronal phenotype.


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