Pulser: user-friendly, graphical user-interface based software for controlling stimuli during data acquisition with Spike2 for Windows

Lidierth, Malcolm

doi:10.1016/j.jneumeth.2004.06.014

Cited by 10 publications

(4 citation statements)

References 3 publications

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“…Phrenic nerve frequency (PNf), TI and TE were derived offline. The duration and timing of stimuli were controlled by a programmable Spike 2 script (Lidierth 2005); stimulus intensity was determined using an isolated stimulator.…”

Section: Methodsmentioning

confidence: 99%

Effects of baroreceptor activation on respiratory variability in rat

McMullan

Farnham

Pilowsky

2009

Respiratory Physiology & Neurobiology

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Controversy surrounds the respiratory responses to baroreceptor activation. Although many reflexes that effect respiration (e.g. chemoreflexes and nociceptive reflexes) frequently affect cardiovascular parameters, the effect of baroreflex stimulation within normal physiological limits is generally considered to affect only blood pressure and heart rate. Even though previous authors have reported that baroreceptor activation can affect respiratory activity, the effects on respiratory frequency and amplitude are highly variable, and changes in perfusion evoked by blood pressure manipulation could account for the observed effects. Here, we determined the respiratory effects of activating arterial baroreceptors by intravenous injection of phenylephrine or angiotensin II, or by electrical stimulation of the aortic depressor nerve (ADN). In urethane-anaesthetized vagotomized rats, 1, 2 and 4 second trains of tetanic ADN stimulation evoked 3.1 ± 1.1%, 11.2 ± 13.6% and 21.9 ± 8.9% increases in inspiratory (TI) time and 26.5 ± 18%, 23.4 ± 15.7% and 34.6 ± 20.9% increases in expiratory (TE) time respectively (P < 0.05 in both cases), but no effect on the amplitude of bursts recorded in the phrenic nerve. Similar effects were observed following pressor trials evoked by intravenous PE (TE: +26.1 ± 9.1%, P<0.01), but not Ang II. Intermittent ADN stimulation (single pulse, 1 Hz) significantly increased the variability of TI during periods of low respiratory drive (P < 0.05) without significantly affecting any other parameters. We propose that a specific baroreceptor-respiratory response exists that is independent of changes in blood flow. In contrast to the effects of baroreceptor stimulation on sympathetic nerve activity, the baro-respiratory response is subtle and highly dependent on respiratory drive.

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Section: Methodsmentioning

confidence: 99%

Effects of baroreceptor activation on respiratory variability in rat

McMullan

Farnham

Pilowsky

2009

Respiratory Physiology & Neurobiology

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“…Duration and timing of stimuli were controlled by a programmable Spike2 script (Lidierth, 2005); stimulus intensity was determined by an isolated stimulator. Typical stimulus intensities for ADN and facial nerves were 5 and 20 V, respectively.…”

Section: Methodsmentioning

confidence: 99%

Circulating angiotensin II attenuates the sympathetic baroreflex by reducing the barosensitivity of medullary cardiovascular neurones in the rat

McMullan

Goodchild

Pilowsky

2007

The Journal of Physiology

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Chronic intravenous angiotensin II (Ang II) has been widely used to establish centrally mediated hypertension in experimental animals, and disruption of Ang II activity is a frontline treatment for hypertensive disease. However, the acute central actions of circulating Ang II are poorly understood. We examined the effects of intravenous pressor doses of Ang II on autonomic activity in anaesthetized rats under neuromuscular blockade, and compared baroinhibition evoked by Ang II pressor ramps to equipressor responses evoked by phenylephrine (PE). Baroinhibition of splanchnic sympathetic nerve activity was attenuated during Ang II trials compared with PE, and rats remained sensitive to electrical stimulation of the aortic depressor nerve at higher arterial pressures during Ang II trials. This was not due to a direct effect of Ang II on aortic nerve baroreceptors. In a separate series of experiments, we provide direct evidence that bulbospinal barosensitive neurones in the rostral ventrolateral medulla are differentially sensitive to pressure ramps evoked by Ang II or PE vasoconstriction. Nineteen out of 41 units were equally sensitive to increased arterial pressure evoked by Ang II or PE. In 17 of 41 units, barosensitivity was attenuated during Ang II trials, and in five of 41 cases units that had previously been barosensitive increased their firing rate during Ang II trials. These results show, for the first time, that circulating Ang II acutely modulates central cardiovascular control mechanisms. We suggest that this results from activation by Ang II of a central pathway originating at the circumventricular organs.

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“…In all cases, stimuli were delivered from an isolated constant current source (Neurolog NL800 or Grass SIU7) and were monitored by recording the voltage drop across a resistor placed in the current return path. Pulse sequences were generated using a stand‐alone timing device (D4030, Digitimer UK) or Pulser software (Lidierth, 2005 b ).…”

Section: Methodsmentioning

confidence: 99%

Local and diffuse mechanisms of primary afferent depolarization and presynaptic inhibition in the rat spinal cord

Lidierth

2006

The Journal of Physiology

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Two types of dorsal root potential (DRP) were found in the spinal cord of urethane-anaesthetized rats. Local DRPs with short latency-to-onset were evoked on roots close to the point of entry of an afferent volley. Diffuse DRPs with a longer latency-to-onset were seen on more distant roots up to 17 segments from the volley entry zone. The switch to long latency-to-onset occurred abruptly as a function of distance along the cord and could not be explained by conduction delays within the dorsal columns. Long-latency DRPs were also present and superimposed on the short-latency DRPs on nearby roots. Both local and diffuse DRPs were evoked by light mechanical stimuli: von Frey hair thresholds were ≤ 1 gram force Changes in excitability of the terminals of sural nerve afferents were used to confirm that both local and diffuse DRPs were associated with primary afferent depolarization (PAD). These effects were potent: the area of the antidromic volley evoked in the sural nerve by intraspinal microstimulation in the L4/5 spinal segment was increased by 109 ± 50% (mean ± S.D.; n = 5) by nearby conditioning stimuli, and by 52 ± 12% (n = 6) with stimuli applied 9-13 mm (5-8 segments) away. The time course of the changes in terminal excitability closely matched those of the DRPs. Reduction of the field potentials evoked in the dorsal horn by stimulation of dorsal roots was also shown to accompany both local and diffuse DRPs. The area of the monosynaptically evoked field potential was reduced by 48 ± 19% (n = 7) with nearby conditioning stimulation and 16 ± 9% (n = 10) with stimulation 9-12 mm distant. Evidence is presented that this inhibition includes a presynaptic component. Similar effects were seen with field potentials evoked by sural nerve stimulation. It is concluded that diffuse DRPs are mediated through propriospinal networks which may contribute to the gating of sensory information flow during natural behaviour as they respond to weak mechanical stimuli and provoke presynaptic inhibition.

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Pulser: user-friendly, graphical user-interface based software for controlling stimuli during data acquisition with Spike2 for Windows

Cited by 10 publications

References 3 publications

Effects of baroreceptor activation on respiratory variability in rat

Effects of baroreceptor activation on respiratory variability in rat

Circulating angiotensin II attenuates the sympathetic baroreflex by reducing the barosensitivity of medullary cardiovascular neurones in the rat

Local and diffuse mechanisms of primary afferent depolarization and presynaptic inhibition in the rat spinal cord

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