Suppression of rhythmic discharges of medullary neurones in organotypic cultures of new-born rats by calcium antagonists

Bingmann, D.; Baker, Robert E.; Ballantyne, D.; Jones, David B.; Widman, Guido

doi:10.1016/0304-3940(95)12047-8

Cited by 5 publications

(2 citation statements)

References 17 publications

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“…Indeed, our own studies have shown that blocking NMDA or non‐NMDA receptors with either APV or DNQX (Baker et al . 1989, Baker et al 1995, unpublished observations), or calcium L‐channel activity with verapamil (Bingmann et al . 1995) failed to abolish SBA in neonatal rat neocortical slices.…”

Section: Discussionmentioning

confidence: 93%

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

Baker

Dijkhuizen

Pelt

et al. 1998

Eur J of Neuroscience

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The present study was undertaken to determine the effects of neurotrophin-3 (NT3) and spontaneous bioelectric activity (SBA) on dendritic elongation and branching in long-term isolated organotypic explants of rat neocortex. Viral vector-directed expression of NT3 was used as an effective means to ensure a continuous, local production of the neurotrophic factor. Quantitative light microscopic measurement of dendritic branching patterns was carried out on Golgi-stained materials. Explants were exposed to an adenoviral vector encoding the genetic sequence for neurotrophin-3 (Ad-NT3), or to exogenous additions of the neuropeptide NT3. In order to test for activity-dependent growth effects under control and experimental conditions, explants were exposed to glutamatergic blockade using a cocktail of APV and DNQX. Both Ad-NT3 and NT3 peptide potently promoted apical and basal dendritic growth (elongation and branching) in pyramidal neurons. This growth was observed to be significant in layers II-IV and V. These growth effects were also not activity dependent, inasmuch as they were elicited from explants in which spontaneous bioelectric activity had been suppressed. Non-pyramidal neurons, throughout the neocortical slice, showed no significant dendritic responses to the prolonged presence of NT3. These findings show that pyramidal dendritic growth in long-term neocortical explants responds to at least one neurotrophic growth factor, NT3, and is independent of intrinsic bioelectric activity. The use of viral vectors in delivering a continuous high level of neurotrophic factor within developing neural tissues demonstrates its potential application to in vivo tissues during development, or in the stimulation of neuritogenesis and neuroregeneration following injuries.

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Section: Discussionmentioning

confidence: 93%

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

Baker

Dijkhuizen

Pelt

et al. 1998

Eur J of Neuroscience

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“…In contrast to other high‐voltage‐activated channels, which are pre‐synaptic and participate in synaptic transmission, L‐type Ca 2+ channels seem to be localized predominantly postsynaptically (Elliot et al 1995) and may serve to shape the discharge patterns of respiratory neurones. L‐type channel blockers alter firing properties of in vitro neonatal rat respiratory neurones (Onimaru et al 1996) and activity of bursting neurones in cultured organotypic medullary tissue (Bingmann et al 1995). In the present investigation we have identified single L‐type Ca 2+ channels in inspiratory neurones and showed the modulation of their activity by mechanisms which may be relevant to various physiological and pathophysiological phenomena.…”

Section: Discussionmentioning

confidence: 99%

L‐type Ca²⁺ channels in inspiratory neurones of mice and their modulation by hypoxia

Mironov

Richter

1998

The Journal of Physiology

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Whole‐cell (ICa) and single Ca2+ channel currents were measured in inspiratory neurones of neonatal mice (4–12 days old). During whole‐cell recordings, ICa slowly declined and disappeared within 10–20 min. The run‐down was delayed during hypoxia, indicating ICa potentiation. Ca2+ channels were recorded in cell‐attached patches using pipettes which contained 110 mm Ba2+. L‐type Ca2+ channels exhibited a non‐ohmic I–V relationship. The slope conductance was 24 pS below and 50 pS above their null potential. The open probability of the channels increased during oxygen depletion, reaching a maximum 2 min after the onset of hypoxia. Restoration of the oxygen supply brought the channel activity back to initial levels. The channel activity was enhanced by 3–30 μmS(–)Bay K 8644, an agonist of L‐type Ca2+ channels. The open probability was increased about 3‐fold and the activation curve was shifted by 20 mV in the hyperpolarizing direction. In the presence of the agonist, channel open time increased and long openings appeared. Agonist‐modulated channels were also potentiated during oxygen depletion. The effect was due to an increase in open time and a decrease in closed time. The channels were inhibited by bath application of nifedipine (10 μm) and nitrendipine (20 μm). Weak bases such as NH4Cl and TMA increased and weak acids such as sodium acetate and propionate decreased activity of the channels, indicating that they are modulated by intracellular pH. Bath application of 1 μm forskolin enhanced the channel activity, whereas 500 μm NaF suppressed it. L‐type Ca2+ channels were modulated by an agonist for mGluR1/5 receptors, (S)‐3,5‐dihydrophenylglycine (DHPG, 5 μm). In its presence, the hypoxic facilitation of channels was abolished. After blockade of L‐type Ca2+ channels, the respiratory response to hypoxia was modified. The transient enhancement of the respiratory rhythm (augmentation) was no longer evident and the secondary depression occurred earlier. We suggest that L‐type Ca2+ channels contribute to the early hypoxic response of the respiratory centre. Glutamate release during hypoxia stimulates postsynaptic metabotropic glutamate receptors, which activate the Ca2+ channels.

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Effects of extracellular calcium and magnesium on central respiratory control in the brainstem–spinal cord of neonatal rat

1998

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Suppression of rhythmic discharges of medullary neurones in organotypic cultures of new-born rats by calcium antagonists

Cited by 5 publications

References 17 publications

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

L‐type Ca²⁺ channels in inspiratory neurones of mice and their modulation by hypoxia

Effects of extracellular calcium and magnesium on central respiratory control in the brainstem–spinal cord of neonatal rat

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Suppression of rhythmic discharges of medullary neurones in organotypic cultures of new-born rats by calcium antagonists

Cited by 5 publications

References 17 publications

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3

L‐type Ca2+ channels in inspiratory neurones of mice and their modulation by hypoxia

Effects of extracellular calcium and magnesium on central respiratory control in the brainstem–spinal cord of neonatal rat

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L‐type Ca²⁺ channels in inspiratory neurones of mice and their modulation by hypoxia