Noradrenaline blocks accommodation of pyramidal cell discharge in the hippocampus

Madison, Daniel V.; Nicoll, RA

doi:10.1038/299636a0

Cited by 562 publications

(246 citation statements)

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“…Because both of these compounds can make pyramidal cells more excitable (54,55), they may allow for greater induction of signaling cascades. Although a possibility, this explanation is unlikely given evidence to the contrary: antidromic stimulation can induce synaptic depression (36), and synaptic ''priming'' if anything reduces the likelihood of LTP induction (56).…”

Section: Discussionmentioning

confidence: 99%

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Dudek

Fields

2002

Proc. Natl. Acad. Sci. U.S.A.

108

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A question of critical importance confronting neuroscientists today is how biochemical signals initiated at a synapse are conveyed to the nucleus. This problem is particularly relevant to the generation of the late phases of long-term potentiation (LTP). Here we provide evidence that some signaling pathways previously associated with late-LTP can be activated in hippocampal CA1 neurons without synaptic activity; somatic action potentials, induced by backfiring the cells, were found to be sufficient for phosphorylation of extracellular signal-regulated kinase-1/2 and cAMP response element-binding protein, as well as for induction of zif268. Furthermore, such antidromic stimulation was adequate to rescue ''tagged'' synapses (early-LTP) from decay. These results show that a synapse-to-nucleus signal is not necessary for late-phase LTPassociated signaling cascades in the regulation of gene expression.

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Section: Discussionmentioning

confidence: 99%

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Dudek

Fields

2002

Proc. Natl. Acad. Sci. U.S.A.

108

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“…Because hippocampal heterotopic neurons in the MAM model receive excessive innervation by catecholaminergic fibers (25)(26)(27), and it is well established that catecholamines modulate Ca 2+ channel activity (40) or hippocampal neuronal excitability (28,40,41,42), we investigated adrenergic modulation of VDCC on heterotopic neurons. Bath application of norepinephrine (NE, 10-100 M), a potent agonist at ␣ 1, ␣ 2 , and ␤-adrenergic receptors, significantly reduced VDCC peak current amplitude in a dose-dependent manner on both CA1 pyramidal control neurons and heterotopic cells (Fig.…”

Section: Adrenergic Modulation Of Calcium Current On Heterotopic Cellsmentioning

confidence: 99%

An Examination of Calcium Current Function on Heterotopic Neurons in Hippocampal Slices from Rats Exposed to Methylazoxymethanol

Calcagnotto

Baraban

2003

Epilepsia

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Summary:Purpose: To study voltage-dependent calcium currents (VDCCs) on hippocampal heterotopic neurons by using whole-cell patch-clamp techniques in brain slices prepared from methylaxozymethanol (MAM)-exposed rats.Methods: Whole-cell voltage-clamp recordings were obtained from visually identified neurons in acute brain slices by using an infrared differential interference contrast (IR-DIC) video microscopy system. Heterotopic neurons were compared with normotopic pyramidal cells in hippocampal slices from MAM-exposed rats or CA1 pyramidal neurons in slices from controls.Results: Heterotopic neurons expressed a prominent VDCC, which exhibited a peak current maximum around -30 mV (holding potential, -60 mV) and an inactivation time constant of 48.2 ± 2.4 ms (n ‫ס‬ 91). VDCC peak current and inactivation time constants were similar for normotopic (n ‫ס‬ 92) and CA1 pyramidal cells (n ‫ס‬ 40). Pharmacologic analysis of VDCC, on heterotopic, normotopic, and CA1 pyramidal cells, revealed an ∼70% blockade of peak Ca 2+ current with nifedipine and amiloride (L-and T-type channel blockers, respectively). Inhibition of VDCC, for all three cell types, also was similar when more specific Ca 2+ channel antagonists were used [e.g., -conotoxin GVIA (N-type), −agatoxin KT (P/Q-type), and sFTX-3.3 (P-type)]. VDCC modulation by norepinephrine (NE) or adrenergic receptor-specific agonists [clonidine (␣ 2 ), isoproterenol (␤), and phenylephrine (␣ 1 )] was similar for heterotopic and CA1 pyramidal cells.Conclusions: Heterotopic neurons do not appear to exhibit Ca 2+ channel abnormalities that could contribute to the reported hyperexcitability associated with MAM-exposed rats. Key Words: Dysplasia-Epilepsy-Heterotopia-Ion channel-Calcium-Patch-clamp.Voltage-dependent calcium channels are an essential pathway for Ca 2+ influx and play critical roles in regulating neuronal excitability (1). Several voltage-dependent calcium channel subtypes have been recognized in the central nervous system (CNS) (2-5), each with characteristic voltage dependence, pharmacology, and single-channel kinetic properties. Often more than one voltage-dependent calcium current (VDCC) type coexists in the same neuron (6,7). Based on differences in kinetic-and voltage-dependent activation and inactivation properties, VDCC are subdivided into low voltageactivated (LVA) and high voltage-activated (HVA) components (8). LVA currents activate at relatively hyperpolarized potentials and inactivate more rapidly than HVA currents (9). In hippocampal CA1 pyramidal neurons, LVA currents are activated close to the resting membrane potential (near -65 mV) and show fast and complete inactivation kinetics. HVA currents are activated at a threshold higher than -30 mV (10). HVA currents are further subdivided, based largely on pharmacologic profiles, into N-type, P/Q-type, L-type, and residual (R-type) components (11). Each Ca 2+ channel subtype has specialized physiologic roles in the CNS. For example, N-and P/Q-type HVA currents are essential for neurotransmitter release f...

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“…18 " 20 We have examined whether these currents could account for the repetitive discharge observed in autonomic neurons of SHR. The amplitude and duration of the hyperpolarizing afterpotentials in neurons of SHR, SD, and WKY were not significantly different from each other ( Table 1).…”

Section: Contribution Of Kmentioning

confidence: 99%

Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

Yarowsky

Weinreich²

1985

Hypertension

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SUMMARY Synaptic transmission and membrane properties of sympathetic neurons in superior cervical ganglia of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (VVKY), and Sprague-Dawley rats (SD) were investigated in vitro by extracellular and intracellular recording. The sympathetic neurons of SHR showed an atypical loss of spike accommodation. The spike discharge was insensitive to the sodium channel blocker tetrodotoxin, but it was reversibly blocked by a variety of calcium antagonists. The loss of accommodation in the neurons of SHR was not due to a loss of M-current, a potassium current involved in controlling spike frequency adaptation in sympathetic neurons. Superfusion of ganglia of SHR with muscarine (10 ^M), which suppresses M-current and leads to a loss of accommodation, potentiated the repetitive discharge. In the presence of muscarine the current-voltage curves in neurons of SHR and SD were shifted to similar extents. Resting membrane potentials of neurons of SHR and WKY were consistently depolarized as compared with neurons of SD. Synaptic efficacy through the ganglia of SHR, assessed by extracellular recordings of presynaptic and postsynaptic compound action potentials at 0.25 Hz stimulation, was elevated when compared with the ganglia of WKY, but was similar to that of the ganglia of SD. These results indicate that strain differences should be considered when attempting to attribute changes in sympathetic neuron membrane properties to hypertension. The sympathetic neurons of SHR appear to have lost their accommodative properties and might possess an exaggerated calcium conductance. This calcium conductance may explain the augmented calcium-dependent release of norepinephrine during sympathetic nerve stimulation in the SHR. (Hypertension 7: 268-276, 1985) KEY WORDS • membrane properties normotensive strains repetitive firing * calcium conductance E XAGGERATED activity in the sympathetic nervous system in the Okamoto-Aoki strain of spontaneously hypertensive rats (SHR) has been implicated in both the development and the maintenance of hypertension in this model. "2 Numerous studies with the SHR have shown that both central and peripheral neurogenic mechanisms are contributory factors, although they may not account for all the elevation in peripheral vascular resistance.2 There is an increased basal sympathetic tone in visceral and nonvisceral sympathetic nerves, and an elevated sympa-

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Noradrenaline blocks accommodation of pyramidal cell discharge in the hippocampus

Cited by 562 publications

References 30 publications

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

An Examination of Calcium Current Function on Heterotopic Neurons in Hippocampal Slices from Rats Exposed to Methylazoxymethanol

Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

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