Calcium channel types contributing to excitatory and inhibitory synaptic transmission between individual hypothalamic neurons

Zeilhofer, Hanns Ulrich; Müller, Thomas; Swandulla, Dieter

doi:10.1007/s004240050131

Cited by 14 publications

(10 citation statements)

References 58 publications

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“…x-CTX has been reported to irreversibly block N-type calcium channels in several preparations (23)(24)(25)(26). The I-V relationship of x-CTX-insensitive current was shifted to the right, which has been described in dissociated hypothalamic neurones (26). 8).…”

Section: Adrenergic Enhancement Of Barium Currentmentioning

confidence: 80%

“…To determine whether N-type calcium channels contributed to PHEN enhancement of I Ba in the VMN, we tested PHEN effects in the presence of the N-type channel blocker x-CTX. x-CTX has been reported to irreversibly block N-type calcium channels in several preparations (23)(24)(25)(26). When slices were preincubated with 2 lM x-CTX for 60 min, PHEN had no effect on peak amplitude of I Ba in any of the neurones from vehicle-(n = 12) or oestradiol-treated (n = 11) female rats (Fig.…”

Section: Adrenergic Enhancement Of Barium Current Through N-type Calcmentioning

confidence: 89%

“…x-CTX has been reported to irreversibly block N-type calcium channels in several preparations (23)(24)(25)(26). x-CTX has been reported to irreversibly block N-type calcium channels in several preparations (23)(24)(25)(26).…”

Section: Adrenergic Enhancement Of Barium Currentmentioning

confidence: 99%

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Voltage‐Dependent Calcium Channels in Ventromedial Hypothalamic Neurones of Postnatal Rats: Modulation by Oestradiol and Phenylephrine

Lee

Kyrozis

Chevaleyre

et al. 2007

J Neuroendocrinology

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Oestradiol actions in the hypothalamus play an important role in reproductive behaviour. Oestradiol treatment in vivo induces alpha(1b)-adrenoceptor mRNA and increases the density of alpha(1B)-adrenoceptor binding in the hypothalamus. Oestradiol is also known to modulate neuronal excitability, in some cases by modulating calcium channels. We assessed the effects of phenylephrine, an alpha(1)-adrenergic agonist, on low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium channels in ventromedial hypothalamic (VMN) neurones from vehicle- and oestradiol-treated female rats. Whole-cell and gramicidin perforated-patch recordings were obtained, with barium as the charge carrier. In the absence of phenylephrine, oestradiol treatment increased the magnitude of LVA currents compared to controls, but had no effect on HVA currents. Phenylephrine enhanced HVA currents in a significantly greater proportion of neurones from oestradiol-treated rats (76%) than from vehicle-treated (41%) rats. The L-channel blocker nifedipine abolished this oestradiol effect on phenylephrine-enhanced HVA currents. Preincubating slices with the N-type channel blocker omega-conotoxin GVIA completely blocked the phenylephrine response, suggesting that the N-type channel is essential. Phenylephrine also stimulated LVA currents in approximately two-thirds of neurones in slices from both vehicle- and oestradiol-treated rats. Our data show that oestradiol increases LVA currents in the VMN. Oestradiol also amplifies alpha(1)-adrenergic signalling by increasing the proportion of neurones showing phenylephrine-stimulated HVA currents mediated by N- and L-type calcium channels. In this way, oestradiol may increase excitatory responses to arousing adrenergic inputs to VMN neurones governing oestradiol-dependent reproductive behaviour.

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Section: Adrenergic Enhancement Of Barium Currentmentioning

confidence: 80%

Section: Adrenergic Enhancement Of Barium Current Through N-type Calcmentioning

confidence: 89%

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Voltage‐Dependent Calcium Channels in Ventromedial Hypothalamic Neurones of Postnatal Rats: Modulation by Oestradiol and Phenylephrine

Lee

Kyrozis

Chevaleyre

et al. 2007

J Neuroendocrinology

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“…We used 1 m GVIA and found that the proportion of N-type Ca 2ϩ current was 15-20% of the total Ca 2ϩ currents. N-Type Ca 2ϩ channels could be involved in GnRH release at nerve endings, because the N-type channel is known to be involved in vasopressin release (20), oxytocin release (26), and synaptic transmission in cultured hypothalamic neurons (37) and several central synapses (38). Immunostaining of N-type Ca 2ϩ channel subunit ␣1B revealed the presence of the Ntype channel not only at nerve terminals, but also in the soma-dendritic region of central neurons (39), so that N-type channels in the GnRH neuron may play some roles in the soma-dendritic region besides at nerve terminals.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Voltage-Gated Calcium Currents in Gonadotropin-Releasing Hormone Neurons Tagged with Green Fluorescent Protein in Rats

et al. 2003

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Functional analysis of GnRH neurons is limited, although these neurons play an important role in neuroendocrine regulation. Therefore, we decided to conduct cell physiological analysis of GnRH neurons. To identify GnRH neurons, we tagged the neurons with green fluorescence protein by a transgenic technique. A dispersed culture of GnRH neurons was prepared from the transgenic rats. After overnight culture, a perforated patch clamp was applied to the identified GnRH neurons to analyze the Ca2+ currents. In neonatal GnRH neurons, high voltage-activated Ca2+ currents were clearly observed, but low voltage-activated Ca2+ current was negligible. Nimodipine (L-type channel blocker) and omega-conotoxin GVIA (N-type channel blocker) each attenuated the current by approximately 20%. The R-type channel blocker SNX-482 attenuated the current by approximately 55%. Inhibition by the P/Q-type channel blocker omega-agatoxin IVA was small. In GnRH neurons around puberty, however, both high and low voltage-activated Ca2+ currents were observed. Inhibitions by nifedipine, omega-conotoxin GVIA, and SNX-482 were similar to those in the neonatal neurons, whereas the inhibition by omega-agatoxin IVA was clearly seen in 40-61% of the GnRH neurons examined. These results indicate that GnRH neurons functionally express L-, N-, P/Q-, R-, and T-type channels. Expressions of P/Q- and T-type channels are developmentally regulated.

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“…These findings are in line with the observation that nociceptin inhibits voltage‐activated N‐type Ca 2+ channels that are sensitive to the Conus geographus toxin ω‐CgTxGVIA (Connor et al , 1996). N‐type Ca 2+ channels together with ω‐AgaIVA‐sensitive P‐ and/or Q‐type Ca 2+ channels are criticlly involved in triggering transmitter release from the presynaptic terminals of central neurones (Turner et al , 1992; Takahashi & Momiyama, 1993; Wheeler et al , 1994; Zeilhofer et al , 1996). Inhibition of excitatory synaptic transmission by nociceptin occurred with an EC 50 of about 450 n m .…”

Section: Discussionmentioning

confidence: 99%

Modulation of excitatory synaptic transmission by nociceptin in superficial dorsal horn neurones of the neonatal rat spinal cord

Liebel

Swandulla

Zeilhofer

1997

British J Pharmacology

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112

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1 The modulatory actions of nociceptin/orphanin FQ on excitatory synaptic transmission were studied in super®cial dorsal horn neurones in transverse slices from 7 to 14 day old rats. 2 Glutamatergic excitatory postsynaptic currents (e.p.s.cs) were recorded from the somata of the neurones in the whole-cell patch-clamp con®guration. E.p.s.cs were evoked by extracellular electrical stimulation (100 ms, 3 ± 10 V) of the ipsilateral dorsal root entry zone by use of a glass electrode. E.p.s.cs with constant short latency (52.3 ms) and with no failures upon stimulation were assumed to be monosynaptic. These e.p.s.cs occurred with an average latency of 1.72+0.098 ms and exhibited a fast decay with a time constant, t, of 4.8+0.53 ms (n=30). 3 Nociceptin reversibly reduced the amplitudes of e.p.s.cs in a concentration-dependent manner in 25 out of 27 cells tested. Average maximum inhibition was 51.6+5.7% (mean+s.e.mean; n=9), at concentrations 43 mM. EC 50 was 485+47 nM and the Hill coecient was 1.29+0.09. 4 Inhibition of synaptic transmission by nociceptin (10 mM) was insensitive to the non-speci®c opioid receptor antagonist naloxone (10 mM) indicating that nociceptin did not act via classical opioid receptors. 5 In order to determine the site of action of nociceptin spontaneous miniature e.p.s.cs (m-e.p.s.cs) were recorded. Nociceptin reduced the frequency of m-e.p.s.cs in 6 out of 7 cells but had no eect on their amplitude distribution or on their time course. These ®ndings suggest a pre-rather than a postsynaptic modulatory site of action. This is in line with the ®nding that current responses elicited by extracellular application of L-glutamate (10 mM) were not aected by nociceptin (10 mM; n=7). 6 No positive correlation was found between the degree of inhibition by nociceptin (10 mM) and by the mixed d-and m-receptor agonist methionine-enkephalin (10 mM). This suggests that both neuropeptides acted on dierent but perhaps overlapping populations of synaptic connections. 7 Our results indicate that nociceptin inhibits excitatory synaptic transmission in the super®cial layers of the rat dorsal horn by acting on presynaptic, presumably ORL 1 receptors. This may be an important mechanism for spinal sensory information processing including nociception.

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Calcium channel types contributing to excitatory and inhibitory synaptic transmission between individual hypothalamic neurons

Cited by 14 publications

References 58 publications

Voltage‐Dependent Calcium Channels in Ventromedial Hypothalamic Neurones of Postnatal Rats: Modulation by Oestradiol and Phenylephrine

Voltage‐Dependent Calcium Channels in Ventromedial Hypothalamic Neurones of Postnatal Rats: Modulation by Oestradiol and Phenylephrine

Characterization of Voltage-Gated Calcium Currents in Gonadotropin-Releasing Hormone Neurons Tagged with Green Fluorescent Protein in Rats

Modulation of excitatory synaptic transmission by nociceptin in superficial dorsal horn neurones of the neonatal rat spinal cord

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