Effects of forskolin on electrical behaviour of myenteric neurones in guinea‐pig small intestine.

Nemeth, Paul R.; Palmer, Jeffrey M.; Wood, Jackie D.; Zafirov, Dimiter H.

doi:10.1113/jphysiol.1986.sp016162

Cited by 80 publications

(62 citation statements)

References 20 publications

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“…First, it is not known whether similar changes occur when the ileum is exposed overnight to morphine at 48C. Second, m-opioid responsive neurones in the myenteric plexus (S neurones) are not aected by agents that elevate cyclic AMP levels (Nemeth et al, 1986;Johnson & Pillai, 1990).…”

Section: Cellular Events Associated With Antagonist-induced Contractimentioning

confidence: 99%

Pharmacological examination of contractile responses of the guinea‐pig isolated ileum produced by μ‐opioid receptor antagonists in the presence of, and following exposure to, morphine

Mundey

Ali

Mason

et al. 2000

British J Pharmacology

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1 We have assessed the potential of several m-opioid receptor antagonists to elicit a response in the guinea-pig isolated ileum in the presence of, and following overnight exposure to, morphine. 2 Naloxone, D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH 2 (CTOP), (7)-5,9a-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphan (MR2266), but not D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH 2 (CTAP), produced a transient inhibition of electrically-evoked contractions of the guinea-pig ileum. The eect of 1 mM CTOP, but not that to MR2266, was inhibited by 1 mM somatostatin. 3 Naloxone (0.3 mM), CTOP (3 mM), CTAP (3 mM) and MR2266 (0.3 mM) antagonized the inhibitory eect of morphine on electrically-evoked contractions of the guinea-pig to a similar degree and, following 60 min exposure to morphine, produced non-sustained contractions. The response to 3 mM CTOP was signi®cantly smaller than that to 3 mM CTAP. None of the antagonists produced a response in the absence of morphine. 4 Following overnight exposure of the ileum to 0.3 mM morphine (48C), and repeated washing to remove the agonist, all four antagonists elicited non-sustained contractions. However, the responses to 3 mM CTOP and 0.3 mM MR2266 were signi®cantly smaller than those elicited by 0.3 mM naloxone and 3 mM CTAP. Somatostatin (1 mM) signi®cantly reduced naloxone-induced contractions, but not those to CTAP. 5 While all four m-opioid antagonists elicited contractions in the presence of, and following prolonged exposure to, morphine, dierences between them were noted which may be a consequence of non-opioid actions.

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Section: Cellular Events Associated With Antagonist-induced Contractimentioning

confidence: 99%

Pharmacological examination of contractile responses of the guinea‐pig isolated ileum produced by μ‐opioid receptor antagonists in the presence of, and following exposure to, morphine

Mundey

Ali

Mason

et al. 2000

British J Pharmacology

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“…In AH/type 2 myenteric neurones, it produces membrane depolarization, increased input resistance and enhancement of excitability (Fig. 4;Nemeth et al 1986). …”

Section: Suppression Offorskolin-induced Excitationmentioning

confidence: 99%

“…Electrical behaviour characteristic of slow synaptic excitation occurs when adenylate cyclase is activated by forskolin (Nemeth, Palmer, Wood & Zafirov, 1986) or when intraneuronal cyclic AMP is elevated experimentally (Palmer, Wood & Zafirov, 1986c).…”

Section: Introductionmentioning

confidence: 99%

Purinergic inhibition in the small intestinal myenteric plexus of the guinea‐pig.

Palmer

Wood

Zafirov

1987

The Journal of Physiology

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SUMMARY1. The actions of adenosine on electrical behaviour of myenteric neurones were investigated with intracellular recording methods in guinea-pig small intestine.2. The actions of adenosine were: membrane hyperpolarization, decreased input resistance, enhancement of post-spike hyperpolarizing potentials and suppression of excitability. These effects were observed exclusively in AH/type 2 myenteric neurones.3. The presence of adenosine in the micromolar range of concentrations prevented or suppressed excitatory responses to forskolin. It also aborted the effects of forskolin when added in combination with this activator of adenylate cyclase. 5. The results suggest that the mechanism of the inhibitory action of adenosine is suppression of the catalytic activity of adenylate cyclase and consequent reduction of intraneuronal levels of cyclic AMP.

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“…A voltage-independent background potassium conductance and a voltage-dependent calcium-activated potassium conductance have been shown to be targeted by the so-called slow excitatory transmitters (Katayama & North, 1978;Grafe et al 1980;Surprenant, 1984;Mihara et al 1986; Surprenant, North & Katayama, 1987;Akasu & Tokimasa, 1989;Morita & Katayama, 1992). There is good indirect evidence to suggest that activation of the 'cyclic AMP cascade' is the primary intracellular transduction process involved in closure of potassium channels by most of these substances (Nemeth, Palmer, Wood & Zafirov, 1986;, 1987Akasu & Tokimasa, 1989). It is not known whether activation of each receptor present on a single enteric neurone will result in an identical cascade of intracellular transduction pathways and alterations in ionic conductances.…”

Section: Introductionmentioning

confidence: 99%

Common ionic mechanisms of excitation by substance P and other transmitters in guinea‐pig submucosal neurones.

Shen

Surprenant

1993

The Journal of Physiology

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SUMMARY1. Intracellular recordings were made from submucosal neurones and singleelectrode voltage-clamp methods were used to record membrane currents. The actions of substance P (SP), 5-hydroxytryptamine (5-HT), muscarine, vasoactive intestinal polypeptide (VIP), forskolin and nerve stimulation were studied.2. Substance P, 5-HT (in the presence of 5-HT3 receptor antagonists), muscarine, VIP, forskolin and slow excitatory synaptic transmission all produced identical responses: an inward current associated with a membrane conductance decrease at the resting potential. The actions of any one occluded the actions of any other and all responses were pertussis-toxin insensitive.3. These agonists produced a voltage-independent decrease in a 'leak' potassium conductance between -40 and -120 mV in 14 % of neurones.4. These agonists decreased a voltage-dependent, calcium-activated potassium conductance between -40 and -80 mV in all other (86 %) neurones. The agonists still evoked an inward current without apparent conductance change at potentials between -90 and -130 mV.5. In a low calcium solution containing cobalt or cadmium, the agonists produced an inward current associated with a conductance increase from -40 to -120 mV. Ion replacement studies indicated this current was due to an increase in a cationselective (mainly sodium) conductance.6. The agonists also reduced the inwardly rectifying potassium current that is activated by somatostatin and x2-adrenoceptor agonists in these neurones. The agonists did not alter the inwardly rectifying potassium current that is present in these neurones in the absence of somatostatin or a2-agonists. 7. Thus, SP, 5-HT, muscarine, VIP and the release of slow excitatory transmitters all appear to act through a common intracellular transduction pathway, an increase in adenylate cyclase. This results in an activation of a sodium-selective cation current and an inhibition of three distinct potassium conductances: the background potassium conductance, the calcium-activated potassium conductance and the inwardly rectifying potassium conductance activated by somatostatin and ac2-adrenoceptor agonists.

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Effects of forskolin on electrical behaviour of myenteric neurones in guinea‐pig small intestine.

Cited by 80 publications

References 20 publications

Pharmacological examination of contractile responses of the guinea‐pig isolated ileum produced by μ‐opioid receptor antagonists in the presence of, and following exposure to, morphine

Pharmacological examination of contractile responses of the guinea‐pig isolated ileum produced by μ‐opioid receptor antagonists in the presence of, and following exposure to, morphine

Purinergic inhibition in the small intestinal myenteric plexus of the guinea‐pig.

Common ionic mechanisms of excitation by substance P and other transmitters in guinea‐pig submucosal neurones.

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