5‐HT<sub>2</sub> receptor characteristics in frontal cortex and 5‐HT<sub>2</sub> receptor‐mediated head‐twitch behaviour following antidepressant treatment to mice

Goodwin, Guy M.; Green, A R; Johnson, Peter M.

doi:10.1111/j.1476-5381.1984.tb10140.x

Cited by 158 publications

(50 citation statements)

References 33 publications

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“…These drugs are able to augment 5-HT transmission by prolonging the residence time of 5-HT in the synaptic cleft (Caldecott-Hazard et al 1991;Wong et al 1990). The majority of antidepressant drugs administered repeatedly to rats, decreased the number of 5-HT2 receptor sites and their function measured as the head-twitch response (Goodwin et al 1984;Green 1987;Peroutka and Snyder 1980). In contrast to the data obtained with administration of drugs, repeated electroconvulsive shock was found to increase the number and function of 5-HT2 receptors (Green et al 1983;Kellaret al 1981;Vetulani et al 1981).…”

Section: Introductionmentioning

confidence: 56%

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Klimek

Zak-Knapik

Pietrasiewicz

1992

Clinical Neuropharmacology

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Section: Introductionmentioning

confidence: 56%

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Klimek

Zak-Knapik

Pietrasiewicz

1992

Clinical Neuropharmacology

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“…It is difficult to predict what the increased GABA9 response would do in terms of overall transynaptic 5-HT function. Cortical postsynaptic 5-HT2 receptors in mice are decreased by antidepressant drugs but increased by ECS (Goodwin et al, 1984). In rats postsynaptic 5-HTIA receptor function has been shown to be decreased by both ECS and antidepressant drugs, although the behavioural response examined is unlikely to have been initiated in the frontal cortex (Goodwin et al, 1987).…”

Section: Discussionmentioning

confidence: 97%

Increased GABA_B receptor function in mouse frontal cortex after repeated administration of antidepressant drugs or electroconvulsive shocks

Gray¹,

Green²

1987

British J Pharmacology

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Addition of baclofen to a medium containing slices of mouse frontal cortex inhibited the potassium‐evoked release of 5‐hydroxytryptamine (5‐HT) in a concentration‐dependent manner. The degree of inhibition was increased in frontal cortex tissue taken from animals treated for 14 days with amitriptyline (10 mg kg−1, twice daily) at all concentrations of baclofen tested (10−6 m − 10−4 m). Administration of either desipramine, mianserin or zimeldine (10 mg kg−1 daily) for 14 days also approximately doubled the degree of inhibition evoked by addition of baclofen (10−5 m) to the medium. One day of treatment with the antidepressant drugs did not alter the inhibitory effect of baclofen on K+‐evoked 5‐HT release. Addition of the antidepressant drugs to the medium had no effect on the K+‐evoked release of 5‐HT. Repeated administration of electroconvulsive shock (5 seizures spread out over 10 days), like amitriptyline, produced a significant enhancement of the baclofen‐induced inhibition of 5‐HT release over the range of baclofen concentrations studied. A single electroconvulsive shock had no effect. These data suggest that repeated administration of the antidepressant drugs or electroconvulsive shock increases the function of the γ‐aminobutyric acid (GABA)B receptor in the frontal cortex modulating 5‐HT release and are consistent with the finding of increased GABAB receptor number in this region following various antidepressant treatments.

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“…The relevance of the enhanced head-twitch response to the antidepressant effect of ECS is unclear since many antidepressant drugs decrease this behavioural change (Ogren et al, 1979;Goodwin et al, 1984). Furthermore, diazepam, which is not an antidepressant, has now also been found to increase the headtwitch response and [3H]-spiperone binding, thereby tending to rule out a crucial role for this change in any antidepressant effect.…”

Section: Implicationsfor the Action Ofantidepressant Treatmentsmentioning

confidence: 99%

Some anticonvulsant drugs alter monoamine‐mediated behaviour in mice in ways similar to electroconvulsive shock; implications for antidepressant therapy

Green¹,

Johnson²,

Mountford³

et al. 1985

British J Pharmacology

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1 The effects in mice of administration of the anticonvulsants, progabide, sodium valproate, diazepam, carbamazepine and phenytoin on 5-hydroxytryptophan (5-HTP)-induced head-twitch, apomorphine-induced locomotion, clonidine-induced sedation, and P-adrenoceptor and 5-HT2 receptor number have been examined. 2 Repeated progabide administration (400 mg kg-', i.p. twice daily for 14 days) enhanced the headtwitch response the effect lasting for over 8 days after the last dose, and also increased 5-HT2 receptor number in frontal cortex. 3 Progabide (400 mg kg-', i.p.) enhanced the head-twitch response when given once daily for 10 days and when given intermittently (5 times over 10 days) but not after 1 day of administration. 4 Repeated Na valproate (400mg kg-',i.p.) also increased the 5-HTP-induced head-twitch response and 5-HT2 receptor number in the frontal cortex when given twice daily for 14 days, but no behavioural enhancement was seen after 10 days' treatment. 5 Diazepam (1.25 mg kg-', i.p.) twice daily for 14 days increased the head-twitch response and 5-HT2 receptor number. 6 Repeated progabide and valproate (but not diazepam) administration attenuated the sedation response to the a2-adrenoceptor agonist, clonidine (0.15mg kg-') but neither drug altered 1-adrenoceptor number in the cerebral cortex. 7 No changes in apomorphine-induced locomotor behaviour were seen after progabide, valproate or diazepam.8 Repeated carbamazepine (20 mg kg-') or phenytoin (40 mg kg-1) administration failed to alter any of the biochemical or behavioural parameters listed above. 9 Like repeated electroconvulsive shock (ECS), progabide altered the head-twitch response, clonidine-induced sedation response and 5-HT2 receptor number. Unlike repeated ECS, it did not alter P-adrenoceptor number or the apormorphine-induced locomotor response. These data suggest that ECS may produce some changes in monoamine function by altering GABA metabolism as has previously been postulated.

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5‐HT₂ receptor characteristics in frontal cortex and 5‐HT₂ receptor‐mediated head‐twitch behaviour following antidepressant treatment to mice

Cited by 158 publications

References 33 publications

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Increased GABA_B receptor function in mouse frontal cortex after repeated administration of antidepressant drugs or electroconvulsive shocks

Some anticonvulsant drugs alter monoamine‐mediated behaviour in mice in ways similar to electroconvulsive shock; implications for antidepressant therapy

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5‐HT2 receptor characteristics in frontal cortex and 5‐HT2 receptor‐mediated head‐twitch behaviour following antidepressant treatment to mice

Cited by 158 publications

References 33 publications

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Effects of Repeated Treatment With Fluoxetine and Citalopram, a 5-Ht Uptake Inhibitors on 5-Ht1a and 5-Ht2 Receptors in the Rat Brain.

Increased GABAB receptor function in mouse frontal cortex after repeated administration of antidepressant drugs or electroconvulsive shocks

Some anticonvulsant drugs alter monoamine‐mediated behaviour in mice in ways similar to electroconvulsive shock; implications for antidepressant therapy

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5‐HT₂ receptor characteristics in frontal cortex and 5‐HT₂ receptor‐mediated head‐twitch behaviour following antidepressant treatment to mice

Increased GABA_B receptor function in mouse frontal cortex after repeated administration of antidepressant drugs or electroconvulsive shocks