Effects of Iprindole on Responses of Single Cortical and Caudate Neurones to Monoamines and Acetylcholine

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1 The technique of microelectrophoresis was used in order to compare the actions of L-3,4-dihydroxyphenylalanine (DOPA) and noradrenaline on single neurones in the cerebral cortices of cats and rats. 2 DOPA could both excite and depress cortical neurones. Cells excited by DOPA were also excited by noradrenaline and cells depressed by DOPA were also depressed by noradrenaline. 3 In the case of both excitatory and depressant responses, DOPA appeared to be less potent than noradrenaline. 4 Responses to DOPA and noradrenaline could be antagonized by phentolamine and propranolol. Responses to acetylcholine were not affected. 5 Responses to acetylcholine, but not responses to DOPA, were antagonized by atropine. 6 The results indicate that locally applied DOPA may mimic the actions of noradrenaline on cortical neurones. Possible mechanisms for these effects of DOPA are discussed.

Section: Methodsmentioning

confidence: 99%

The Action of Micro‐electrophoretically Applied 1‐3,4‐dihydroxyphenylalanine (Dopa) on Single Cortical Neurones

Bevan

Bradshaw

Szabadi

1976

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“…The oxygen-halothane mixture was administered through a face-mask throughout the experiment. The methods for the surgical preparation of the animals, and the manufacture of multi-barrelled glass micropipettes for extracellular recording and microelectrophoretic drug application, have been described elsewhere (Bradshaw, Roberts & Szabadi, 1973a;Bradshaw, Szabadi & Roberts, 1973b;Bevan et al, 1975).…”

Section: Methodsmentioning

confidence: 99%

“…Recent evidence indicates that these responses are mediated by pharmacologically distinct receptors: the excitatory responses by a-adrenoceptors, and the depressant responses by ,B-adrenoceptors (Bevan, Bradshaw & Szabadi, 1977). Dopamine, like NA, can both excite and depress cortical neurones (Bevan, Bradshaw & Szabadi, 1975;Stone, 1976;Bunney & Aghajanian, 1976;Sharma, 1977). Evidence has recently been obtained suggesting that the excitatory responses to the catecholamines may be mediated by two populations of receptors: a-adrenoceptors and specific excitatory dopamine receptors (Bevan, Bradshaw, Pun, Slater & Szabadi, 1978).…”

Section: Introductionmentioning

confidence: 99%

The Action of Microelectrophoretically Applied (3,4‐dihydroxy‐phenylamino)‐2‐imidazoline (Dpi) on Single Cortical Neurones

Bevan

Bradshaw

Pun

et al. 1979

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1The technique of microelectrophoresis was used in order to compare the actions of the imidazoline derivative, (3,4-dihydroxy-phenylamino-2-imidazoline (DPI), with those of dopamine and phenylephrine on single neurones in the cerebral cortex of the rat anaesthetized with halothane. 2 DPI and phenylephrine were almost exclusively excitatory, whereas dopamine could evoke both excitatory and depressant responses. 3 In the case of excitatory responses, DPI appeared to be more potent than dopamine, and was approximately equipotent with phenylephrine. 4 The dopamine antagonist, haloperidol, could discriminate between excitatory responses to DPI and dopamine: responses to dopamine were abolished, whereas responses to DPI, and to a control agonist, acetylcholine, were unaffected. 5 The a-adrenoceptor antagonist, phenoxybenzamine, antagonized equally excitatory responses to DPI and phenylephrine. Responses to acetylcholine were not affected. 6 It is concluded that DPI does not stimulate dopamine receptors on cortical neurones; the excitatory responses of these cells to DPI may be mediated by ac-adrenoceptors.

“…0007-1188/79/030501-10 $01.00 gest that ACh is inactivated by reuptake in the CNS (Katz & Chase, 1971). Further experiments showed that iprindole, a tricyclic with little effect on NA uptake (Gluckman & Baum, 1969), could potentiate neuronal responses to this amine (Bevan, Bradshaw & Szabadi, 1975a).…”

Section: Introductionmentioning

confidence: 99%

“…Further experiments showed that iprindole, a tricyclic with little effect on NA uptake (Gluckman & Baum, 1969), could potentiate neuronal responses to this amine (Bevan, Bradshaw & Szabadi, 1975a).…”

Section: Introductionmentioning

confidence: 99%

Potentiation of Responses to Monoamines by Antidepressants After Destruction of Monoamine Afferents

Jones

Roberts²

1979

1Stereotaxic lesioning and microiontophoretic techniques were used to study the effects of lesions of the medial forebrain bundle (MFB) on the potentiation by antidepressant drugs of responses to monoamines of cortical neurones. 2 Active uptake of noradrenaline (NA) and 5 hydroxytryptamine (5-HT) by synaptosomes from the motor and somatosensory cortex was reduced to approximately 20%, 10 to 14 days following lesion of the MFB in rats. 3 Unilateral lesions of the MFB caused changes in responsiveness of neurones to NA and 5-HT, applied by iontophoresis, in the cortex ipsilateral to the lesion. Excitatory responses to both amines were observed less frequently and depression was the predominant response. Excitatory responses on the lesioned side were significantly smaller than on the unlesioned side, but the size of depressant responses was unaltered. 4 Viloxazine strongly potentiated responses of cortical neurones to NA and 5-HT on both sides of the brain of MFB-lesioned rats. There were no significant differences in the potentiation of responses to monoamines on the lesioned or unlesioned sides of the brain. 5 Desipramine potentiated responses to NA of neurones in the cortex ipsilateral to MFB lesions. 6 Chlorimipramine potentiated responses to 5-HT of neurones in the cortex ipsilateral to MFB lesions. 7 It is concluded that antidepressants can potentiate responses to monoamines despite a profound reduction in presynaptic terminals. The potentiation is unlikely to be the result of blockade of monoamine uptake into presynaptic terminals, and is probably a postsynaptic effect of the antidepressant drugs.