Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim

Araki, Hiroaki; Kawashima, Kazuaki; Uchiyama, Yoshimi; Aihara, Hironaka

doi:10.1016/0014-2999(85)90078-0

Cited by 27 publications

(4 citation statements)

References 18 publications

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“…; Sigma-Aldrich) was dissolved in sterile saline and administered twice daily for 13 days (chronic) to rats. This dose of desipramine is a prototypical dose, displaying reliable antidepressant activity in animal models predictive of antidepressant activity, such as the rat FST (Araki et al, 1985;Kawashima et al, 1986). The drug was administered alone, simultaneous with i.c.v.…”

Section: Methodsmentioning

confidence: 99%

Brain-Derived Tumor Necrosis Factor-α and Its Involvement in Noradrenergic Neuron Functioning Involved in the Mechanism of Action of an Antidepressant

Reynolds

Ignatowski²,

Sud³

et al. 2004

J Pharmacol Exp Ther

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The present study documents a role for brain-derived tumor necrosis factor-␣ (TNF) in the mechanism of action of the antidepressant drug desmethylimipramine (desipramine). To establish this role, field stimulation and superfusion of rat hippocampal slices was employed to investigate the regulation of norepinephrine (NE) release by TNF. Chronic desipramine administration transforms TNF-mediated inhibition of NE release to facilitation, dependent upon ␣ 2 -adrenergic receptor activation. Chronic i.c.v. microinfusion of polyclonal TNF antibody (pTNF-Ab) similarly transforms TNF inhibition of NE release to facilitation. To determine whether this transformation is due to desipramine-induced inhibition of TNF bioactivity in the brain, rats were i.c.v. microinfused with recombinant rat TNF (rrTNF) for 14 days, either alone or with simultaneous i.p. desipramine administration. TNF regulation of NE release in hippocampal slices isolated from these rats was compared with slices isolated from rats chronically administered desipramine alone. Although simultaneous microinfusion of rrTNF with chronic desipramine administration prevents the transformation induced by desipramine, microinfusion of rrTNF enhances TNF inhibition of NE release. These cellular events correspond to changes in immobility, analyzed by the forced swim test (FST). Intracerebroventricular microinfusion of rrTNF increases the duration of immobility of rats in the FST, compared with rats microinfused with aCSF. Desipramine administered chronically decreases immobility duration, which is mimicked by i.c.v. microinfusion of pTNF-Ab and prevented by simultaneous i.c.v. microinfusion of rrTNF. Thus, i.c.v. microinfusion of rrTNF with concomitant desipramine administration opposes decreases in neuron-associated TNF levels, required to transform presynaptic sensitivity to TNF, which is necessary for the drug to be efficacious.The etiology of depression as well as the mechanism of action of antidepressant drugs has been investigated for over 40 years, yet precise mechanisms that direct the expression of mood are unknown. Several theories have been postulated that implicate altered release of the neurotransmitter norepinephrine (NE) (Schildkraut, 1965) in the pathogenesis of depression. The classic Monoamine Theory of Depression proposes that symptoms of depression are due to an imbalance in the bioavailability of the monoamines, NE and serotonin, within the central nervous system (Schildkraut, 1965;Willner, 1985). Therefore, antidepressant drug-induced regulation of NE availability, as well as adrenergic receptors that regulate the release of NE, have been extensively investigated (Banerjee et al., 1977;Crews and Smith, 1978). A "dysregulation hypothesis" has also been proposed, which implicates an impaired negative feedback on presynaptic neurons due to dysfunctional presynaptic ␣ 2 -adrenergic receptors (Siever and Davis, 1985;Maes et al., 1999). These receptors are primary regulators of NE release from noradrenergic neurons and are classically known to ...

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Section: Methodsmentioning

confidence: 99%

Brain-Derived Tumor Necrosis Factor-α and Its Involvement in Noradrenergic Neuron Functioning Involved in the Mechanism of Action of an Antidepressant

Reynolds

Ignatowski²,

Sud³

et al. 2004

J Pharmacol Exp Ther

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“…The mesolimbic DA system plays an important role in orchestrating adaptive behavior under stress [2,5] and in learning and memory processes [2,14]. Evidence for the involvement of mesolimbic DA structures in mediating the effects o f antidepressants has also been reported [6,7].…”

Section: Resultsmentioning

confidence: 98%

Effects of amphazide (a hydrazide of phosphorylated carboxylic acids) and tetramezine (a diaziridine derivative) on central dopaminergic structures

1996

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Amphazide and tetramezine, two recently synthesized compounds with antidepressant and nootropic activities; were found to have dopamine-positive activity in animals injected with apomorphine, L-Dopa, or haloperidol. Amphazide expressed this activity in most tests only when given in multiple doses, whereas tetramezine expressed it well even after a single dose.Key Words: amphazide; tetramezine; dopamine-positive activity Dopaminergic (DA) structures are involved in memory processes, promoting the recall of what was learned long ago [13,15] and, when activated, contributing to effective restoration of forgotten habits [15]. There is evidence that the DA system is implicated in mediating the effects of certain antidepressants [1,3].The purpose of this study was to investigate how central DA structures might be influenced by two recently synthesized compounds with antidepressant and nootropic activities --amphazide, which is a hydrazide of phosphorylated carboxylic acids, and tetramezine, which is a diaziridine derivative. MATERIALS AND METHODSThe study was conducted on 170 random-bred mice (body weight 17-22 g) and 50 random-bred rats (body weight 150-200 g).Amphazide and tetramezine (TM) were injected intraperitoneally at 90 mg/kg body weight either once or ten times once daily, and their effects on apomorphine-induced hypothermia and stereotypy, LDopa-induced hypothermia and alterations in exploratory and motor activities, and haloperidol-induced catalepsy were evaluated. State Medical University, KazanHypothermia was produced in mice by a subcutaneous injection of apomorphine at 25 mg/kg, and their body temperature was recorded with an electric thermometer 1 and 2 h postinjection.The total duration of sterotypy and the intensities of its components (licking, sniffing, and gnawing) were measured in rats 1 h after a subcutaneous injection of apomorphine at 20 mg/kg. Skin temperature and exploratory and motor activities (the number of holes explored and of lines crossed in an open field) were recorded in mice 1 h after a subcutaneous injection of L-Dopa at 150 mg/kg.The severity of catalepsy was evaluated by the ability of mice to retain an awkward posture (with the hind legs on a support 30 mm high and the forelegs on the table) for 60 sec at 10, 60, and 120 min after haloperidol injection at 5 mg/kg.The results were statistically analyzed by Student's t test. RESULTSAmphazide potentiated the effects of apomorphine only in multiple doses, enhancing the hypothermia in mice (Fig. 1) and prolonging the stereotypy in rats (Table 1); the recording of individual stereotypy components in rats showed longer sniffing times in comparison with the control group. In contrast, TM

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“…A role of MeA in behavioral responses in the FST is supported by evidence obtained in non-stressed animals that demonstrated decrease in immobility following local MeA treatment with imipramine or a selective V 1b receptor antagonist [ 32 , 34 ]. Regarding angiotensinergic receptors in the MeA, we reported recently that MeA treatment with losartan decreased the immobility time in the FST in non-stressed animals [ 42 ].…”

Section: Discussionmentioning

confidence: 97%

“…The role of MeA in depressive-like behaviors is supported by evidence that intra-MeA microinjection of tricyclic antidepressants, V 1b receptor antagonist, the monoamine oxidase inhibitor antidepressant drug minaprine or estradiol decreased immobility in the FST [ 31 , 32 , 33 ]. Besides, lesion of catecholaminergic terminals within the MeA inhibited the antidepressant-like effect evoked by systemic injection of tricyclic antidepressants and electroconvulsive shock [ 34 , 35 ]. However, the local neurochemical mechanisms involved in behavioral control by MeA is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Angiotensinergic Neurotransmissions in the Medial Amygdala Nucleus Modulate Behavioral Changes in the Forced Swimming Test Evoked by Acute Restraint Stress in Rats

Marchi-Coelho

Costa-Ferreira

Reis‐Silva

et al. 2021

Cells

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We investigated the role of angiotensin II type 1 (AT1 receptor) and type 2 (AT2 receptor) and MAS receptors present in the medial amygdaloid nucleus (MeA) in behavioral changes in the forced swimming test (FST) evoked by acute restraint stress in male rats. For this, rats received bilateral microinjection of either the selective AT1 receptor antagonist losartan, the selective AT2 receptor antagonist PD123319, the selective MAS receptor antagonist A-779, or vehicle 10 min before a 60 min restraint session. Then, behavior in the FST was evaluated immediately after the restraint (15 min session) and 24 h later (5 min session). The behavior in the FST of a non-stressed group was also evaluated. We observed that acute restraint stress decreased immobility during both sessions of the FST in animals treated with vehicle in the MeA. The decreased immobility during the first session was inhibited by intra-MeA administration of PD123319, whereas the effect during the second session was not identified in animals treated with A-779 into the MeA. Microinjection of PD123319 into the MeA also affected the pattern of active behaviors (i.e., swimming and climbing) during the second session of the FST. Taken together, these results indicate an involvement of angiotensinergic neurotransmissions within the MeA in behavioral changes in the FST evoked by stress.

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Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim

Cited by 27 publications

References 18 publications

Brain-Derived Tumor Necrosis Factor-α and Its Involvement in Noradrenergic Neuron Functioning Involved in the Mechanism of Action of an Antidepressant

Brain-Derived Tumor Necrosis Factor-α and Its Involvement in Noradrenergic Neuron Functioning Involved in the Mechanism of Action of an Antidepressant

Effects of amphazide (a hydrazide of phosphorylated carboxylic acids) and tetramezine (a diaziridine derivative) on central dopaminergic structures

Angiotensinergic Neurotransmissions in the Medial Amygdala Nucleus Modulate Behavioral Changes in the Forced Swimming Test Evoked by Acute Restraint Stress in Rats

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