Animal experiment:

Rats: The Wistar (WIS) and Wistar Kyoto (WKY) rats are divided into four groups: (1) a control WIS rat group, (2) an imipramine-treated WIS rat group, (3) a control WKY rat group and (4) an imipramine-treated WKY rat group. Distilled water (10 mL/kg) or imipramine solution (10 mg/10 mL/kg) is orally administered for 28 days except on the day of the open field test, when nothing is administered in order to avoid the acute effect of single administration on the open field test[5]. Mice: C57BL/6 mice subjected to repeated social defeat (RSD), home cage control (HCC) are randomLy selected into four groups: RSD/imipramine, RSD/vehicle, HCC/imipramine, and HCC/vehicle. Mice in the RSD/imipramine received daily intraperitoneal (i.p.) injections of imipramine (20 mg/kg) for 24 days after the 6 cycles of RSD. HCC/imipramine received daily i.p. imipramine at the same dose while RSD/vehicle and HCC/vehicle groups received i.p. injections of vehicle (sodium chloride, 0.9%) for 24 days at the same time point[3].

Imipramine (hydrochloride) is a tricyclic antidepressant and is mainly used in the treatment of major depression and enuresis [1].

Antidepressants are antagonists of many neurotransmitter receptors in human brain [3].

Imipramine is the first tricyclic antidepressant that acts mainly as an inhibitor of serotonin and norepinephrine transporters [2]. In radioligand binding assays, imipramine inhibited serotonin and norepinephrine transporters with KD values of 1.4 and 37 nM, respectively [2]. Imipramine is also inhibited histamine H1 receptor, muscarinic acetylcholine receptor and α1-adrenergic receptor with Kd values of 37, 46, and 32 nM, respectively [4].

In rodents, imipramine abolished the depressive syndrome produced by the acute administration of reserpine. Imipramine also possessed central anticholinergic activity and attenuate the activity of the centrally acting muscarinic agents tremorine and oxotremorine. Imipramine inhibited the presynaptic uptake of NA and 5-HT, and relatively weak against DA [1].

References:
[1].  Spencer PS. Review of the pharmacology of existing antidepressants. Br J Clin Pharmacol. 1977;4Suppl 2:57S-68S.
[2].  Tatsumi M, Groshan K, Blakely RD, et al. Pharmacological profile of antidepressants and related compounds at human monoamine transporters. Eur J Pharmacol. 1997 Dec 11;340(2-3):249-58.
[3].  Cusack B, Nelson A, Richelson E. Binding of antidepressants to human brain receptors: focus on newer generation compounds. Psychopharmacology (Berl). 1994 May;114(4):559-65.