The Quinpirole Hypolocomotive Effects are Strain and Route of Administration Dependent in SHR and SLA16 Isogenic Rats

Abstract

The SHR and SLA16 inbred strains present behavioral differences in anxiety/emotionality that could be under the influence of dopaminergic neurotransmission. In order to investigate the role of D2 receptors in modulating such differences, an agonist (quinpirole) and an antagonist (haloperidol) of this receptor were administered, either via systemic injection (IP), or microinjected into the ventral area of the hippocampus (vHIP). Quinpirole and haloperidol IP decreased locomotor activity, only in SLA16 rats in the open-field (OF), and in both strains in the elevated plus-maze (EPM). Quinpirole also increased the preference for the aversive areas of the EPM. Quinpirole vHIP decreased locomotor activity in both strains. Haloperidol vHIP did not elicit behavioural changes and no differences in the levels of D2 receptors and of dopamine transporter in the hippocampus were found. Results indicate that systemic activation/blocking of D2 receptors caused a strain-dependent hypolocomotion, whereas activation of D2 receptors in the vHIP, but not D2 receptor antagonism, regardless of dose, decreased general locomotor activity in the two strains. Therefore, we suggest that genomic differences in the chromosome 4 can influence the locomotor activity regulated by the D2 dopaminergic receptor, especially in the vHIP.

The Distinct Functions of Dopaminergic Receptors on Pain Modulation: A Narrative Review

“…Briefly, systematic administration of a high dosage of quinpirole may have affected the locomotor and exploratory activities of rats, while IT infusion of low doses had no significant effect on locomotion. Besides, the effects of D2 receptor agonists on locomotion might be strain-dependent, as shown in spontaneously hypertensive Neural Plasticity rat (SHR) and SLA16 isogenic (SHR.Lewis-Anxrr16; anxietyrelated response #16) rat strains [53]. In summary, the dosage of drugs, route of administration, and strain of animals should be considered when investigating the possible analgesic effects of DAergic drugs.…”

Dopaminergic Modulation of Orofacial Mechanical Hypersensitivity Induced by Infraorbital Nerve Injury

“…The A11 nucleus contains almost 2.5 times more GABA-containing neurons as compared with dopamine-containing neurons, and noxious facial stimulation activates GABA-containing neurons in the A11 nucleus [15], suggesting that GABA-containing neurons in the A11 nucleus might be involved in the regulation of dopaminergic neuron activity. Dopamine D2 agonist and GABA A receptor agonist were reported to affect motor function [33][34][35][36]. Therefore, the change of head-withdrawal threshold measured in our study might be the result of not only attenuation of mechanical hypersensitivity but also change of motor function by quinpirole and muscimol.…”

Deciphering Spinal Endogenous Dopaminergic Mechanisms That Modulate Micturition Reflexes in Rats with Spinal Cord Injury

“…All drugs were prepared in three concentrations to examine the effects of low, middle and high doses administered sequentially at an interval of at least 30 min ( Table 1 ). The half-life information of each drug except SKF 38393 ( Setler et al, 1978 ) was available in the literature: 1.5 h for L-DOPA ( Calabrese et al, 2007 ; Contin and Martinelli, 2010 ), 1.8 h for carbidopa ( Brooks, 2008 ), 33 min for APO ( Gancher, 1995 ), 4.8 h for remoxipride ( King et al, 1990 ; Movin-Osswald and Hammarlund-Udenaes, 1991 ), 9.5 h for quinpirole ( Ballester González et al, 2015 ; Pértile et al, 2017 ), and 30 min for SCH 23390 ( Hietala et al, 1992 ; Giorgi et al, 1993 ). When L-DOPA was tested, rats also received carbidopa (in a 1:10 ratio to the dose of L-DOPA) in the solution to inhibit peripheral effects of L-DOPA, as described below.…”