The effect of selective opioid receptor agonists and antagonists on epileptiform activity in morphine-dependent infant mice hippocampal slices

Hippocampal slices of mouse brain were used to estimate how selective agonist and antagonist of opioid
receptors alter Low-Mg+2 artificial cerebrospinal fluid (LM-ACSF)-induced epileptiform activities in normal and
morphine-dependent mice. Brain slices were obtained from control and morphine-dependent mice. The
morphine-dependent group received morphine once a day for 5 consecutive days, and the control group
received saline. All injections were administered subcutaneously (s.c) in a volume of 0.1 mL on postnatal days
14–18. Brain slices were perfused with LM-ACSF along with selective agonist and antagonist of μ, κ and δ opioid
receptors. Changes in spike count per unit of time were used as indices to quantify the effects of LM-ACSF
exposure in the slices. In both groups, DAMGO (selective μ opioid receptor agonist) and DPDPE (selective δ
opioid receptor agonist) suppressed while Dyn-A (selective κ opioid receptor agonist) potentiated the epileptiform activity. Meanwhile, BFN-A (selective μ opioid receptor antagonist) recovered epileptiform activity in
normal brain slices but not in morphine-dependent ones. NTI (selective δ opioid receptor antagonist) and norBNI (selective κ opioid receptor antagonist) decreased epileptiform activity. It seems that the excitatory effect of
morphine on epileptiform activity was mediated through kappa receptors and its inhibitory effect was mediated
via the mu receptor and, to a lesser degree, through the delta receptor. The pattern of effect was similar in
normal and morphine-dependent slices, but the intensity of the effect was significantly stronger in normal mice.
Finding of this study might be considered for further research and attention in epilepsy treatment