A distinct impact of repeated morphine exposure on synaptic plasticity at Schaffer collateral‐CA1, temporoammonic‐CA1, and perforant pathway‐dentate gyrus synapses along the longitudinal axis of the hippocampus

Abstract

We aimed to study how morphine affects synaptic transmission in the dentate gyrus and CA1 regions along the hippocampal long axis. For this, recording and measuring of field excitatory postsynaptic potentials (fEPSPs) were utilized to test the effects of repeated morphine exposure on paired-pulse evoked responses and long-term potentiation (LTP) at Schaffer collateral-CA1 (Sch-CA1), temporoammonic-CA1 (TA-CA1) and perforant pathway-dentate gyrus (PP-DG) synapses in transverse slices from the dorsal (DH), intermediate (IH), and ventral (VH) hippocampus in adult male rats. After repeated morphine exposure, the expression of opioid receptors and the α1 and α5 GABA A subunits were also examined. We found that repeated morphine exposure blunt the difference between the DH and the VH in their basal levels of synaptic transmission at Sch-CA1 synapses that were seen in the control groups. Significant paired-pulse facilitation of excitatory synaptic transmission was observed at Sch-CA1 synapses in slices taken from all three hippocampal segments as well as at PP-DG synapses in slices taken from the VH segment in the morphine-treated groups as compared to the control groups. Interestingly, significant paired-pulse inhibition of excitatory synaptic transmission was observed at TA-CA1 synapses in the DH slices from the morphine-treated group as compared to the control group. While primedburst stimulation (a protocol reflecting normal neuronal firing) induced a robust LTP in hippocampal subfields in all control groups, resulting in a decaying LTP at TA-CA1 synapses in the VH slices and at PP-DG synapses in both the IH and VH slices taken from the morphine-treated rats. In the DH of morphine-treated rats, we found increased levels of the mRNAs encoding the α1 and α5 GABA A subunits as compared to the control group. Taken together, these findings suggest the potential mechanisms through which repeated morphine exposure causes differential changes in circuit excitability and synaptic plasticity in the dentate gyrus and CA1 regions along the hippocampal long axis.

Avoidance and escape conditioning adjust adult neurogenesis to conserve a fit hippocampus in adult male rodents

“…Herein, consistent with previous reports (Anvari et al, 2023;Dubovyk & Manahan-Vaughan, 2018;Kenney & Manahan-Vaughan, 2013;Maggio & Segal, 2007;Papatheodoropoulos & Kostopoulos, 2000;Schreurs et al, 2017), LTP of synaptic transmission at PP-DG synapses was characterized with a different profile along the hippocampal long axis.…”

Acute adolescent morphine exposure improves dark avoidance memory and enhances long‐term potentiation of ventral hippocampal CA1 during adulthood in rats

“…The hippocampus was immediately dissected, and the ventral part of the hippocampus was separated and glued to a piece of agar jelly (3 g of agar powder dissolved in 70 mL distilled water) on the stage of a vibroslicer (Campden Instrument, NVSLM1, Sarasota FL, USA) and was immediately immersed in cold aCSF. Transverse slices (400 μm) were cut and transferred to a recovery chamber that was continuously perfused at a rate of 2 mL/min with aCSF at room temperature (22–25°C), and the slices were left there for 1.5 h recovery time before the start of the recording 24 …”

“…Transverse slices (400 μm) were cut and transferred to a recovery chamber that was continuously perfused at a rate of 2 mL/min with aCSF at room temperature (22-25 C), and the slices were left there for 1.5 h recovery time before the start of the recording. 24…”