Chronic Methamphetamine Alters Neural Oscillations and Synaptic Plasticity in the Hippocampus in Guinea Pigs, In Vivo
Location
Suwanee, GA
Start Date
15-5-2018 1:00 PM
Description
Chronic methamphetamine (METH) users perform poorly compared to controls on memory tasks. The neural mechanisms that underlie these deficits are unclear. This was the focus of the study. We treated male guinea pigs with 10 mg/kg/day METH (N=12) or phosphate buffered saline (PBS, N= 8) for 7 days. Drugs were continuously infused using ALZET mini-pumps. After 7 days of treatment a subset of guinea pigs from each group (METH = 6 and PBS = 4) were anesthetized with urethane (1500 mg/kg) and local field potentials across the CA3/CA1 synapses were obtained from the hippocampus in vivo. Similar recordings were conducted in the remaining subset of guinea pigs (i.e., METH = 6 and PBS = 4) after 7 days of drug washout. We found that METH-treated guinea pigs had increased spontaneous cell discharges and had reduced slow wave oscillations. By contrast, PBS controls exhibited fewer spontaneous discharges and had prominent slow wave oscillations whose peaks contained robust ‘ripples’, a hallmark of transfer of information from the hippocampus to neocortical structures. We also found that long-term potentiation (LTP, a cellular correlate of learning and memory) was attenuated in the METH-treated guinea pigs compared to PBS controls. The effects of METH on CA1 cell discharges, oscillations and LTP were still present even after the 7-day washout. Our results show that METH-induced changes to CA1 network properties may partly underlie the reported memory impairments associated with the drug.
Embargo Period
8-14-2018
Chronic Methamphetamine Alters Neural Oscillations and Synaptic Plasticity in the Hippocampus in Guinea Pigs, In Vivo
Suwanee, GA
Chronic methamphetamine (METH) users perform poorly compared to controls on memory tasks. The neural mechanisms that underlie these deficits are unclear. This was the focus of the study. We treated male guinea pigs with 10 mg/kg/day METH (N=12) or phosphate buffered saline (PBS, N= 8) for 7 days. Drugs were continuously infused using ALZET mini-pumps. After 7 days of treatment a subset of guinea pigs from each group (METH = 6 and PBS = 4) were anesthetized with urethane (1500 mg/kg) and local field potentials across the CA3/CA1 synapses were obtained from the hippocampus in vivo. Similar recordings were conducted in the remaining subset of guinea pigs (i.e., METH = 6 and PBS = 4) after 7 days of drug washout. We found that METH-treated guinea pigs had increased spontaneous cell discharges and had reduced slow wave oscillations. By contrast, PBS controls exhibited fewer spontaneous discharges and had prominent slow wave oscillations whose peaks contained robust ‘ripples’, a hallmark of transfer of information from the hippocampus to neocortical structures. We also found that long-term potentiation (LTP, a cellular correlate of learning and memory) was attenuated in the METH-treated guinea pigs compared to PBS controls. The effects of METH on CA1 cell discharges, oscillations and LTP were still present even after the 7-day washout. Our results show that METH-induced changes to CA1 network properties may partly underlie the reported memory impairments associated with the drug.