title: Morphine dependence increases the response to a brief pentylenetetrazol administration in rat hippocampal CA1 in vitro.
abstract: OBJECTIVE
  Herein we used electrophysiologic approaches in hippocampal area CA1 to estimate how morphine treatment alters the pentylenetetrazol (PTZ) effects.
  
  
  METHODS
  Hippocampal slices taken from either control animals or animals made dependent via chronic morphine administration were examined. Changes in the population spike and epileptiform amplitudes were used as indices to quantify the effects of PTZ exposure in the control and morphine-dependent slices. Hippocampal slices taken either from control animals or from animals made dependent upon morphine were exposed to PTZ, either with or without morphine, naloxone, or morphine + naloxone.
  
  
  RESULTS
  Morphine dependence increased a PTZ-induced long-term potentiation (LTP) of the population spike in CA1 in vitro. This LTP was not found in rats that had spontaneously withdrawn morphine or withdrawn with naloxone in vivo after chronic morphine intake. Morphine or naloxone in vitro blocked the PTZ-induced LTP changes in control and morphine-dependent slices. However, PTZ-induced multiple population spikes (epileptiform activity) in CA1 was not blocked by naloxone.
  
  
  CONCLUSIONS
  It is concluded that dependence on morphine enhances PTZ-induced plastic and epileptic changes in CA1 excitability. We suggest that this model of neuronal activity in dependent slices could present an opportunity for studying the mechanisms underlying the increased likelihood of seizures in morphine users.
authors.affiliation: Department of Physiology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
authors.forename: Zakaria
authors.initials: Z
authors.lastname: Jafarzadeh
authors.forename: Yaghoub
authors.initials: Y
authors.lastname: Fathollahi
authors.forename: Saeed
authors.initials: S
authors.lastname: Semnanian
authors.forename: Azar
authors.initials: A
authors.lastname: Omrani
authors.forename: Feresteh
authors.initials: F
authors.lastname: Salmanzadeh
authors.forename: Mahmoud Elahdadi
authors.initials: ME
authors.lastname: Salmani
mesh_terms: D000818:Animals; D003292:Convulsants / Q000494:pharmacology*; D004195:Disease Models, Animal; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology*; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology*; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology; D008297:Male; D009020:Morphine / Q000008:administration & dosage; D009021:Morphine Dependence / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009294:Narcotics / Q000008:administration & dosage; D009434:Neural Pathways / Q000502:physiology; D010433:Pentylenetetrazole / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D018709:Statistics, Nonparametric; D013375:Substance Withdrawal Syndrome / Q000473:pathology / Q000503:physiopathology
chemical_list: D003292:Convulsants; D009292:Narcotic Antagonists; D009294:Narcotics; D009270:Naloxone; D009020:Morphine; D010433:Pentylenetetrazole