Prenatal cocaine exposure leads to enhanced long-term potentiation in region CA1 of hippocampus.
*Prenatal Exposure Delayed Effects; Animals; Cocaine/*administration & dosage/pharmacology; Electrophysiology; Female; Hippocampus/*drug effects/physiology; In Vitro Techniques; Long-Term Potentiation/*drug effects; Narcotics/*administration & dosage/pharmacology; Neuronal Plasticity/drug effects; Pregnancy; Rabbits; Reference Values; Synapses/drug effects
Cocaine use by pregnant women is currently of concern for its social and economic impact. Clinical studies of cocaine exposed offspring are limited by methodological constraints. In this study we used a rabbit model to examine the effects of gestational cocaine exposure on substrates of learning and memory. Rabbits, 30 to 40 days old, were examined for alterations in synaptic plasticity using an intact hippocampal slice preparation. Extracellular recordings revealed in utero cocaine exposure predisposed slices to larger long-term potentiation compared to controls.
Little J Z; Teyler T J
Brain research. Developmental brain research
1996
1996-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0165-3806(95)00187-5" target="_blank" rel="noreferrer noopener">10.1016/0165-3806(95)00187-5</a>
In utero cocaine exposure decreases dopamine D1 receptor modulation of hippocampal long-term potentiation in the rabbit.
Animals; Cocaine/*pharmacology; Dopamine D1/*drug effects; Female; Hippocampus/*drug effects; Long-Term Potentiation/*drug effects; Rabbits; Receptors; Uterus/*drug effects
Cocaine increases the synaptic concentration of neurotransmitters by inhibiting catecholamine transporters. Disturbances of behavior and cellular physiology have been associated with prenatal cocaine exposure and are related to changes in dopamine transmission. Recently we found the magnitude of long-term potentiation (LTP) was greater in hippocampal slices from cocaine exposed offspring. In the hippocampus, D1 dopamine receptor antagonists inhibit the expression of LTP while agonists facilitate it. To test the functionality of the D1 receptor we examined the effect of the D1 antagonist SCH-23390 on LTP using a rabbit model of gestational cocaine exposure. Tetanization during exposure to the D1 antagonist
Little J Z; Teyler T J
Neuroscience letters
1996
1996-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0304-3940(96)12960-8" target="_blank" rel="noreferrer noopener">10.1016/0304-3940(96)12960-8</a>
GABAa receptor-mediated field potentials are enhanced in area CA1 following prenatal cocaine exposure.
*Prenatal Exposure Delayed Effects; AMPA/physiology; Animals; Bicuculline/analogs & derivatives/pharmacology; Cocaine/*pharmacology; Female; GABA-A/*physiology; GABA-B/physiology; Hippocampus/drug effects/*physiology; In Vitro Techniques; Membrane Potentials/drug effects/physiology; N-Methyl-D-Aspartate/physiology; Pregnancy; Quinoxalines/pharmacology; Rabbits; Receptors; Synapses/drug effects/physiology
Prenatal cocaine exposure results in several documented changes in neurotransmitter receptor number and structure. Increases have been reported for cortical catecholamine and indoleamine receptor number and binding affinity, in the subunit expression of glutamatergic NMDA and AMPA receptors in the striatum, and in GABA immunoreactivity in the anterior cingulate cortex. We sought information on the functional consequences of cocaine-induced alterations in receptor structure/number. Since hippocampal amino acid neurotransmitters are of critical importance and have been shown to be affected by cocaine, we studied field potentials produced by synaptic activation of isolated glutamatergic NMDA and AMPA receptors and GABAa and GABAb responsive receptors in area CA1 of rabbit hippocampal slices. We found the GABAa receptor population produced significantly larger field potentials in cocaine-exposed offspring compared to controls, while other receptors produced responses similar to controls.
Little J Z; Teyler T J
Brain research. Developmental brain research
1998
1998-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0165-3806(98)00100-x" target="_blank" rel="noreferrer noopener">10.1016/s0165-3806(98)00100-x</a>