3-Mercaptopropionic acid administration increases the affinity of [3H]Quinuclidinyl benzilate binding to membranes of the striatum and cerebellum

Molecular and Chemical Neuropathology

1994

Acetylcholinesterase activity (AChE) was assayed in rat CNS membrane fractions after administration of the convulsant 3-mercaptopropionic acid (150 mg/kg, ip). In comparison with saline-injected controls, total AChE activity decreased 12-20% in striatum and cerebellum during seizure and postseizure but failed to change in cerebral cortex. Specific AChE activity, assayed in the presence of 10(-4) M ethopropazine (a butyrylcholinesterase inhibitor), decreased 15-25% in striatum and cerebellum, increased 20-45% in hippocampus, but remained unchanged in cerebral cortex. Saline injection alone increased AChE activity in striatum (68%) and cerebellum (36%) but failed to modify enzyme activity in hippocampus and cerebral cortex. To conclude, AChE sensitivity to convulsant and saline administration is tissue-specific and not restricted to cholinergic areas.

Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 77%

See 1 more Smart Citation

Area-specific modification of acetylcholinesterase activity following 3-mercaptopropionic acid-induced seizures

Girardi

Molecular and Chemical Neuropathology

1994

“…Previous work from this laboratory has shown that convulsant MP modifies GABA system by decreasing GAD activity and GABA levels as well as alterating of cerebellar Purkinje cell morphology [ 8 , 9 ]. With a convulsant MP dose, [ 3 H]-QNB binding to muscarinic receptors is enhanced in CNS, an effect due to an increase in affinity without changes in binding site number [ 10 , 11 ]. However, a subconvulsant MP dose fails to induce any change [ 10 - 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous work from this laboratory has shown that the administration of the convulsant drug 3-mercaptopropionic acid (MP), a GAD inhibitor [ 7 ], modifies not only GABA synthesis [ 8 , 9 ] but also binding of antagonist [ 3 H]-quinuclidinyl benzilate ([ 3 H]-QNB) to central muscarinic receptors, an effect due to an increase in affinity without modifications in binding site number [ 10 - 12 ].…”

Section: Introductionmentioning

confidence: 99%

Convulsant bicuculline modifies CNS muscarinic receptor affinity

2006

BMC Neurosci

Background: Previous work from this laboratory has shown that the administration of the convulsant drug 3-mercaptopropionic acid (MP), a GAD inhibitor, modifies not only GABA synthesis but also binding of the antagonist [ 3 H]-quinuclidinyl benzilate ([ 3 H]-QNB) to central muscarinic receptors, an effect due to an increase in affinity without modifications in binding site number. The cholinergic system has been implicated in several experimental epilepsy models and the ability of acetylcholine to regulate neuronal excitability in the neocortex is well known. To study the potential relationship between GABAergic and cholinergic systems with seizure activity, we analyzed the muscarinic receptor after inducing seizure by bicuculline (BIC), known to antagonize the GABA-A postsynaptic receptor subtype.

Area-dependent CNS membrane response of muscarinic receptor to convulsant 3-mercaptopropionic acid

Molecular and Chemical Neuropathology

1997

It has already been shown that the administration of convulsant 3-mercaptopropionic acid at 150 mg/kg enhances binding affinity of muscarinic antagonist [3H]quinuclidinyl benzilate ([3H]QNB) to certain rat CNS membranes without affecting site number. Herein we employed a 100 mg/kg dose and tested [3H]QNB binding to cerebellar, hippocampal, and striatal membranes obtained from rats killed at preseizure, seizure, and postseizure stages. In cerebellum, binding increased 24, 65, and 19% a1 preseizure, seizure, and postseizure stages, respectively; in hippocampus, values were 12 and 20% higher at pre- and seizure stages, but failed to differ from controls at postseizure; in striatum, increases of 10 and 18% were recorded at seizure and postseizure, with no changes at preseizure. Neither a subconvulsant dose (20 mg/kg) nor in vitro drug addition had any effect on binding. Results indicate a differential response to the convulsant, with reversible changes in cerebellum and hippocampus, and a delayed response in striatum, supporting the concept of area-dependent neuronal plasticity.