Subject(s)
Brain/growth & development , Glycoproteins/metabolism , Maternal-Fetal Exchange , Membrane Proteins/metabolism , Protein-Energy Malnutrition/metabolism , Animals , Brain/metabolism , Cell Membrane/metabolism , Cell Membrane/physiopathology , Female , Fucose/metabolism , Pregnancy , Rats , Rats, Inbred Strains , Synaptic Membranes/metabolism , Synaptic Membranes/physiopathologyABSTRACT
Antibodies to GM1 ganglioside injected into the sensorimotor cortex of the rat induce recurrent epileptiform activity. We now find that the divalent F(ab')2 and monovalent Fab' fragments derived from antiganglioside IgG molecules are able to induce epileptiform seizures. This result supports the view that the binding of antibodies to ganglioside receptors in the synaptic membrane is sufficient in itself to initiate changes in membrane processes which lead to epileptiform spiking. These changes do not appear to be dependent on linking of ganglioside receptors or on the presence of serum factors such as complement.
Subject(s)
Epilepsy/physiopathology , Immunoglobulin Fab Fragments/immunology , Animals , Cerebral Cortex , Electroencephalography , G(M1) Ganglioside/immunology , Immunoglobulin G/immunology , Immunoglobulin M/immunology , Male , Rats , Rats, Inbred Strains , Receptors, Neurotransmitter/metabolism , Synaptic Membranes/physiopathologyABSTRACT
The convulsant bicuculline (BICUC) had both synaptic and nonsynaptic actions on mouse spinal cord neurons in primary dissociated cell culture. BICUC antagonized postsynaptic responses to the inhibitory neurotransmitter GABA (a synaptic action) and produced direct membrane depolarization by blocking a membrane potassium conductance and directly prolonging calcium-dependent action potentials (nonsynaptic actions). In cultured spinal cord neurons, BICUC also produced paroxysmal depolarizing events (PDE), which might be equivalent to in vivo convulsant-induced bursting in spinal cord neurons or paroxysmal depolarizing shifts (PDS) in cortical neurons. Thus, the concentrations of BICUC producing both synaptic and nonsynaptic actions overlapped those producing paroxysmal activity. The results suggest that in addition to antagonism of GABA-mediated synaptic inhibition, direct nonsynaptic actions of BICUC may be required for some neurons to develop PDS.
Subject(s)
Bicuculline/pharmacology , Synaptic Membranes/physiopathology , Action Potentials/drug effects , Animals , Calcium/pharmacology , Cells, Cultured , Electrophysiology , Ganglia, Spinal/cytology , Ganglia, Spinal/physiopathology , Membrane Potentials/drug effects , Mice , Spinal Cord/cytology , Spinal Cord/physiopathology , gamma-Aminobutyric Acid/pharmacologyABSTRACT
Convulsive manifestations are synchronized mass-discharges which are caused by a dysfunction of the dynamic equilibrium between excitation and inhibition. This is caused by a change in membrane activity which increases or decreases the effectiveness of neurotransmitters. We showed the effect of ions on membrane activity and epileptic discharges.
