Membrane currents underlying bursting pacemaker activity and spike frequency adaptation in invertebrates.
Invertebrate systems have proved to be quite useful for the development of an understanding of some processes in the central nervous system (CNS). An understanding of the basic mechanisms of epilepsy will result from understanding not only how populations of neurons interact but also how the physiological processes in individual neurons are altered in epileptogenesis. Because invertebrate neurons have been so accessible to experimentation, it has been possible to explore in detail the basic mechanisms controlling neuronal excitability using these cells and to make some useful predictions about electrophysiological mechanisms that may be present in central neurons. This chapter deals with two electrophysiological processes that have been observed in invertebrate neurons and that may have some relevance to understanding the basic mechanisms of epilepsy. We review first the past and current studies of invertebrate burst firing neurons. It appears that the electrophysiological mechanisms producing burst firing may be present in CNS neurons participating in epileptogenesis. With caution, the information gleaned from invertebrate studies may be applicable to higher systems. The second process we consider is the phenomenon of spike frequency adaptation seen in invertebrates. Spike frequency adaptation is the process by which the firing rate of the neuron declines despite the maintenance of a constant stimulus. This process is not so thoroughly studied as burst firing, but it appears to represent a cellular mechanism designed to suppress prolonged periods of repetitive firing. Clearly, the suppression of such a process would produce excessive neuronal excitability, while its enhancement might have some anticonvulsant effects. The extreme sensitivity of spike frequency adaptation to barbiturates suggests such a possibility. These two electrophysiological processes are interesting in themselves and also because they may underlie the genesis or control of seizures. However, the greater significance is that, to understand the basic mechanisms of epilepsy, we may be well advised to examine neuronal processes in systems not considered to have seizure susceptibility.
D V
DV
Lewis
J R
JR
Huguenard
W W
WW
Anderson
W A
WA
Wilson
D000200:Action Potentials; D000222:Adaptation, Physiological; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D005110:Extracellular Space / Q000378:metabolism; D006329:Heart Conduction System / Q000166:cytology / Q000502:physiology*; D007448:Invertebrates / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology*; D007700:Kinetics; D008955:Models, Cardiovascular; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D013997:Time Factors
D007473:Ion Channels; D018377:Neurotransmitter Agents; D011188:Potassium; D002118:Calcium