Properties and origin of spikelets in thalamocortical neurones in vitro.
Spikelets, or fast prepotentials as they are frequently referred to, are a common feature of the electrophysiology of central neurones and are invariably correlated with the presence of electrotonic coupling via gap junctions. Here we report that in the presence of the metabotropic glutamate receptor agonists, trans-ACPD or DHPG, thalamocortical neurones of the cat dorsal lateral geniculate nucleus maintained in vitro exhibit stereotypical spikelets that possess similar properties to those described in other brain areas. These spikelets were routinely observed in the presence of antagonists of fast chemical synaptic transmission, were resistant to the application of a variety of voltage-dependent Ca(2+) channel blockers but were abolished by tetrodotoxin. In addition, spikelets were reversibly blocked by the putative gap junction blocker carbenoxolone and were nearly always accompanied by dye-coupling. These results indicate that thalamocortical neurones may be electrotonically coupled via gap junctions with spikelets representing attenuated action potentials from adjoining cells. We suggest that the presence of electrotonic communication between thalamocortical neurones would have major implications for the understanding of both physiological (Steriade et al., 1993; Sillito et al., 1994; Alonso et al., 1996; Neuenschwander and Singer, 1996; Weliky and Katz, 1999) and pathological (Steriade and Contreras, 1995; Pinault et al., 1998) synchronised electrical activity in the thalamus.
Hughes
S W
SW
School of Biosciences, Cardiff University, Museum Avenue, CF10 3US, Cardiff, UK.
Blethyn
K L
KL
Cope
D W
DW
Crunelli
V
V
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002229:Carbenoxolone / Q000494:pharmacology; D002415:Cats; D002450:Cell Communication / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology*; D005829:Geniculate Bodies / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014793:Visual Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014795:Visual Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology*
D000897:Anti-Ulcer Agents; D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D026941:Sodium Channel Blockers; D002229:Carbenoxolone