Premium
Cellular mechanisms of orexin actions on paraventricular nucleus neurones in rat hypothalamus
Author(s) -
Follwell Matthew J.,
Ferguson Alastair V.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.030049
Subject(s) - parvocellular cell , neuroscience , depolarization , magnocellular cell , population , tetrodotoxin , excitatory postsynaptic potential , chemistry , biology , hypothalamus , medicine , biophysics , inhibitory postsynaptic potential , environmental health
Using whole‐cell patch clamp techniques we have examined the cellular mechanisms underlying the effects of orexin A (OX‐A) on electrophysiologically identified magnocellular and parvocellular neurones in the rat hypothalamic paraventricular nucleus (PVN). The majority of magnocellular neurones (67 %) showed concentration‐dependent, reversible depolarizations in response to OX‐A. These effects were abolished in tetrodotoxin (TTX), suggesting them to be indirect effects on this population of neurones. OX‐A also caused increases in excitatory postsynaptic current (EPSC) frequency and amplitude in magnocellular neurones. The former effects were again blocked in TTX while increases in mini‐EPSC amplitude remained. Depolarizing effects of OX‐A on magnocellular neurones were also found to be abolished by kynurenic acid, supporting the conclusion that these effects were the result of activation of a glutamate interneurone. Parvocellular neurones (73 % of those tested) also showed concentration‐dependent, reversible depolarizations in response to OX‐A. In contrast to magnocellular neurones, these effects were maintained in TTX, indicating direct effects of OX‐A on this population of neurones. Voltage clamp analysis using slow voltage ramps demonstrated that OX‐A enhanced a non‐selective cationic conductance with a reversal potential of ‐40 mV in parvocellular neurones, effects which probably explain the depolarizing effects of this peptide in this subpopulation of PVN neurones. These studies have identified separate cellular mechanisms through which OX‐A influences the excitability of magnocellular and parvocellular PVN neurones.