Neurotensin excitation of rat ventral tegmental neurones.
- 1 January 1994
- journal article
- Published by Wiley in The Journal of Physiology
- Vol. 474 (1) , 119-129
- https://doi.org/10.1113/jphysiol.1994.sp020007
Abstract
1. Whole-cell patch-clamp recordings were made from ventral tegmental area neurones in rat midbrain slices in vitro. In principal cells, which are presumed to contain dopamine, neurotensin (< or = 1 microM) caused an inward current at -60 mV in thirty of forty-seven neurones and had no effect on the remainder. In secondary neurones, neurotensin caused an inward current in twelve of thirty-three cells. 2. The inward current evoked by neurotensin reached a maximum amplitude of about 80 pA, and declined over several minutes when the application was discontinued. The current was most commonly accompanied by a decrease in membrane conductance and reversed polarity at a strongly hyperpolarized potential; this reversal potential was less negative in a higher extracellular potassium concentration. Neurotensin also caused an inward current even in potassium-free internal and external solutions; this current was accompanied by a conductance increase, reversed close to 0 mV and was inhibited by reduction of the extracellular sodium concentration (from 150 to 20 mM). 3. The inward current was associated with a large increase in noise; this persisted in calcium-free solutions but was inhibited by low sodium concentration. The increase in noise was more prominent at hyperpolarized potentials. The amplitude of the unitary current underlying the increase in noise was estimated from the ratio of the variance to the mean as about 1.5 pA at -100 mV. 4. When the recording was made with an electrode containing guanosine 5'-thio-triphosphate, the steady inward current evoked by neurotensin did not reverse when the application was discontinued. When the recording electrode contained pertussis toxin, the action of neurotensin was not different although outward currents evoked by dopamine and baclofen declined with time. 5. It is concluded that neurotensin excites ventral tegmental area neurones by activating a pertussis toxin-insensitive guanosine nucleotide-binding protein. This leads to a reduction in membrane potassium conductance and an increase in membrane sodium conductance, the relative contribution of which varies from cell to cell.Keywords
This publication has 39 references indexed in Scilit:
- Differential G protein-mediated coupling of D2 dopamine receptors to K+ and Ca2+ currents in rat anterior pituitary cellsNeuron, 1992
- Neurotensin attenuates dopamine D2 agonist quinpirole-induced inhibition of midbrain dopamine neuronsNeuropharmacology, 1990
- Structure and functional expression of the cloned rat neurotensin receptorNeuron, 1990
- Neurotensin Binding to DopamineJournal of Neurochemistry, 1990
- Stimulation‐Induced Release of Coexistent Transmitters in the Prefrontal Cortex: An In Vivo Microdialysis Study of Dopamine and Neurotensin ReleaseJournal of Neurochemistry, 1989
- Binding of [3H]Neurotensin in Human Brain: Properties and DistributionJournal of Neurochemistry, 1986
- Neurotensin stimulates inositol phospholipid hydrolysis in rat brain slicesBrain Research, 1984
- Occurrence of neurotensinlike immunoreactivity in subpopulations of hypothalamic, mesencephalic, and medullary catecholamine neuronsJournal of Comparative Neurology, 1984
- Neurotensin receptor localization by light microscopic autoradiography in rat brainBrain Research, 1981
- Synaptic events in sympathetic gangliaProgress in Neurobiology, 1978