Recording of mouse ventral tegmental area dopamine-containing neurons.
We examined the electrophysiologic and pharmacologic properties of dopamine-containing ventral tegmental area neurons in the mouse using extracellular single-unit recording techniques in both chloral hydrate-anesthetized mice and in vitro mouse midbrain slices. In vivo the ventral tegmental area neurons had long-duration action potentials (2 to 5 ms) and discharged at 1 to 9 spikes/s with either a decremental burst pattern or a regular pattern. Systemic administration of the dopamine agonist, apomorphine, decreased their firing rate, and the dopamine receptor blocker, haloperidol, reversed this effect. Similarly, systemic administration of the dopamine-releasing agent, d-amphetamine, suppressed their discharge rate, an effect blocked by pretreatment of the animals with alpha-methyl-p-tyrosine. When recorded in vitro from midbrain slices, ventral tegmental area neurons showed electrophysiologic properties similar to those found in vivo; however, the neurons recorded in vitro fired at a significantly faster rate and their firing pattern tended to be more pacemaker-like, especially when recordings were made in an incubation medium that blocked synaptic transmission (i.e., low calcium/high magnesium). The activity of most of these neurons was suppressed by addition of apomorphine to the incubation medium, an effect reversed by haloperidol. Pretreatment with alpha-methyl-p-tyrosine produced no significant change in the discharge pattern or rate for cells recorded in vitro. These data indicate that mouse ventral tegmental area dopamine neurons in vivo exhibit the same electrophysiologic and pharmacologic properties as do rat and cat dopamine-containing neurons and that in vitro they fire with pacemaker regularity in a low-calcium/high-magnesium medium. The in vitro preparation offers an approach to examining the fundamental properties of ventral tegmental area dopamine-containing neurons in the absence of afferent inputs.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003913:Dextroamphetamine / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D006220:Haloperidol / Q000494:pharmacology; D006719:Homovanillic Acid / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008781:Methyltyrosines / Q000494:pharmacology; D051379:Mice; D013681:Tegmentum Mesencephali / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005971:Glutamates; D008781:Methyltyrosines; D015102:3,4-Dihydroxyphenylacetic Acid; D018698:Glutamic Acid; C022260:alpha-methyltyrosine methyl ester; D005680:gamma-Aminobutyric Acid; D006220:Haloperidol; D001058:Apomorphine; D003913:Dextroamphetamine; D004298:Dopamine; D006719:Homovanillic Acid