Firing properties of substantia nigra dopaminergic neurons in freely moving rats

Freeman, Arthur; Meltzer, Leonard T.; Bunney, Benjamin S.

doi:10.1016/0024-3205(85)90448-5

Cited by 226 publications

(130 citation statements)

References 16 publications

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“…However, in terms of absolute magnitude, the increase was relatively week (~12 imp/s). This response pattern well agrees with preferential excitations of presumed DA neurons induced by arousing somato-sensory stimuli in awake animals, as shown both in the SNc (Freeman et al, 1985;Freeman and Bunney, 1987;Steinfels et al, 1983;Strecker et al, 1985;Schultz, 1986;Trulson, 1985) and VTA (Guarraci and Kapp, 1999;Freeman and Bunney, 1987;Kiyatkin, 1988;Horvitz et al, 1997;Schultz, 1986). These data are also consistent with large body of neurochemical data (DA metabolism, [DA] evaluated by microdialysis or electrochemistry) suggesting increased DA release, especially in cortical projections, associated with arousing and aversive stimulation (Abercrombie et al, 1989;Deutch et al, 1985;Fadda et al, 1978;Feenstra et al, 2000Feenstra et al, , 2001Kiyatkin, 1995;Le Moal and Simon, 1991;Thierry et al, 1976).…”

Section: Sensory Responses Of Ls and Ss Vta Neuronssupporting

confidence: 86%

“…In contrast to the striatum, which is comprised of primarily GABA-containing spiny cells (Parent and Hazrati, 1995), VTA neuronal population is highly heterogeneous, with cells containing many different neurotransmitters (DA, GABA, glutamate or GLU, peptides) (Bjorklund and Lindvall, 1984;Swanson, 1982). Although VTA cells were extensively studied in vitro and anesthetized preparations (Chiodo, 1988;Grace and Bunney, 1984), data in awake conditions are limited and point at the high variability in their electrophysiological properties and important differences in their activity and responsiveness to sensory stimuli (Dahan et al, 2007;Freeman et al, 1985;Horvitz et al, 1997;Kiyatkin, 1988;Rebec, 1998, 2001;Schultz, 1986). By recording impulse activity of single VTA neurons following iv cocaine administration and tail-press stimulation, we tried to answer two primary questions.…”

Section: Introductionmentioning

confidence: 99%

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Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Brown

Kiyatkin

2008

Brain Research

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Intravenous (iv) cocaine mimics salient somato-sensory stimuli in their ability to induce rapid physiological effects, which appear to involve its action on peripherally located neural elements and fast neural transmission via somato-sensory pathways. To further clarify this mechanism, single-unit recording with fine glass electrodes was used in awake rats to examine responses of ventral tegmental area (VTA) neurons, both presumed dopamine (DA) and non-DA, to iv cocaine and tail-press, a typical somato-sensory stimulus. To exclude the contribution of DA mechanisms to the observed neuronal responses to sensory stimuli and cocaine, recordings were conducted during full DA receptor blockade (SCH23390+eticloptide).Iv cocaine (0.25 mg/kg delivered over 10 s) induces significant excitations of ~63% of long-spike (presumed DA) and ~70% of short-spike (presumed non-DA) VTA neurons. In both subgroups, neuronal excitations occurred with short latencies (4-8 s), peaked at 10-20 s (30-40% increase over baseline) and disappeared at 30-40 s after the injection onset. Most long-(67%) and short-spike (89%) VTA neurons also showed phasic responses to tail-press (5-s). All responsive long-spike cells were excited by tail-press; excitations were very rapid (peak at 1 s) and strong (100% rate increase over baseline) but brief (2-3 s). In contrast, both excitations (60%) and inhibitions (29%) were seen in short-spike cells. These responses were also rapid and transient, but excitations of short-spike units were more prolonged and sustained (10-15 s) than in long-spike cells.These data suggest that in awake animals iv cocaine, like somato-sensory stimuli, rapidly and transiently excites VTA neurons of different subtypes. Therefore, along with direct action on specific brain substrates, central effects of cocaine may occur via indirect mechanism, involving peripheral neural elements, visceral sensory nerves and rapid neural transmission. Via this mechanism, cocaine, like somato-sensory stimuli, can rapidly activate DA neurons and induce phasic DA release, creating the conditions for DA accumulation by a later occurring and prolonged direct inhibiting action on DA uptake. By providing a rapid neural signal and triggering transient neural activation, such a peripherally driven action might play a crucial role in the sensory effects of COC, thus contributing to learning and development of drug-taking behavior.

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Section: Sensory Responses Of Ls and Ss Vta Neuronssupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Brown

Kiyatkin

2008

Brain Research

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“…For example, since acute haloperidol and other D 2 receptor antagonists have been shown to increase the firing rate of dopaminergic neurons, [7][8][9][10]17,26 one might expect to detect more spontaneously firing dopaminergic neurons while advancing an electrode through the substantia nigra, since these cells normally fire relatively slowly and since the drug increased the average number of spikes per second. It is possible that the elevation of firing rate of dopaminergic neurons induced by acute haloperidol administration simply increased the chances of finding dopaminergic neurons using the typical cells per track method.…”

Section: Alternative Explanations For the Changes In Number Of Cells mentioning

confidence: 99%

“…It is possible that the elevation of firing rate of dopaminergic neurons induced by acute haloperidol administration simply increased the chances of finding dopaminergic neurons using the typical cells per track method. The rate of advancement of the microelectrode is a critical variable for these measurements and lack of standardization of the rate of electrode advance may account in part for the large (approximately two-fold) differences in the number of cells per track in mesencephalic DA nuclei recorded under control conditions reported in various papers (e.g., Refs 6,9,17,33 and 55). Along these lines, it is interesting to note that the mean number of spontaneously active cells per track found in the present experiment (1.84), while using a very slow, controlled rate of advance (2 µm/s), is somewhat higher than for controls in many other studies, and is similar to the average reported for the substantia nigra after acute administration of DA receptor antagonists in several studies using the conventional cells per track measurement.…”

Section: Alternative Explanations For the Changes In Number Of Cells mentioning

confidence: 99%

Do silent dopaminergic neurons exist in rat substantia nigra in vivo?

Dai

Tepper

1998

Neuroscience

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“…These neurones fire at approximately 5 Hz in conscious animals but may express this firing in either regularly paced action potentials or in short bursts (Grace andBunney, 1983, 1984;Freeman et al, 1985). It has been shown by Gonon and colleagues that both the frequency and pattern of afferent activity determines the magnitude of dopamine release in the terminal fields (see Gonon, 1997).…”

Section: Introductionmentioning

confidence: 99%

Time window of autoreceptor‐mediated inhibition of limbic and striatal dopamine release

Phillips

Hancock

Stamford

2002

Synapse

118

101

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Forebrain dopamine release is under the local control of D2 family (D2 and D3) autoreceptors. In this study, autoreceptor-mediated modulation of forebrain dopamine release was investigated using amperometry in brain slices following local electrical stimulation. 350 m-thick slices of nucleus accumbens or dorsolateral neostriatum were prepared from male Wistar rats (150 -200 g) and superfused with artificial cerebrospinal fluid at 32°C. Dopamine release was evoked by electrical pulses (0.1 ms, 10 mA) across bipolar tungsten stimulating electrodes and measured at carbon fibre microelectrodes using fixed potential amperometry (ϩ300 mV vs. Ag/AgCl). Peak dopamine release on stimulation (single pulse) was 0.75 M (neostriatum) and 1.37 M (nucleus accumbens). Metoclopramide (1 M) had no significant effect on DA efflux from a single pulse in either region. Using paired pulse stimuli, dopamine release on the second pulse varied according to the interval between the two pulses. At very long intervals (Ͼ20 sec), dopamine release was similar to that for the first pulse. At shorter intervals, dopamine efflux was attenuated. Metoclopramide had no effect on second pulse dopamine release when the pulse was applied at short (Ͻ0.1 sec) or long (Ͼ5.0 sec) intervals after the first. At intermediate intervals, metoclopramide significantly increased second pulse dopamine release. The peak dopamine autoreceptor effect occurred at ϳ550 ms in neostriatum and ϳ700 ms in nucleus accumbens. The onset time is due both to diffusion of dopamine from the release sites to the autoreceptors and receptoreffector mechanisms. These findings may have implications for the local control of forebrain dopamine function in physiological and pathological states. Synapse 44: 15-22, 2002.

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Firing properties of substantia nigra dopaminergic neurons in freely moving rats

Cited by 226 publications

References 16 publications

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons

Do silent dopaminergic neurons exist in rat substantia nigra in vivo?

Time window of autoreceptor‐mediated inhibition of limbic and striatal dopamine release

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