Dopaminergic Involvement in Nociceptive Sensitivity/Behavioral Reactivity Regulation During Aversive States of Different Nature in the Rat

Kiyatkin, Eugene A.

doi:10.3109/00207458908986188

Cited by 7 publications

(8 citation statements)

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“…These data show differences in the temporal scale between these closely interrelated processes: very quick and short-lasting unit activation, closely correlated with stimuli-induced behaviours, and delayed ( -80 s) and longer-term (20-30 min) increase in DA levels, which reached a peak after termination of stimulation. Hence, these data are in agreement with numerous electrophysiological, dialysis and electrochemical observations, which show high reactiveness of mesolimbic DA cells and quick changes in nucleus accumbens extracellular DA concentrations with respect to various biologically significant stimuli (Trulson, 1985;Louilot et al, 1986;Schultz, 1986;Kiyatkin, 1988;Mitchell and Gratton, 1991;Phillips el al., 1991;Damsma et al, 1992;Doherty and Gratton, 1992;Imperato et al, 1992).…”

Section: Discussionsupporting

confidence: 92%

Cocaine Enhances the Changes in Extracellular Dopamine in Nucleus Accumbens Associated with Reinforcing Stimuli: A High‐speed Chronoamperometric Study in Freely Moving Rats

Kiyatkin

1993

Eur J of Neuroscience

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Numerous data suggest that the mesocorticolimbic dopamine (DA) system is critically involved in the organization and regulation of goal-directed behaviours of various types as well as in the mediation of the psychogenic effects of cocaine. To test the hypothesis that cocaine not only alters levels of extracellular DA within the mesolimbic DA system, but in addition changes the response of this system to reinforcing environmental stimuli, a study using high-speed chronoamperometry was done to evaluate the effects of cocaine (15 mg/kg, i.p.) on extracellular DA in the nucleus accumbens and to assess the effects of cocaine on the response evoked by the presentation of tail-pinch and palatable food. Cocaine was found to induce long-term biphasic changes in extracellular DA (an increase followed by a decrease) and, more importantly, to enhance DA increases evoked by both tail-pinch and food. The powerful enhancing action of cocaine on DA release, triggered by significant environmental stimuli and associated with behaviours of different types, is considered to be a possible primary mechanism of its rewarding or euphorigenic effect.

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Section: Discussionsupporting

confidence: 92%

Cocaine Enhances the Changes in Extracellular Dopamine in Nucleus Accumbens Associated with Reinforcing Stimuli: A High‐speed Chronoamperometric Study in Freely Moving Rats

Kiyatkin

1993

Eur J of Neuroscience

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“…Although rats administered a mixture of D1-and D2-selective DA antagonists were hypoactive and showed greatly diminished motor responses to sensory stimuli and COC, they were awake and usually vocalized to tail-touch and, especially, tail-pinch. These data are generally consistent with our early work that showed haloperidol, a mixed D1-and D-2 antagonist, greatly reduces motor responses to noxious stimuli, while slightly potentiating affective (vocalization) responses to the same stimuli (Kiyatkin, 1989). Despite hypoactivity, striatal neurons during DA receptor blockade in awake, unrestrained rats had impulse activity similar to (but with slightly higher rates) drug-free animals and showed virtually identical neuronal responses to somato-sensory stimuli and iontophoretic GLU (Kiyatkin and Rebec, 1999b).…”

supporting

confidence: 81%

I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats

Kiyatkin

Brown

2007

Neuroscience

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Cocaine's (COC) direct interaction with the dopamine (DA) transporter is usually considered the most important action underlying the psychomotor stimulant and reinforcing effects of this drug. However, some physiological, behavioral and psycho-emotional effects of COC are very rapid and brief and they remain intact during DA receptor blockade, suggesting possible involvement of peripheral non-DA neural mechanisms.To assess this issue, single-unit recording with microiontophoresis was used to examine changes in impulse activity of dorsal and ventral striatal neurons to intravenous (iv) COC (0.25-0.5 mg/kg) in the same rats under two conditions: awake with dopamine (DA) receptor blockade and anesthetized with urethane. In the awake preparation ~70% striatal neurons showed rapid and transient (latencỹ 6 s, duration ~15 s) COC-induced excitations. These effects were stronger in ventral than dorsal striatum. During anesthesia, these phasic effects were fully blocked and COC slowly decreased neuronal discharge rate. COC-methiodide (COC-M), a derivative that cannot cross the blood-brain barrier, also caused phasic excitations in the awake, but not anesthetized condition. In contrast to regular COC, COC-M had no tonic effect on discharge rate in either preparation. Most striatal neurons that were phasically excited by both COC forms also showed short-latency excitations during tailtouch and tail-pinch in the awake preparation, an effect strongly attenuated during anesthesia. Finally, most striatal neurons that in awake conditions were phasically excited by somato-sensory stimuli and COC salts were also excited by iontophoretic glutamate (GLU). Although striatal neurons were sensitive to GLU in both preparations, the response magnitude at the same GLU current was higher in awake than anesthetized conditions. These data suggest that in awake animals iv COC, like somato-sensory stimuli, transiently excites striatal neurons via its action on peripheral neural elements and rapid neural transmission. While the nature of these neuronal elements needs to be clarified using other analytical techniques, they might involve voltage-gated K + and Na + channels, which have a high affinity for COC and are located on terminals of visceral sensory nerves that densely innervate peripheral vessels. Therefore, along with direct action on specific brain substrates, central excitatory effects of COC may occur via indirect action, involving afferents of visceral sensory nerves and rapid neural transmission. By providing a rapid sensory signal and triggering transient neural activation, such a peripherally triggered action might play a crucial role in the sensory effects of COC, thus contributing to learning and development of drug-taking behavior.* Correspondence should be addressed to Eugene A. Kiyatkin at the above address. Fax: (410) 550-5553; tel.: (410) 550-5551; e-mail: ekiyatki@intra.nida.nih.gov. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our cus...

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“…immediate pain) have been shown to increase dopamine activity in mesolimbic areas traditionally associated with reward, although regional variations exist in degree and time course [45–53]. This increase in striatal dopamine release is supportive of other lines of investigation suggesting a role for striatal dopamine in the response to acute stress; for example, destruction of the dopaminergic neurons of the nigrostriatal bundle reduces the capacity of rats to respond appropriately to stress [54].…”

Section: Neurobiologymentioning

confidence: 71%

Section: Behavioral Measuresmentioning

confidence: 99%

“…lithium chloride), intracranial electrode stimulation, or intraperitoneal acetic acid administration [9–12]. Behavioral measures (i.e., ultrasonic vocalizations and behavioral reactivity) can then be used to interpret the degree to whether the aforementioned stimuli are indeed aversive [9, 13]. Ultrasound vocalizations at 22 kHz are important components of the unconditioned defensive behavior repertoire in rats and a reliable measure of fear and aversion in laboratory animals [194].…”

Section: Behavioral Measuresmentioning

confidence: 99%

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Neurobiology of aversive states

Umberg

Pothos

2011

Physiology & Behavior

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Hoebel and colleagues are often known as students of reward and how it is coded in the CNS. This article, however, attempts to focus on the significant advances by Hoebel and others in dissecting out behavioral components of distinct aversive states and in understanding the neurobiology of aversion and the link between aversive states and addictive behaviors. Reward and aversion are not necessarily dichotomous and may reflect an affective continuum contingent upon environmental conditions. Descriptive and mechanistic studies pioneered by Bart Hoebel have demonstrated that the shift in the reward-aversion spectrum may be, in part, a result of changes in central dopamine/ACh ratio, particularly in the NAc. The path to aversion appears to include a specific neurochemical signature: reduced dopamine activity and increased ACh activity in “reward centers” of the brain. Opioid receptors may have a neuromodulatory role on both of these neurotransmitters.

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Dopaminergic Involvement in Nociceptive Sensitivity/Behavioral Reactivity Regulation During Aversive States of Different Nature in the Rat

Cited by 7 publications

References 70 publications

Cocaine Enhances the Changes in Extracellular Dopamine in Nucleus Accumbens Associated with Reinforcing Stimuli: A High‐speed Chronoamperometric Study in Freely Moving Rats

Cocaine Enhances the Changes in Extracellular Dopamine in Nucleus Accumbens Associated with Reinforcing Stimuli: A High‐speed Chronoamperometric Study in Freely Moving Rats

I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats

Neurobiology of aversive states

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