Intracerebral microdialysis: I. Experimental studies of diffusion kinetics

Lindefors, Nils; Amberg, Gustav; Ungerstedt, Urban

doi:10.1016/0160-5402(89)90011-9

Cited by 217 publications

(94 citation statements)

References 16 publications

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“…Diffusion constants of most drugs have not been determined, although data for TTX (Zhuravin and Bures, 1991) and some neurotransmitters are available (Rice et al, 1985). Estimates can be calculated on the basis of diffusion constants in liquids and recovery data in vivo (Lindefors et al, 1989), which are relatively simple to measure, but the penetration into the brain tissue has to be determined experimentally for each individual drug, because factors such as binding to macromolecules and receptors and uptake into cells cannot be estimated from diffusion constants in liquids or recovery data (Benveniste, 1989). This was clearly demonstrated by the study of Boehnke and Rasmusson (2001), where TTX and lidocaine, despite comparable molecular weights, differed in spreading and time of duration of the effect.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Manipulation of Neuronal Ensemble Activity by Reverse Microdialysis in Freely Moving Rats: A Comparative Study of the Effects of Tetrodotoxin, Lidocaine, and Muscimol

Duuren

Plasse²,

Blom³

et al. 2007

J Pharmacol Exp Ther

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To be able to address the question how neurotransmitters or pharmacological agents influence activity of neuronal populations in freely moving animals, the combidrive was developed. The combidrive combines an array of 12 tetrodes to perform ensemble recordings with a moveable and replaceable microdialysis probe to locally administer pharmacological agents. In this study, the effects of cumulative concentrations of tetrodotoxin, lidocaine, and muscimol on neuronal firing activity in the prefrontal cortex were examined and compared. These drugs are widely used in behavioral studies to transiently inactivate brain areas, but little is known about their effects on ensemble activity and the possible differences between them. The results show that the combidrive allows ensemble recordings simultaneously with reverse microdialysis in freely moving rats for periods at least up to 2 wk. All drugs reduced neuronal firing in a concentration dependent manner, but they differed in the extent to which firing activity of the population was decreased and the in speed and extent of recovery. At the highest concentration used, both muscimol and tetrodotoxin (TTX) caused an almost complete reduction of firing activity. Lidocaine showed the fastest recovery, but it resulted in a smaller reduction of firing activity of the population. From these results, it can be concluded that whenever during a behavioral experiment a longer lasting, reversible inactivation is required, muscimol is the drug of choice, because it inactivates neurons to a similar degree as TTX, but it does not, in contrast to TTX, affect fibers of passage. For a short-lasting but partial inactivation, lidocaine would be most suitable.Until recently, neurophysiological analysis of information processing in the brain was primarily based on the examination of firing activity of single cells during behavior, as measured with repetitive presentations of stimuli (Gerstein and Kiang, 1960). However, this could not provide an answer to the question of how information is represented by the pattern of activity distributed across a population of neurons. With the emergence of techniques to record large numbers of neurons simultaneously ("ensemble recordings"), it became possible to examine information coding at the level of cell populations (Wilson and McNaughton, 1993). However, an issue that has not been addressed thus far is how neurotransmitters influence the activity of these cell populations.To gain more insight in the interaction between neurotransmitters or pharmacological agents and neuronal firing activity, we sought to develop a method in which drugs could be locally administered while performing ensemble recordings in freely moving rats. Because drugs should ideally be delivered with a constant concentration throughout the experimental session within the entire recording area, reverse microdialysis is preferred over either local injections, because with injections additional fluid is introduced into the brain, causing a change in pressure; or iontophoresis,...

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Section: Discussionmentioning

confidence: 99%

Pharmacological Manipulation of Neuronal Ensemble Activity by Reverse Microdialysis in Freely Moving Rats: A Comparative Study of the Effects of Tetrodotoxin, Lidocaine, and Muscimol

Duuren

Plasse²,

Blom³

et al. 2007

J Pharmacol Exp Ther

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“…Compounds were quantified by electrochemical detection using a glassy carbon working electrode set at þ 400 mV against a silver-silver chloride reference electrode (WE-3G; Eicom, Kyoto, Japan), giving a detection limit for dopamine of about 0.02 pg/sample at a 2:1 signal-to-noise ratio. The probes had an in vitro recovery of approximately 12% for dopamine, but the reported concentrations were not adjusted for recovery in vivo because these estimations are inaccurate (Benveniste et al, 1989;Lindefors et al, 1989). Previous experiments in which we have used the same technique and procedure have shown that the dopamine efflux is more or less stabilized 16 h after probe insertion, EM-2-and EM-1-induced accumbal dopamine efflux H Okutsu et al and that the release seen at that time is largely dependent on neuronal release as more than 70% of the release is TTX sensitive (Saigusa et al, 2001).…”

Section: Dialysis and Neurochemical Measurementsmentioning

confidence: 99%

Endomorphin-2 and Endomorphin-1 Promote the Extracellular Amount of Accumbal Dopamine via Nonopioid and Mu-Opioid Receptors, Respectively

Okutsu

Watanabe

Takahashi

et al. 2005

Neuropsychopharmacol

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Activation of mu-opioid receptors in the nucleus accumbens (NAc) is known to increase accumbal dopamine efflux in rats. Endomorphin-2 (Tyr-Pro-Phe-Phe-NH 2 ; EM-2) and endomorphin-1 (Tyr-Pro-Trp-Phe-NH 2 ; EM-1) are suggested to be the endogenous ligands for the mu-opioid receptor. As the ability of EM-2 and EM-1 to alter the accumbal extracellular dopamine level has not yet been studied in freely moving rats, the present study was performed, using a microdialysis technique that allows on-line monitoring of the extracellular dopamine with a temporal resolution of 5 min. A 25 min infusion of either EM-2 or EM-1 into the NAc (5, 25, and 50 nmol) produced a dose-dependent increase of the accumbal dopamine level. The EM-2 (50 nmol)-and EM-1 (25 and 50 nmol)-induced dopamine efflux were abolished by intra-accumbal perfusion of tetrodotoxin (2 mM). Intra-accumbal perfusion of the mu-opioid receptor antagonist CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH 2 ; 3 nmol) failed to affect the EM-2 (50 nmol)-induced dopamine release, whereas it significantly inhibited the EM-1 (25 and 50 nmol)-induced dopamine release. The EM-1 (50 nmol)-induced accumbal dopamine efflux was significantly reduced by the systemic administration of the putative mu1-opioid receptor antagonist naloxonazine (15 mg/kg, intraperitoneally (i.p.), given 24 h before starting the perfusion). Systemic administration of the aspecific opioid receptor antagonist naloxone (1 mg/kg, i.p., given 10 or 20 min before starting the perfusion) also failed to affect the EM-2 (50 nmol)-induced dopamine efflux, whereas it significantly inhibited the EM-1 (25 and 50 nmol)-induced dopamine efflux. The present study shows that the intra-accumbal infusion of EM-2 and EM-1 increases accumbal dopamine efflux by mechanisms that fully differ. It is concluded that the effects of EM-2 are not mediated via opioid receptors in contrast to the effects of EM-1 that are mediated via mu1-opioid receptors in the NAc.

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“…In contrast, the effects of the dopaminergic treatment of the nucleus accumbens on the dopamine release in the striatum extended to both sides of the brain, implying that a direct or indirect projection from the nucleus accumbens to both the left and the right striatum is required for mediating these biochemical effects. Although the nature of these connections remains to be determined, there are at least three candidates in this respect: (a) the pathway which connects the nucleus accumbens via the A 10 cells in the ventral tegmental region with the ventrolateral striatum (Loughlin and Fallon, 1982;Heimer et al, 1991;Zahm and Heimer, 1993), (b) the pathway which connects the nucleus accumbens via the A 9 cells in the substantia nigra pars compacta with the ventrolateral striatum (Fass and Butcher, 1981;Groenewegen et al, 1991;Wouterlood et al, 1992;Zahm and Heimer, 1993), and (c) the pathway which connects the nucleus accumbens via pallido-nigral fibres with the ventrolateral striatum Heimer, 1990, 1993). Future studies are required to determine whether these pathways are indeed differentially involved in the effects found in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Baseline levels were the mean of the last three samples before drug injection. The probes had an in vitro recovery of 10-12% for dopamine, but the reported concentrations (pg/50 ¡i\ of dialysate) were not adjusted for recovery in vivo because these estimations are inaccu rate (Benveniste et al, 1989;Benveniste and Huttemeier, 1990;Lindefors et al, 1989). Contralateral turnings (de fined as complete 360° turns) were counted visually by a trained observer who had no prior knowledge of the drug treatment.…”

Section: 1 Animals and Surgerymentioning

confidence: 99%

Stimulation of acetylcholine or dopamine receptors in the nucleus accumbens differentially alters dopamine release in the striatum of freely moving rats

Koshikawa

Yoshida

Kitamura

et al. 1996

European Journal of Pharmacology

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The present study examined whether unilateral stimulation of acetylcholine or dopamine receptors in the nucleus accumbens induces an asymmetry in dopamine transmission in the ventrolateral striatum. For this purpose, a microdialysis technique was used to measure dopamine release in both sides of the ventrolateral striatum following unilateral injections of carbachol (5 ¿¿g/0.5 j j l \ ) or a mixture of dopamine Dj and dopamine D 2 receptor agonists (l-phenyl-2,3,4,5-tetrahydro-ltf-3-benzazepine-7,8-diol 5 fig + quinpirole 10 ¿¿g/0.5 /xl) into the nucleus accumbens. The results show that carbachol injection increased dopamine release in the ipsilateral striatum without changing dopamine release in the contralateral striatum, whereas the dopamine D , / D 2 receptor agonist mixture injected unilaterally into the nucleus accumbens produced an increase followed by a decrease in dopamine release in the ipsilateral striatum, but only a decrease in dopamine release in the contralateral striatum. The biochemical effects of the cholinergic treatment greatly outlasted the drug-induced contralateral turning, whereas the biochemical effects of the dopaminergic treatment showed a good correlation with the drug-induced contralateral turning. The present study provides biochemical evidence that unilateral stimulation of acetylcholine or dopamine receptors in the nucleus accumbens elicits an asymmetry in dopaminergic activity in the ventrolateral striatum. The present study also provides biochemical evidence that two distinct neural substrates are involved in the effects of cholinergic and dopaminergic manipulation of the nucleus accumbens.

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Intracerebral microdialysis: I. Experimental studies of diffusion kinetics

Cited by 217 publications

References 16 publications

Pharmacological Manipulation of Neuronal Ensemble Activity by Reverse Microdialysis in Freely Moving Rats: A Comparative Study of the Effects of Tetrodotoxin, Lidocaine, and Muscimol

Pharmacological Manipulation of Neuronal Ensemble Activity by Reverse Microdialysis in Freely Moving Rats: A Comparative Study of the Effects of Tetrodotoxin, Lidocaine, and Muscimol

Endomorphin-2 and Endomorphin-1 Promote the Extracellular Amount of Accumbal Dopamine via Nonopioid and Mu-Opioid Receptors, Respectively

Stimulation of acetylcholine or dopamine receptors in the nucleus accumbens differentially alters dopamine release in the striatum of freely moving rats

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