Afferent connections of the nucleus accumbens of the snake, Elaphe guttata, studied by means of in vitro and in vivo tracing techniques in combination with TH immunohistochemistry

1997 ◽  
Vol 225 (2) ◽  
pp. 101-104 ◽  
Author(s):  
Lilian Perez-Santana ◽  
Oscar Marı́n ◽  
Wilhelmus J.A.J Smeets
Keyword(s):  
Nucleus Accumbens ◽  
Afferent Connections ◽  
Tracing Techniques ◽  
Elaphe Guttata

scholarly journals In vivo functional diversity of midbrain dopamine neurons within identified axonal projections

2019 ◽  
Author(s):  
Navid Farassat ◽  
Kauê M. Costa ◽  
Stefan Albert ◽  
Lora Kovacheva ◽  
Josef Shin ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Functional Diversity ◽  
Multiple Scales ◽  
Dopamine Neurons ◽  
Unit Recording ◽  
Data Set ◽  
Midbrain Dopamine ◽  
Firing Properties

AbstractThe functional diversity of midbrain dopamine (DA) neurons ranges across multiple scales, from differences in intrinsic properties and synaptic connectivity to selective task engagement in behaving animals. Distinct in vitro biophysical features of DA neurons have been associated with different axonal projection targets. However, it is unknown how this translates to different firing patterns of projection-defined DA subpopulations in the intact brain. We combined retrograde tracing with single-unit recording and juxtacellular labelling in mouse brain to create the first single cell-resolved in vivo functional topography of the midbrain DA system. We identified surprising differences in burst firing among those DA neurons projecting to dorsolateral striatum, which were organized along the medio-lateral substantia nigra (SN) axis. Furthermore, burst properties also differentiated DA neurons in the medial SN that projected either to dorsal or ventral striatum. In contrast, DA neurons projecting to lateral shell of nucleus accumbens displayed identical firing properties, irrespective of whether they were located in the SN or ventral tegmental area (VTA), thus breaching classical anatomical boundaries. Finally, we found robust differences in mean firing rates and pause durations among VTA DA neurons projecting to either lateral or medial shell of nucleus accumbens. Together, our data set establishes a high-resolution functional landscape of midbrain DA neurons, which will facilitate the identification of selective functions and pathophysiological changes within the midbrain DA system.

Cocaine increases stimulation-evoked serotonin efflux in the nucleus accumbens

2022 ◽  
Author(s):  
Jason Yuen ◽  
Abhinav Goyal ◽  
Aaron E Rusheen ◽  
Abbas Z Kouzani ◽  
Michael Berk ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Illicit Drugs ◽  
Serotonin Release ◽  
Sprague Dawley ◽  
Nucleus Accumbens Core ◽  
Fast Scan Cyclic Voltammetry ◽  
Carbon Fiber Microelectrode ◽  
Before And After

Cocaine is one of the most common illicit drugs globally, but the role of serotonin in its mechanism of action is insufficiently characterised. Consequently, we investigated the acute effects of the psychomotor stimulant cocaine on electrical stimulation-evoked serotonin (phasic) release in the nucleus accumbens core (NAcc) of urethane-anesthetized (1.5 g/kg i.p.) male Sprague-Dawley rats using N-shaped fast-scan cyclic voltammetry (N-FSCV). A single carbon fiber microelectrode was first implanted in the NAcc. Stimulation was applied to the medial forebrain bundle using 60 Hz, 2 ms, 0.2 mA, 2 s biphasic pulses before and after cocaine (2 mg/kg i.v.) was administered. Stimulation-evoked serotonin release significantly increased 5 minutes after cocaine injection compared to baseline (153±21 nM vs 257±12 nM; p = 0.0042; n = 5) but was unaffected by saline injection (1 ml/kg i.v.; n = 5). N-FSCV's selective measurement of serotonin release in vivo was confirmed pharmacologically via administration of the selective serotonin reuptake inhibitor escitalopram (10 mg/kg i.p.) which effectively increased the signal in a separate group of rats (n = 5). Selectivity to serotonin was further confirmed in vitro in which dopamine was minimally detected by N-FSCV with a serotonin to dopamine response ratio of 1:0.04 (200 nM of serotonin:1 mM dopamine ratio; p = 0.0048; n = 5 electrodes). This study demonstrates a noteworthy influence of cocaine on serotonin dynamics, and confirms that N-FSCV can effectively and selectively measure phasic serotonin release in the NAcc.

Sodium depletion and aldosterone decrease dopamine transporter activity in nucleus accumbens but not striatum

1999 ◽  
Vol 276 (5) ◽  
pp. R1339-R1345 ◽  
Author(s):  
Mitchell F. Roitman ◽  
Terrell A. Patterson ◽  
Randall R. Sakai ◽  
Ilene L. Bernstein ◽  
Dianne P. Figlewicz
Keyword(s):  
Nucleus Accumbens ◽  
Direct Action ◽  
Rotating Disk ◽  
Rotating Disk Electrode ◽  
Sodium Depletion ◽  
Rotating Disk Electrode Voltammetry ◽  
Motivated Behaviors ◽  
Na Depletion

Motivated behaviors, including sodium (Na) appetite, are correlated with increased dopamine (DA) transmission in the nucleus accumbens (NAc). DA transporter (DAT) modulation affects DA transmission and may play a role in motivated behaviors. In vivo Na depletion, which reliably induces Na appetite, was correlated with robust decreases in DA uptake via the DAT in the rat NAc with rotating disk electrode voltammetry [1,277 ± 162 vs. 575 ± 89 pmol ⋅ s−1 ⋅ g−1; Vmax of transport for control vs. Na-depleted tissue]. Plasma aldosterone (Aldo) levels increase after in vivo Na depletion and contribute to Na appetite. Decreased DAT activity in the NAc was observed after in vitro Aldo treatment (428 ± 28 vs. 300 ± 25 pmol ⋅ s−1 ⋅ g−1). Neither treatment affected DAT activity in the striatum. These results suggest that a direct action of Aldo is one possible mechanism by which Na depletion induces a reduction in DAT activity in the NAc. Reduced DAT activity may play a role in generating increased NAc DA transmission during Na appetite, which may underlie the motivating properties of Na for the Na-depleted rat.

Hyperlocomotion during Recovery from Isoflurane Anesthesia Is Associated with Increased Dopamine Turnover in the Nucleus Accumbens and Striatum in Mice

1997 ◽  
Vol 86 (2) ◽  
pp. 464-475 ◽  
Author(s):  
Masahiro Irifune ◽  
Tomoaki Sato ◽  
Takashige Nishikawa ◽  
Takashi Masuyama ◽  
Masahiro Nomoto ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Nucleus Accumbens ◽  
High Performance ◽  
Gas Flow ◽  
Brain Regions ◽  
Dopamine Neurons ◽  
Dopamine Turnover

Background It was recently reported that isoflurane increases dopamine release in the striatum in rats both in vivo and in vitro, and that isoflurane inhibits uptake of dopamine in the rat brain synaptosomes. However, the functional role of these effects of isoflurane on dopamine neurons is uncertain. Dopaminergic mechanisms within the nucleus accumbens and striatum play an important role in the control of locomotor activity, and a change in dopamine turnover depends essentially on a change in impulse flow in the dopamine neurons. In this study, the effects of isoflurane on locomotor activity and on dopamine turnover were investigated in discrete brain regions in mice. Methods Mice were placed in individual airtight clear plastic chambers and spontaneously breathed isoflurane in 25% oxygen and 75% nitrogen (fresh gas flow, 4 l/min). Locomotor activity was measured with an Animex activity meter. Animals were decapitated after treatments with or without isoflurane, and the concentrations of monoamines and their metabolites in different brain areas were measured by high-performance liquid chromatography. Results During the 10 min after the cessation of the 20-min exposure to isoflurane, there was a significant increase in locomotor activity in animals breathing 1.5% isoflurane but not 0.7% isoflurane. This increase in locomotor activity produced by 1.5% isoflurane was abolished by a low dose of haloperidol (0.1 mg/kg), a dopamine receptor antagonist. Regional brain monoamine assays revealed that 1.5% isoflurane significantly increased the 3,4-dihydroxyphenylacetic acid:dopamine ratio (one indicator of transmitter turnover) in the nucleus accumbens and striatum, but a concentration of 0.7% did not. This significant increase in dopamine turnover in these regions continued during 20 min after the cessation of the administration of 1.5% isoflurane. Conclusions These results suggest that isoflurane-induced hyperlocomotion during emergence may be associated with increased dopamine turnover in the nucleus accumbens and striatum.

scholarly journals Rapid changes in extracellular glutamate induced by natural arousing stimuli and intravenous cocaine in the nucleus accumbens shell and core

2012 ◽  
Vol 108 (1) ◽  
pp. 285-299 ◽  
Author(s):  
Ken T. Wakabayashi ◽  
Eugene A. Kiyatkin
Keyword(s):  
Nucleus Accumbens ◽  
High Speed ◽  
Behavioral Activation ◽  
Nucleus Accumbens Shell ◽  
Excitatory Neurotransmitter ◽  
Motivated Behavior ◽  
Rapid Changes ◽  
Electrochemical Signal

Glutamate (Glu) is a major excitatory neurotransmitter, playing a crucial role in the functioning of the nucleus accumbens (NAc), a critical area implicated in somatosensory integration and regulation of motivated behavior. In this study, high-speed amperometry with enzyme-based biosensors was used in freely moving rats to examine changes in extracellular Glu in the NAc shell and core induced by a tone, tail pinch (TP), social interaction with a male conspecific (SI), and intravenous (iv) cocaine (1 mg/kg). To establish the contribution of Glu to electrochemical signal changes, similar recordings were conducted with null (Glu0) sensors, which were exposed to the same chemical and physical environment but were insensitive to Glu. TP, SI, and cocaine, but not a tone, induced relatively large and prolonged current increases detected by both Glu and Glu0 sensors. However, current differentials revealed very rapid, much smaller, and transient increases in extracellular Glu levels, more predominantly in the NAc shell than core. In contrast to monophasic responses with natural stimuli, cocaine induced a biphasic Glu increase in the shell, with a transient peak during the injection and a slower postinjection peak. Therefore, Glu is phasically released in the NAc after exposure to natural arousing stimuli and cocaine; this release is rapid, stimulus dependent, and structure specific, suggesting its role in triggering neural and behavioral activation induced by these stimuli. This study also demonstrates the need for multiple in vitro and in vivo controls to reveal relatively small, highly phasic, and transient fluctuations in Glu levels occurring under behaviorally relevant conditions.

scholarly journals Parvalbumin interneurons in the nucleus accumbens regulate impairment of risk avoidance in DISC1 transgenic mice

2020 ◽  
Author(s):  
Xinyi Zhou ◽  
Bifeng Wu ◽  
Qian Xiao ◽  
Wei He ◽  
Ying Zhou ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Cognitive Abilities ◽  
Social Preference ◽  
Patch Clamp Recording ◽  
Risk Avoidance ◽  
Electrophysiological Recordings ◽  
Potential Risks ◽  
Frequency Of Action Potentials

AbstractOne strong survival instinct in animals is to approach things that are of benefit and avoid risk. In humans, a large portion of mental disorders are accompanied by cognition-related impairments including the inability to recognize potential risks. One of the most important genes involved in risk behavior is disrupted-in-schizophrenia-1 (DISC1), and animal models where this gene has some dysfunction show cognitive impairments. However, whether DISC1 mice models have an impairment in avoiding potential risks is still not fully understood. In the present study, we used DISC1-N terminal truncation (DISC1-NTM) mice to study cognitive abilities related to potential risks. We found that DISC1-NTM mice were impaired in risk avoidance on the elevated plus maze (EPM) test, and showed impairment in social preference in a three-chamber social interaction test. Staining for c-Fos following the EPM indicated that the nucleus accumbens (NAc) was associated with risk avoidance behavior in DISC1-NTM mice. Meanwhile, in vivo electrophysiological recordings showed that firing rates of fast spiking neurons (FS) in the NAc significantly decreased in DISC1-NTM mice following tamoxifen administration. In addition, theta band power was lower when mice shuttled from the safe (closed) arms to the risky (open) arms, an effect which disappeared after induction of the truncated DISC1 gene. Furthermore, we found through in vitro patch clamp recording that the frequency of action potentials stimulated by current injection was lower in parvalbumin (PV) neurons in the NAc of DISC1-NTM mice than their wild-type littermates. Risk-avoidance impairments in DISC1-NTM mice were rescued using optogenetic tools that activated NAcPV neurons. Finally, we inhibited activitiy of NAcPV neurons in PV-Cre mice, which mimicked the risk-avoidance impairment found in the DISC1-NTM mice during tests on the elevated zero maze. Taken together, our findings confirmed a cognitive impairment in DISC1-NTM mice related to risk recognition and suggests that reduced excitability of NAcPV neurons may be responsible.

Effects of the A2A adenosine receptor antagonist KW6002 in the nucleus accumbens in vitro and in vivo

2006 ◽  
Vol 83 (1) ◽  
pp. 114-121 ◽  
Author(s):  
L.K. Harper ◽  
S.R. Beckett ◽  
C.A. Marsden ◽  
A.C. McCreary ◽  
S.P.H. Alexander
Keyword(s):  
Nucleus Accumbens ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
A2a Adenosine Receptor ◽  
Adenosine Receptor Antagonist

Olanzapine: a basic science update

1999 ◽  
Vol 174 (S37) ◽  
pp. 36-40 ◽  
Author(s):  
Franklin Bymaster ◽  
Kenneth W. Perry ◽  
David L. Nelson ◽  
David T. Wong ◽  
Kurt Rasmussen ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Muscarinic Receptors ◽  
Receptor Binding ◽  
Dopaminergic Neurons ◽  
Adrenergic Receptors ◽  
Receptor Subtypes ◽  
Binding Studies

Olanzapine, an atypical antipsychotic, has a broad receptor binding profile, which may account for its pharmacological effects in schizophrenia. In vitro receptor binding studies showed a high affinity for dopamine D2, D3, and D4 receptors; all 5-HT2 receptor subtypes and the 5-HT6 receptor; muscarinic receptors, especially the M1 subtype; and α1-adrenergic receptors. In vivo studies showed that olanzapine had potent activity at D2 and 5 -HT2A receptors, but much less activity at D1 and muscarinic receptors, and that it inhibited dopaminergic neurons in the A10 but not the A9 tract, suggesting that this agent will not cause extrapyramidal side-effects (EPS). Microdialysis studies showed that olanzapine increased the extracellular levels of norepinephrine and dopamine, but not 5-HT, in the prefrontal cortex, and increased extracellular dopamine levels in the neostriatum and nucleus accumbens, areas ofthe brain associated with schizophrenia. Studies of gene expression showed that olanzapine 10 mg/kg also increased Fos expression in the prefrontal cortex, the dorsolateral striatum, and the nucleus accumbens. These findings are consistent with the effectiveness of olanzapine on both negative and positive symptoms and suggest that, with careful dosing, olanzapine should not cause EPS.

scholarly journals Reduced Firing of Nucleus Accumbens Parvalbumin Interneurons Impairs Risk Avoidance in DISC1 Transgenic Mice

2021 ◽  
Author(s):  
Xinyi Zhou ◽  
Bifeng Wu ◽  
Wenhao Liu ◽  
Qian Xiao ◽  
Wei He ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Mental Disorders ◽  
Social Preference ◽  
Patch Clamp Recording ◽  
Risk Avoidance ◽  
Electrophysiological Recordings ◽  
Potential Risks ◽  
Frequency Of Action Potentials

AbstractA strong animal survival instinct is to approach objects and situations that are of benefit and to avoid risk. In humans, a large proportion of mental disorders are accompanied by impairments in risk avoidance. One of the most important genes involved in mental disorders is disrupted-in-schizophrenia-1 (DISC1), and animal models in which this gene has some level of dysfunction show emotion-related impairments. However, it is not known whether DISC1 mouse models have an impairment in avoiding potential risks. In the present study, we used DISC1-N terminal truncation (DISC1-NTM) mice to investigate risk avoidance and found that these mice were impaired in risk avoidance on the elevated plus maze (EPM) and showed reduced social preference in a three-chamber social interaction test. Following EPM tests, c-Fos expression levels indicated that the nucleus accumbens (NAc) was associated with risk-avoidance behavior in DISC1-NTM mice. In addition, in vivo electrophysiological recordings following tamoxifen administration showed that the firing rates of fast-spiking neurons (FS) in the NAc were significantly lower in DISC1-NTM mice than in wild-type (WT) mice. In addition, in vitro patch clamp recording revealed that the frequency of action potentials stimulated by current injection was lower in parvalbumin (PV) neurons in the NAc of DISC1-NTM mice than in WT controls. The impairment of risk avoidance in DISC1-NTM mice was rescued using optogenetic tools that activated NAcPV neurons. Finally, inhibition of the activity of NAcPV neurons in PV-Cre mice mimicked the risk-avoidance impairment found in DISC1-NTM mice during tests on the elevated zero maze. Taken together, our findings confirm an impairment in risk avoidance in DISC1-NTM mice and suggest that reduced excitability of NAcPV neurons is responsible.

Sign in / Sign up

Export Citation Format

Share Document