Systemic opiate administration has heterogeneous effects on activity recorded from nucleus accumbens neurons in vivo

Hakan, Robert L.; Henriksen, Steven J.

doi:10.1016/0304-3940(87)90105-4

Cited by 39 publications

(40 citation statements)

References 16 publications

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“…Previously, single-pulse stimulation of the fimbria was found to elicit driven spikes, excitatory, inhibitory and complex response patterns; fimbria-responsive units were not found to be regionally distributed (Hakan and Henriksen, 1987). Similarly, in the present study, fimbria-responsive units were encountered in both anterior (n = 33) and posterior (n = 34) NAS.…”

Section: Convergence Of Amygdala and Fimbria Efferentsmentioning

confidence: 55%

“…= 16.2 + 5.0msec). As previously reported for fimbria stimulation (Hakan and Henriksen, 1987), amygdala stimulation produced response patterns other than fixed-latency excitations. Inhibition of firing was recognized when spontaneous firing rates decreased by at least 50%, although in most cases complete cessation of firing for an interval following stimulation was observed.…”

Section: Amygdala-responsive Nas Unitsmentioning

confidence: 59%

“…However, unit data was combined from different animals in which the precise placement of amygdala electrodes varied, thereby minimizing any bias of stimulating only one site in the amygdala. In contrast, experience with a larger population of NAS neurons indicates that robust responses to fimbria stimulation occur only when stimulating electrodes are placed in the ventolateral tip of the fimbria, and that these responses show no topographical arrangement within the NAS (Hakan and Henriksen, 1987). Thus, integration of hippocampal and amygdala input can occur within individual NAS units, but the fact that most neurons fail to exhibit such integration and the possibility that these inputs are anatomically segregated suggests that some parallel processing of NAS inputs also occurs.…”

Section: Discussionmentioning

confidence: 83%

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Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

Callaway

Hakan

Henriksen

1991

J. Neural Transmission

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The nucleus accumbens septi (NAS) receives afferent input from the amygdala via the stria terminalis and from the hippocampus via the fimbria. Extracellular recordings from 196 NAS neurons in halothane-anesthetized rats revealed heterogeneous response patterns following stimulation of the amygdala. The observation that 30% of anterior NAS units but only 16% of posterior NAS units were responsive to amygdala stimulation suggested a topographical arrangement of amygdala efferents. Comparing the effects of amygdala and fimbria stimulation revealed that the two afferent pathways converge onto individual NAS neurons, but that the two sites of stimulation can differentially influence other neurons. The present results clarify the topographical distribution of amygdala input to the NAS, confirm that inputs from two limbic structures are integrated within the NAS, and further illustrate the electrophysiological heterogeneity of NAS neurons.

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Section: Convergence Of Amygdala and Fimbria Efferentsmentioning

confidence: 55%

Section: Amygdala-responsive Nas Unitsmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 83%

See 1 more Smart Citation

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

Callaway

Hakan

Henriksen

1991

J. Neural Transmission

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“…Medium spiny neurons make up over 90% of the neurons in the accumbens (Meredith, 1999). Electrical recordings from these neurons show opioids inhibit their activity (McCarthy et al, 1977; Hakan and Henriksen, 1987). This suppression of activity over a majority of the neurons in the accumbens might appear as no change in BOLD signal intensity or a negative BOLD.…”

Section: Discussionmentioning

confidence: 99%

BOLD Imaging in Awake Wild-Type and Mu-Opioid Receptor Knock-Out Mice Reveals On-Target Activation Maps in Response to Oxycodone

et al. 2016

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Blood oxygen level dependent (BOLD) imaging in awake mice was used to identify differences in brain activity between wild-type, and Mu (μ) opioid receptor knock-outs (MuKO) in response to oxycodone (OXY). Using a segmented, annotated MRI mouse atlas and computational analysis, patterns of integrated positive and negative BOLD activity were identified across 122 brain areas. The pattern of positive BOLD showed enhanced activation across the brain in WT mice within 15 min of intraperitoneal administration of 2.5 mg of OXY. BOLD activation was detected in 72 regions out of 122, and was most prominent in areas of high μ opioid receptor density (thalamus, ventral tegmental area, substantia nigra, caudate putamen, basal amygdala, and hypothalamus), and focus on pain circuits indicated strong activation in major pain processing centers (central amygdala, solitary tract, parabrachial area, insular cortex, gigantocellularis area, ventral thalamus primary sensory cortex, and prelimbic cortex). Importantly, the OXY-induced positive BOLD was eliminated in MuKO mice in most regions, with few exceptions (some cerebellar nuclei, CA3 of the hippocampus, medial amygdala, and preoptic areas). This result indicates that most effects of OXY on positive BOLD are mediated by the μ opioid receptor (on-target effects). OXY also caused an increase in negative BOLD in WT mice in few regions (16 out of 122) and, unlike the positive BOLD response the negative BOLD was only partially eliminated in the MuKO mice (cerebellum), and in some case intensified (hippocampus). Negative BOLD analysis therefore shows activation and deactivation events in the absence of the μ receptor for some areas where receptor expression is normally extremely low or absent (off-target effects). Together, our approach permits establishing opioid-induced BOLD activation maps in awake mice. In addition, comparison of WT and MuKO mutant mice reveals both on-target and off-target activation events, and set an OXY brain signature that should, in the future, be compared to other μ opioid agonists.

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“…Electrophysiology has shown that opiates and opioid peptides can reduce excitability of NAC neurons through actions at -opioid receptors (McCarthy et al, 1977;Hakan and Henriksen, 1987). Furthermore, pre-and postsynaptic effects of -opioid receptor stimulation (Hori et al, 1992;Capogna et al, 1993;Siggins et al, 1995) provide mechanisms for -opioid receptor modulation of synaptic transmission (Yuan et al, 1992).…”

mentioning

confidence: 99%

Ultrastructural Immunocytochemical Localization of μ-Opioid Receptors in Rat Nucleus Accumbens: Extrasynaptic Plasmalemmal Distribution and Association with Leu⁵-Enkephalin

et al. 1996

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-Opioid receptors and their endogenous ligands, including Leu 5 -enkephalin (LE), are distributed abundantly in the nucleus accumbens (NAC), a region implicated in mechanisms of opiate reinforcement. We used immunoperoxidase and/or immunogoldsilver methods to define ultrastructural sites for functions ascribed to -opioid receptors and potential sites for activation by LE in the NAC. An antipeptide antibody raised against an 18 amino acid sequence of the cloned -opioid receptor (MOR) C terminus showed that MOR-like immunoreactivity (MOR-LI) was localized predominantly to extrasynaptic sites along neuronal plasma membranes. The majority of neuronal profiles containing MOR-LI were dendrites and dendritic spines. The dendritic plasma membranes immunolabeled for MOR were near sites of synaptic input from LE-labeled terminals and other unlabeled terminals forming either inhibitory or excitatory type synapses. Unmyelinated axons and axon terminals were also intensely but less frequently immunoreactive for MOR. Observed sites for potential axonal associations with LE included coexistence of MOR and LE within the same terminal, as well as close appositions between differentially labeled axons. Astrocytic processes rarely contained detectable MOR-LI, but also were sometimes observed in apposition to LE-labeled terminals. We conclude that in the rat NAC, MOR is localized prominently to extrasynaptic neuronal and more rarely to glial plasma membranes that are readily accessible to released LE and possibly other opioid peptides and opiate drugs. The close affiliation of MOR with spines receiving excitatory synapses and dendrites receiving inhibitory synapses provides the first direct morphological evidence that MOR selectively modulates postsynaptic responses to cortical and other afferents.

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Systemic opiate administration has heterogeneous effects on activity recorded from nucleus accumbens neurons in vivo

Cited by 39 publications

References 16 publications

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

BOLD Imaging in Awake Wild-Type and Mu-Opioid Receptor Knock-Out Mice Reveals On-Target Activation Maps in Response to Oxycodone

Ultrastructural Immunocytochemical Localization of μ-Opioid Receptors in Rat Nucleus Accumbens: Extrasynaptic Plasmalemmal Distribution and Association with Leu⁵-Enkephalin

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Systemic opiate administration has heterogeneous effects on activity recorded from nucleus accumbens neurons in vivo

Cited by 39 publications

References 16 publications

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation

BOLD Imaging in Awake Wild-Type and Mu-Opioid Receptor Knock-Out Mice Reveals On-Target Activation Maps in Response to Oxycodone

Ultrastructural Immunocytochemical Localization of μ-Opioid Receptors in Rat Nucleus Accumbens: Extrasynaptic Plasmalemmal Distribution and Association with Leu5-Enkephalin

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Ultrastructural Immunocytochemical Localization of μ-Opioid Receptors in Rat Nucleus Accumbens: Extrasynaptic Plasmalemmal Distribution and Association with Leu⁵-Enkephalin