Reversal of Diminished Inhibitory Sensory Gating in Cocaine Addicts by a Nicotinic Cholinergic Mechanism

Adler, Lawrence E.; Olincy, Anti; Cawthra, Ellen; Hoffer, Michelle; Nagamoto, Herbert T.; Amass, Leslie; Freedman, Robert

doi:10.1016/s0893-133x(00)00242-6

Cited by 36 publications

(16 citation statements)

References 58 publications

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“…Findings of hippocampal involvement in the sensory gating response have also not been reported during MEG studies of healthy and clinical populations (Hanlon et al, 2005; Huang et al, 2003; Thoma et al, 2003) although these studies typically examined earlier time epochs (M50 and M100) rather than the time epoch (200–300 ms) associated with hippocampal activity during invasive studies. For example, previous evidence of hippocampal involvement in sensory gating has been reported in animal studies of single-cell recordings (Freedman et al, 1996), during pre-surgical mesial-temporal lobectomy human evaluations (Boutros et al, 2005; Boutros et al, 2008; Grunwald et al, 2003), and in pharmacological stimulation of the hippocampal interneurons with nicotinic acetylcholine-mediated neurotransmission (Adler et al, 2001). A recent FMRI study also reported hyperactivation of the hippocampus in patients with schizophrenia compared to normal controls using a click-train paradigm (Tregellas et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

The neural networks underlying auditory sensory gating

et al. 2009

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One of the most consistent electrophysiological deficits reported in the schizophrenia literature is a failure to inhibit, or properly gate, the neuronal response to the second stimulus of an identical pair (i.e., sensory gating). Although animal and invasive human studies have consistently implicated the auditory cortex, prefrontal cortex and hippocampus in mediating the sensory gating response, localized activation in these structures has not always been reported during non-invasive imaging modalities. In the current experiment, event-related FMRI and a variant of the traditional gating paradigm were utilized to examine how the gating network differentially responded to the processing of pairs of identical and non-identical tones. Two single-tone conditions were also presented so that they could be used to estimate the HRF for paired stimuli, reconstructed based on actual hemodynamic responses, to serve as a control non-gating condition. Results supported an emerging theory that the gating response for both paired-tones conditions was primarily mediated by auditory and prefrontal cortex, with potential contributions from the thalamus. Results also indicated that the left auditory cortex may play a preferential role in determining the stimuli that should be inhibited (gated) or receive further processing due to novelty of information. In contrast, there was no evidence of hippocampal involvement, suggesting that future work is needed to determine what role it may play in the gating response.

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Section: Discussionmentioning

confidence: 99%

The neural networks underlying auditory sensory gating

et al. 2009

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“…Since dopamine D2 receptor antagonists reverse the amphetamine-induced gating deficit, it has been proposed that enhanced dopamine neurotransmission results in disrupted gating (Stevens et al, 1996;Krause et al, 2003). Furthermore, enhanced catecholamine neurotransmission by amphetamine (Light et al, 1999) or cocaine (Adler et al, 2001) leads to impaired gating in humans. Interestingly, it has been demonstrated that amphetamine-or cocaine-induced gating deficit can be reversed not only with D2 antagonists, but with nicotine or nicotinic agonists as well (Stevens et al, 1995(Stevens et al, , 1999Adler et al, 2001), presumably interacting with inhibitory neuronal circuitry involved in gating, i.e., GABAergic interneurons in the hippocampus (Stevens et al, 1999;Freedman et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, enhanced catecholamine neurotransmission by amphetamine (Light et al, 1999) or cocaine (Adler et al, 2001) leads to impaired gating in humans. Interestingly, it has been demonstrated that amphetamine-or cocaine-induced gating deficit can be reversed not only with D2 antagonists, but with nicotine or nicotinic agonists as well (Stevens et al, 1995(Stevens et al, , 1999Adler et al, 2001), presumably interacting with inhibitory neuronal circuitry involved in gating, i.e., GABAergic interneurons in the hippocampus (Stevens et al, 1999;Freedman et al, 2000). Subsequent experiments indicated a key role for the ␣7 nAChR in nicotine-induced improvement in auditory gat- ing and in gating mechanisms in general.…”

Section: Discussionmentioning

confidence: 99%

The Selective α7 Nicotinic Acetylcholine Receptor Agonist PNU-282987 [N-[(3R)-1-Azabicyclo[2.2.2]oct-3-yl]-4-chlorobenzamide Hydrochloride] Enhances GABAergic Synaptic Activity in Brain Slices and Restores Auditory Gating Deficits in Anesthetized Rats

Hajós

Hurst²,

Hoffmann³

et al. 2004

J Pharmacol Exp Ther

218

149

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Schizophrenic patients are thought to have an impaired ability to process sensory information. This deficit leads to disrupted auditory gating measured electrophysiologically as a reduced suppression of the second of paired auditoryevoked responses (P50) and is proposed to be associated with decreased function and/or expression of the homomeric ␣7 nicotinic acetylcholine receptor (nAChR). Here, we provide evidence that N- [(3R)-1-azabicyclo[2.2.2]oct-3-yl]-4-chlorobenzamide hydrochloride (PNU-282987), a novel selective agonist of the ␣7 nAChR, evoked whole-cell currents from cultured rat hippocampal neurons that were sensitive to the selective ␣7 nAChR antagonist methyllycaconitine (MLA) and enhanced GABAergic synaptic activity when applied to hippocampal slices. Amphetamine-induced sensory gating deficit, determined by auditory-evoked potentials in hippocampal CA3 region, was restored by systemic administration of PNU-282987 in chloral hydrate-anesthetized rats.

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“…Because nicotine′s demonstrated modulatory effect on sensory gating lasts less than 60 minutes (Adler et al, 2001;Adler et al, 1992), recordings were not conducted until at least 1 hour after any participant had smoked. None of the smokers were recorded during a withdrawal period that exceeded normal daily routine (number of smokers = 5, 4, and 8 for auditory, somatosensory and combined studies respectively).…”

Section: Participantsmentioning

confidence: 99%

Gamma and beta neural activity evoked during a sensory gating paradigm: Effects of auditory, somatosensory and cross-modal stimulation

Kisley

Cornwell

2006

Clinical Neurophysiology

115

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Objective.-Stimulus-driven salience is determined involuntarily, and by the physical properties of a stimulus. It has recently been theorized that neural coding of this variable involves oscillatory activity within cortical neuron populations at beta frequencies. This was tested here through experimental manipulation of inter-stimulus interval (ISI).Methods.-Non-invasive neurophysiological measures of event-related gamma (30-50 Hz) and beta (12-20 Hz) activity were estimated from scalp-recorded evoked potentials. Stimuli were presented in a standard "paired-stimulus" sensory gating paradigm, where the S1 (conditioning) stimulus was conceptualized as long-ISI, or "high salience," and the S2 (test) stimulus as short-ISI, or "low salience." Three separate studies were conducted: auditory stimuli only (N=20 participants), somatosensory stimuli only (N=20), and a cross-modal study for which auditory and somatosensory stimuli were mixed (N=40).Results.-Early (20-150 ms) stimulus-evoked beta activity was more sensitive to ISI than temporally-overlapping gamma band activity, and this effect was seen in both auditory and somatosensory studies. In the cross-modal study, beta activity was significantly modulated by the similarity (or dissimilarity) of stimuli separated by a short ISI (0.5 s); a significant cross-modal gating effect was nevertheless detected.Conclusions.-With regard to the early sensory-evoked response recorded from the scalp, the interval between identical stimuli especially modulates beta oscillatory activity.Significance.-This is consistent with developing theories regarding the different roles of temporally-overlapping oscillatory activity within cortical neuron populations at gamma and beta frequencies, particularly the claim that the latter is related to stimulus-driven salience.

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Reversal of Diminished Inhibitory Sensory Gating in Cocaine Addicts by a Nicotinic Cholinergic Mechanism

Cited by 36 publications

References 58 publications

The neural networks underlying auditory sensory gating

The neural networks underlying auditory sensory gating

The Selective α7 Nicotinic Acetylcholine Receptor Agonist PNU-282987 [N-[(3R)-1-Azabicyclo[2.2.2]oct-3-yl]-4-chlorobenzamide Hydrochloride] Enhances GABAergic Synaptic Activity in Brain Slices and Restores Auditory Gating Deficits in Anesthetized Rats

Gamma and beta neural activity evoked during a sensory gating paradigm: Effects of auditory, somatosensory and cross-modal stimulation

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