Blockade of epinephrine priming of the cerebral auditory evoked response by cortical cholinergic deafferentation

Berntson, Gary G.; Shafi, Reema; Sarter, Martin

doi:10.1016/s0306-4522(02)00702-9

Cited by 27 publications

(35 citation statements)

References 85 publications

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“…Consistent with this interpretation, systemic application of epinephrine activates the vagus nerve there by activating the nucleus tractus solitarius and the LC. The LC, through the release of norepinephrine activates the nucleus basalis, modulating sensory processing in the auditory cortex ("epinephrine priming") in a cholinergic dependent manner, whereas cholinergic deafferentation induced through chemical lesions of basal forebrain cholinergic neurons prevents this effect (Berntson et al, 2003b).…”

Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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Abstract-Vagus nerve stimulation (VNS) is an FDA approved treatment for drug-resistant epilepsy and depression.Recently, we demonstrated the capacity for repeatedly pairing sensory input with brief pulses of VNS to induce input specific reorganization in rat auditory cortex. This was subsequently used to reverse the pathological neural and perceptual correlates of hearing loss induced tinnitus. Despite its therapeutic potential, VNS mechanisms of action remain speculative. In this study, we report the acute effects of VNS on intra-cortical synchrony, excitability, and sensory processing in anesthetized rat auditory cortex. VNS significantly increased and decorrelated spontaneous multi-unit activity, and suppressed entrainment to repetitive noise burst stimulation at 6 -8 Hz but not after application of the muscarinic antagonist scopolamine. Collectively, these experiments demonstrate the capacity for VNS to acutely influence cortical synchrony and excitability and strengthen the hypothesis that acetylcholine and muscarinic receptors are involved in VNS mechanisms of action. These results are discussed with respect to their possible implications for sensory processing, neural plasticity, and epilepsy.

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Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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“…Ketamine administration increases epinephrine levels in the ketamine-resistant strain (FVB/Hsd), which show no alterations in AEPs. One rodent study showed systemic epinephrine increased the N1-P2 AEP amplitude, suggesting that epinephrine may modulate late latency AEPs (Berntson et al, 2003). Similarly, human studies have proposed that the hippocampus plays a role in sensory gating of late latency AEPs (Grunwald et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Ketamine Produces Lasting Disruptions in Encoding of Sensory Stimuli

Maxwell

Ehrlichman²,

Liang³

et al. 2005

J Pharmacol Exp Ther

131

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The current study analyzed the acute, chronic, and lasting effects of ketamine administration in four inbred mouse strains (C3H/HeHsd, C57BL/6Hsd, FVB/Hsd, and DBA/2Hsd) to evaluate vulnerability to ketamine as a drug of abuse and as a model of schizophrenia. Serum half-life of ketamine was similar between all strains (approximately 13 min). Also, the ratio of brain-to-serum ketamine levels was 3:1. Examination of multiple phases of auditory processing using auditory-evoked potentials (AEPs) following acute ketamine (0, 5, and 20 mg/kg) treatment revealed C3H/HeHsd mice to be most vulnerable to ketamine-induced alterations in AEPs, whereas FVB/Hsd mice exhibited the least electrophysiological sensitivity to ketamine. Overall, the precortical P1-evoked potential component increased in amplitude and latency, whereas the cortically generated N1 and P2 components decreased in amplitude and latency following acute ketamine across all strains. Brain catecholamine analyses indicated that ketamine decreased hippocampus epinephrine levels in C3H/HeHsd but elevated hippocampus epinephrine levels in FVB/Hsd, suggesting one potential mechanism for AEP vulnerability to ketamine. Based on results of the acute study, the immediate and lasting effects of chronic low-dose ketamine on AEPs were examined among C3H/HeHsd (sensitive) and FVB/Hsd (insensitive) mice. We observed a decrement of the N1 amplitude that persisted at least 1 week after the last exposure to ketamine across both strains. This lasting deficit in information processing occurred in the absence of acute changes among the FVB/Hsd mice. Implications for both ketamine abuse and N-methyl-D-aspartate hypofunction models of schizophrenia are discussed.

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“…NBM corticopetal cholinergic neurons could facilitate the modulatory effect adrenal hormones have on the PFC LFP during acquisition of fear memory and via this mechanism modulate fear memory. Pharmacologically enhancing arousal by systemic epinephrine administration enhances sensory evoked LFPs in the PFC and RSC (Berntson, Shafi, Knox, and Sarter, 2003b; Knox, Sarter, and Berntson, 2004) and both NBM cholinergic lesions and blockade of α1 noradrenergic receptors in the NBM attenuate these effects (Berntson et al, 2003b; Knox et al, 2004). Locus coeruleus neurons could secrete norepinephrine onto NBM corticopetal cholinergic neurons during acquisition of fear memory, which would cause an increase in ACh release in the PFC that is critical for fear memory formation in the conditioned suppression paradigm (LC➔NBM➔PFC).…”

Section: Bf Cholinergic Neurons In Fear and Extinction Memorymentioning

confidence: 99%

The role of basal forebrain cholinergic neurons in fear and extinction memory

Knox

2016

Neurobiology of Learning and Memory

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Cholinergic input to the neocortex, dorsal hippocampus (dHipp), and basolateral amygdala (BLA) is critical for neural function and synaptic plasticity in these brain regions. Synaptic plasticity in the neocortex, dHipp, ventral Hipp (vHipp), and BLA has also been implicated in fear and extinction memory. This finding raises the possibility that basal forebrain (BF) cholinergic neurons, the predominant source of acetylcholine in these brain regions, have an important role in mediating fear and extinction memory. While empirical studies support this hypothesis, there are interesting inconsistencies among these studies that raise questions about how best to define the role of BF cholinergic neurons in fear and extinction memory. Nucleus basalis magnocellularis (NBM) cholinergic neurons that project to the BLA are critical for fear memory and contextual fear extinction memory. NBM cholinergic neurons that project to the neocortex are critical for cued and contextual fear conditioned suppression, but are not critical for fear memory in other behavioral paradigms and in the inhibitory avoidance paradigm may even inhibit contextual fear memory formation. Medial septum and diagonal band of Broca cholinergic neurons are critical for contextual fear memory and acquisition of cued fear extinction. Thus, even though the results of previous studies suggest BF cholinergic neurons modulate fear and extinction memory, inconsistent findings among these studies necessitates more research to better define the neural circuits and molecular processes through which BF cholinergic neurons modulate fear and extinction memory. Furthermore, studies determining if BF cholinergic neurons can be manipulated in such a manner so as to treat excessive fear in anxiety disorders are needed.

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Blockade of epinephrine priming of the cerebral auditory evoked response by cortical cholinergic deafferentation

Cited by 27 publications

References 85 publications

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Ketamine Produces Lasting Disruptions in Encoding of Sensory Stimuli

The role of basal forebrain cholinergic neurons in fear and extinction memory

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