Chronic Ethanol Exposure Increases <sup>3</sup>H‐GABA Release in Rat Hippocampus by Presynaptic Muscarinic Receptor Modulation

Hu, Ming; Walker, David A.; Vickroy, Thomas W.; Peris, Joanna

doi:10.1111/j.1530-0277.1999.tb04048.x

Cited by 8 publications

(4 citation statements)

References 35 publications

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“…Unlike CIE, chronically treated rodents show morphological changes and neuronal loss in hippocampus and cortex (Farr, Scherrer, Banks, Flood, & Morley, 2005; Mandyam, 2013; Walker, Barnes, Zornetzer, Hunter, & Kubanis, 1980). Chronic ethanol treatment diminishes LTP in the hippocampus and, again, this correlates with deficits in spatial learning (Hu, Walker, Vickroy, & Peris, 1999; Peris et al, 1997). Effects on LTD have received less attention, but chronic exposure appears to dampen this form of plasticity as well (Thinschmidt, Walker, & King, 2003).…”

Section: Chronic Effects Of Ethanol On Hippocampal Plasticitymentioning

confidence: 95%

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Zorumski¹,

Mennerick²,

Izumi³

2014

Alcohol

142

113

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Alcoholism is associated with acute and long-term cognitive dysfunction including memory impairment, resulting in substantial disability and cost to society. Thus, understanding how ethanol impairs cognition is essential for developing treatment strategies to dampen its adverse impact. Memory processing is thought to involve persistent, use-dependent changes in synaptic transmission, and ethanol alters the activity of multiple signaling molecules involved in synaptic processing, including modulation of the glutamate and gamma-aminobutyric acid (GABA) transmitter systems that mediate most fast excitatory and inhibitory transmission in the brain. Effects on glutamate and GABA receptors contribute to ethanol-induced changes in long-term potentiation (LTP) and long-term depression (LTD), forms of synaptic plasticity thought to underlie memory acquisition. In this paper, we review the effects of ethanol on learning-related forms of synaptic plasticity with emphasis on changes observed in the hippocampus, a brain region that is critical for encoding contextual and episodic memories. We also include studies in other brain regions as they pertain to altered cognitive and mental function. Comparison of effects in the hippocampus to other brain regions is instructive for understanding the complexities of ethanol’s acute and long-term pharmacological consequences.

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Section: Chronic Effects Of Ethanol On Hippocampal Plasticitymentioning

confidence: 95%

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Zorumski¹,

Mennerick²,

Izumi³

2014

Alcohol

142

113

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“…Chronic exposure to ethanol diminishes the magnitude of LTP in the hippocampus (Peris et al, 1997). Unlike the dual role of GABA and glutamate in decreasing LTP in the CIE paradigm, LTP in the CET model is altered due to changes in GABAergic inhibition and acetylcholine transmission (Hu, Walker, Vickroy, & Peris, 1999; Peris et al, 1997). Although the precise mechanism of CET-induced potentiation of hippocampal GABAergic inhibition remains to be determined, it may involve muscarinic receptor stimulation of GABAergic interneurons within the hippocampus (Hu et al, 1999; Peris et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Unlike the dual role of GABA and glutamate in decreasing LTP in the CIE paradigm, LTP in the CET model is altered due to changes in GABAergic inhibition and acetylcholine transmission (Hu, Walker, Vickroy, & Peris, 1999; Peris et al, 1997). Although the precise mechanism of CET-induced potentiation of hippocampal GABAergic inhibition remains to be determined, it may involve muscarinic receptor stimulation of GABAergic interneurons within the hippocampus (Hu et al, 1999; Peris et al, 1997). Another form of synaptic plasticity, long-term depression (LTD), involves low-frequency stimulation and is also thought to be involved in learning and memory processes (for review, see Collingridge, Peineau, Howland, & Wang, 2010).…”

Section: Introductionmentioning

confidence: 99%

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Vetreno

Hall

Savage

2011

Neurobiology of Learning and Memory

126

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Chronic alcoholism is associated with impaired cognitive functioning. Over 75% of autopsied chronic alcoholics have significant brain damage and over 50% of detoxified alcoholics display some degree of learning and memory impairment. However, the relative contributions of different etiological factors to the development of alcohol-related neuropathology and cognitive impairment are questioned. One reason for this quandary is that both alcohol toxicity and thiamine deficiency result in brain damage and cognitive problems. Two alcohol-related neurological disorders, alcohol-associated dementia and Wernicke-Korsakoff syndrome have been modeled in rodents. These pre-clinical models have elucidated the relative contributions of ethanol toxicity and thiamine deficiency to the development of dementia and amnesia. What is observed in these models-from repeated and chronic ethanol exposure to thiamine deficiency-is a progression of both neural and cognitive dysregulation. Repeated binge exposure to ethanol leads to changes in neural plasticity by reducing GABAergic inhibition and facilitating glutamatergic excitation, longterm chronic ethanol exposure results in hippocampal and cortical cell loss as well as reduced hippocampal neurotrophin protein content critical for neural survival, and thiamine deficiency results in gross pathological lesions in the diencephalon, reduced neurotrophic protein levels, and neurotransmitters levels in the hippocampus and cortex. Behaviorally, after recovery from repeated or chronic ethanol exposure there is impairment in working or episodic memory that can recover with prolonged abstinence. In contrast, after thiamine deficiency there is severe and persistent spatial memory impairments and increased perseverative behavior. The interaction between ethanol and thiamine deficiency does not produce more behavioral or neural pathology, with the exception of reduction of white matter, than long-term thiamine deficiency alone.

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“…Studies in the hippocampus show that chronic EtOH exposure decreased long-term potentiation (LTP) by increasing the electrically stimulated (but not basal) release of tritiated GABA pre-loaded in CA1 hippocampal slices (Tremwel et al 1994). The GABA uptake or GABA A R function was not altered, and this effect may be due to alterations in the muscarinic receptor regulation of GABA release at presynaptic terminals (Hu et al 1999). In addition, studies using the GABA B receptor agonist baclofen to reduce release of tritiated GABA suggest that a change in GABA B auto-receptors on GABAergic terminals may also contribute to this effect of chronic EtOH exposure on LTP (Peris et al 1997) (see later GABA B paragraph).…”

Section: Chronic Ethanol and Gabaergic Transmission: Presynaptic Effectsmentioning

confidence: 95%

Synaptic Effects Induced by Alcohol

Lovinger

Roberto

2010

Current Topics in Behavioral Neurosciences

117

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Ethanol (EtOH) has effects on numerous cellular molecular targets, and alterations in synaptic function are prominent among these effects. Acute exposure to EtOH activates or inhibits the function of proteins involved in synaptic transmission, while chronic exposure often produces opposing and/or compensatory/homeostatic effects on the expression, localization, and function of these proteins. Interactions between different neurotransmitters (e.g., neuropeptide effects on release of small molecule transmitters) can also influence both acute and chronic EtOH actions. Studies in intact animals indicate that the proteins affected by EtOH also play roles in the neural actions of the drug, including acute intoxication, tolerance, dependence, and the seeking and drinking of EtOH. This chapter reviews the literature describing these acute and chronic synaptic effects of EtOH and their relevance for synaptic transmission, plasticity, and behavior. KeywordsGABA; Glutamate; Monoamine; Neuropeptide; Neurotransmitter receptor; Presynaptic; Postsynaptic; Protein phosphorylation; Synaptic plasticity; Intoxication; Tolerance; Dependence Acute Ethanol ActionsEthanol (EtOH) produces intoxication through actions on the central nervous system (CNS) at concentrations ranging from low to ~100 mM (at least in non-tolerant humans and experimental animals). A number of proteins involved in synaptic transmission are altered by EtOH effects within this concentration range. The target proteins include, but are not limited to, ion channels, neurotransmitter receptors, and intracellular signaling proteins. The first section of this article will review the literature describing the most prominent acute EtOH effects on synaptic transmission in the CNS. This review is not meant to be comprehensive, but rather to cover those effects that have been observed most consistently and are thought to contribute to intoxication.

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Chronic Ethanol Exposure Increases ³H‐GABA Release in Rat Hippocampus by Presynaptic Muscarinic Receptor Modulation

Cited by 8 publications

References 35 publications

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Synaptic Effects Induced by Alcohol

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Chronic Ethanol Exposure Increases 3H‐GABA Release in Rat Hippocampus by Presynaptic Muscarinic Receptor Modulation

Cited by 8 publications

References 35 publications

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Synaptic Effects Induced by Alcohol

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Chronic Ethanol Exposure Increases ³H‐GABA Release in Rat Hippocampus by Presynaptic Muscarinic Receptor Modulation