Consequences of adolescent alcohol use on adult hippocampal neurogenesis and hippocampal integrity

Wooden, Jessica I.; Thompson, Keith; Guerin, Steven; Nawarawong, Natalie N.; Nixon, Kimberly

doi:10.1016/bs.irn.2021.08.005

Cited by 16 publications

(11 citation statements)

References 133 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More notable is that the pharmacological inactivation of the hippocampus prevents the reinstatement of ethanol seeking triggered by ethanol context, indicating a direct role of the hippocampus in ethanol-context memories and motivation to seek ethanol [50]. Furthermore, ethanol seeking in ethanol-dependent animals could be resulting from neuroplastic and neuroadaptive changes in the DG associated with adult hippocampal neurogenesis (reviewed in [24,[51][52][53][54][55][56]). Such neuroplastic changes could involve the proliferative burst in the progenitor cells in the DG 72 h into withdrawal from CIE, a time frame associated with negative affect [16,23].…”

Section: Discussionmentioning

confidence: 99%

“…Unlike the SVZ, in the DG, human subjects with AUD show reduced levels of progenitor cells and neurogenesis [70,71], supporting the various animal studies that detect similar changes in models of moderate to severe AUD. Therefore, the inhibitory effect of ethanol on the regenerative capacity of the adult hippocampus is considered a precursor for ethanolinduced neurodegeneration in the hippocampus [54,55]. Furthermore, it appears that the withdrawal and early abstinence-induced rebound effect in progenitor cells in the DG is associated with hyperactivity stemming from the neurocircuitry underlying the ethanol withdrawal-induced kindling-like behaviors [24].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Progenitor Cells Play a Role in Reinstatement of Ethanol Seeking in Adult Male and Female Ethanol Dependent Rats

Nonoguchi,

Jin,

Narreddy

et al. 2023

IJMS

View full text Add to dashboard Cite

Female and male glial fibrillary acidic protein-thymidine kinase (GFAP-TK) transgenic rats were made ethanol dependent via a six-week chronic intermittent ethanol vapor (CIE) and ethanol drinking (ED) procedure. During the last week of CIE, a subset of male and female TK rats was fed valcyte to ablate dividing progenitor cells and continued the diet until the end of this study. Following week six, all CIE rats experienced two weeks of forced abstinence from CIE-ED, after which they experienced relapse to drinking, extinction, and reinstatement of ethanol seeking sessions. CIE increased ED in female and male rats, with females having higher ethanol consumption during CIE and relapse sessions compared with males. In both sexes, valcyte reduced the levels of Ki-67-labeled progenitor cells in the subgranular zone of the dentate gyrus and did not alter the levels in the medial prefrontal cortex (mPFC). Valcyte increased ED during relapse, increased lever responses during extinction and, interestingly, enhanced latency to extinguish ethanol-seeking behaviors in males. Valcyte reduced the reinstatement of ethanol-seeking behaviors triggered by ethanol cues in females and males. Reduced seeking by valcyte was associated with the normalization of cytokines and chemokines in plasma isolated from trunk blood, indicating a role for progenitor cells in peripheral inflammatory responses. Reduced seeking by valcyte was associated with increases in tight junction protein claudin-5 and oligodendrogenesis in the dentate gyrus and reduction in microglial activity in the dentate gyrus and mPFC in females and males, demonstrating a role for progenitor cells in the dentate gyrus in dependence-induced endothelial and microglial dysfunction. These data suggest that progenitor cells born during withdrawal and abstinence from CIE in the dentate gyrus are aberrant and could play a role in strengthening ethanol memories triggered by ethanol cues via central and peripheral immune responses.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Progenitor Cells Play a Role in Reinstatement of Ethanol Seeking in Adult Male and Female Ethanol Dependent Rats

Nonoguchi,

Jin,

Narreddy

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…For vimentin, the brain was surveyed and two regions with visibly distinct vimentin + immunoreactivity were selected for quantification: the hippocampus (profile counts above) and the forceps minor of the corpus callosum (CC fm ). Past work has shown that adolescents have damage in these two regions in particular [73][74][75]. In sections where the CC fm was visible, three images were taken at 40×: Box A placed proximally, Box B placed dorsally, and Box C placed laterally.…”

Section: Quantificationmentioning

confidence: 99%

“…Brains were surveyed for vimentin immunoreactivity (vim+IR) in the IP group (PND 44) and in the IP+2BC group (PND 111). The hippocampus and forceps minor of the corpus callosum were chosen for quantification due to prior reports of damage in these regions [73][74][75]. In the corpus callosum (Figure 6A,B-E), densitometry was performed and two-way ANOVA revealed no main effects, though a significant interaction [F(1, 25) = 10.30, p = 0.0036], reflected that AIE rats had a 33 ± 0.02% increase in vim+IR (p = 0.03) following i.p.…”

Section: Aie Increased Astrocyte Reactivity In Adolescence But Not Fo...mentioning

confidence: 99%

Adolescent Intermittent Ethanol Drives Modest Neuroinflammation but Does Not Escalate Drinking in Male Rats

Wooden,

Peacoe,

Anasooya Shaji

et al. 2023

Cells

View full text Add to dashboard Cite

During adolescence, the brain is highly susceptible to alcohol-induced damage and subsequent neuroimmune responses, effects which may enhance development of an alcohol use disorder (AUD). Neuroimmune reactions are implicated in adolescent alcohol exposure escalating adulthood drinking. Therefore, we investigated whether intermittent alcohol exposure in male, adolescent rats (AIE) escalated adult drinking via two-bottle choice (2BC). We also examined the influence of housing environment across three groups: standard (group-housed with enrichment during 2BC), impoverished (group-housed without enrichment during 2BC), or isolation (single-housed without bedding or enrichment throughout). In the standard group immediately after AIE/saline and after 2BC, we also examined the expression of microglial marker, Iba1, reactive astrocyte marker, vimentin, and neuronal cell death dye, FluoroJade B (FJB). We did not observe an escalation of adulthood drinking following AIE, regardless of housing condition. Further, only a modest neuroimmune response occurred after AIE in the standard group: no significant microglial reactivity or neuronal cell death was apparent using this model, although some astrocyte reactivity was detected in adolescence following AIE that resolved by adulthood. These data suggest that the lack of neuroimmune response in adolescence in this model may underlie the lack of escalation of alcohol drinking, which could not be modified through isolation stress.

show abstract

“…To date, how alcohol affects neurogenesis is still poorly understood, but it is possible that it alters the cell cycle and interferes with proliferation and/or decreases BDNF action that promotes cell survival and differentiation [ 206 , 209 ]. Recently, some authors have proposed that understanding the role of neurogenesis in adolescent alcohol use and misuse is critical to our understanding of adolescent susceptibility to alcohol pathology and the increased likelihood of developing alcohol problems in adulthood [ 210 ]. Findings from human adolescent studies suggest that binge drinking is associated with poorer cognitive functioning on a broad range of neuropsychological assessments, including learning, memory, visuospatial functioning, psychomotor speed, attention, executive functioning, and impulsivity, which are deficits involved in the prognosis and addiction severity [ 211 ].…”

Section: Involvement Of Bdnf In Alcohol Abuse During Adolescencementioning

confidence: 99%

BDNF and its Role in the Alcohol Abuse Initiated During Early Adolescence: Evidence from Preclinical and Clinical Studies

Cutuli

Sampedro-Piquero

2022

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) is a crucial brain signaling protein that is integral to many signaling pathways. This neurotrophin has shown to be highly involved in brain plastic processes such as neurogenesis, synaptic plasticity, axonal growth, and neurotransmission, among others. In the first part of this review, we revise the role of BDNF in different neuroplastic processes within the central nervous system. On the other hand, its deficiency in key neural circuits is associated with development of psychiatric disorders, including alcohol abuse disorder. Many people begin to drink alcohol during adolescence, and it seems that changes in BDNF are evident after the adolescent engaged regularly in alcohol use. Therefore, the second part of this manuscript addresses the involvement of BDNF during adolescent brain maturation and how this process can be negatively affected by alcohol abuse. Finally, we propose different BNDF enhancers, both behavioral and pharmacological, which should be considered in the treatment of problematic alcohol consumption initiated during the adolescence.

show abstract

Consequences of adolescent alcohol use on adult hippocampal neurogenesis and hippocampal integrity

Cited by 16 publications

References 133 publications

Progenitor Cells Play a Role in Reinstatement of Ethanol Seeking in Adult Male and Female Ethanol Dependent Rats

Progenitor Cells Play a Role in Reinstatement of Ethanol Seeking in Adult Male and Female Ethanol Dependent Rats

Adolescent Intermittent Ethanol Drives Modest Neuroinflammation but Does Not Escalate Drinking in Male Rats

BDNF and its Role in the Alcohol Abuse Initiated During Early Adolescence: Evidence from Preclinical and Clinical Studies

Contact Info

Product

Resources

About