Effects of chronic alcohol consumption and withdrawal on the somatostatin‐immunoreactive neurons of the rat hippocampal dentate hilus

Abstract

Previous studies have demonstrated that the dentate granule and the CA3 pyramidal cells of the rat hippocampal formation are neuronal populations vulnerable to the toxic effects of ethanol. It also has been shown that the resulting alterations do not end after withdrawal from ethanol. As the neurons in the dentate hilus are heavily interconnected with the dentate granule cells, the authors decided to examine the fate of the hilar neurons after chronic alcohol consumption and withdrawal, inasmuch as the hilar somatostatin-immunoreactive (SS-I) neurons were found to be sensitive to cerebral ischemia and to seizures. The following groups of adult rats were studied: (1) alcohol-fed for 6 and 12 months; (2) alcohol-fed for 6 months and then switched to water for a further 6 months; (3) pair-fed controls; and (4) controls fed ad libitum. The authors determined the numerical density of hilar neurons and the number of its SS-I subpopulation. These were found to be significantly reduced in both the alcohol-fed and withdrawal groups when compared with the respective age-matched controls. The consequent loss of the integrative action of the hilar neurons, including the SS-Is, could explain some of the alcohol-related functional deficits as well as their persistence after withdrawal.

Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure

“…GABAergic interneurons are particularly vulnerable to a variety of insults, including excitotoxicity (Shetty et al, 2009; Shetty and Turner, 2001), ischemic events (Bering et al, 1997; Johansen, 1993), and traumatic brain injury (Lowenstein et al, 1992; Schiavone et al, 2017). Previous research has also demonstrated that interneurons in a variety of brain regions are susceptible to damage by both developmental and postnatal EtOH exposure (Andrade et al, 1992; Moore et al, 1998). Developmental exposure to EtOH reduces interneuron populations in cortical areas (Miller, 2006; Moore et al, 1998; Smiley et al, 2015), and in the cerebellum (Nirgudkar et al, 2016).…”

Discrete cue‐conditioned alcohol‐seeking after protracted abstinence: pattern of neural activation and involvement of orexin1 receptors

“…Few studies to date, however, have examined the substrates involved following periods of extended abstinence (Valdez et al ., 2002; Adams et al ., 2010). It has been documented that abstinence from alcohol results in a number of functional neuronal alterations that may contribute to propensity to relapse, including enhanced corticostriatal synaptic plasticity (Xia et al ., 2006), altered hippocampal inhibitory mechanisms and synaptic structure (Faingold et al ., 2004), and modification to neurotransmitter and receptor expression and function (Andrade et al ., 1992; Vizi et al ., 2000; Chandler et al ., 2006). It is unknown how these alterations may contribute to the mechanisms involved in relapse.…”

Activation of somatostatin‐synthesizing neurons in the hippocampal formation through kindling‐induced seizures

“…It is known that neurons of the hippocampal formation are highly susceptible to insults and can degenerate as a result of various injuries. Neurons of the dentate gyrus and subpopulations of hippocampal pyramidal cells are affected following, for example, Alzheimer's disease, alcoholism, ischemia, and epileptic seizures (Chan-Palay, 1987;Andrade et al, 1992;Matsuyama et al, 1993;Obenaus et al, 1993;Sloviter, 1987). Attempts to characterize these neurons neurochemically have shown that they contain a variety of putative neurotransmitters, such as glutamate, GABA, neuropeptide Y (NPY) or somatostatin (SS'I'; de Lanerolle and Spencer, 1991;Kohler et al, 1987).…”

“…Attempts to characterize these neurons neurochemically have shown that they contain a variety of putative neurotransmitters, such as glutamate, GABA, neuropeptide Y (NPY) or somatostatin (SS'I'; de Lanerolle and Spencer, 1991;Kohler et al, 1987). Of these hippocampal neurons, those containing SST have been found to degenerate the earliest and most consistently following insults (Andrade et al, 1992;Chan-Palay, 1987;Matsuyama et al, 1993) including epileptic seizures (Robbins et al, 1991;Sloviter, 1987). The reasons for the early degeneration of SST neurons are not known and could be due to direct or indirect effects of each pathogenesis on the ability of these neurons to function.…”