Event Title

Stimulating GABAA-α1 Receptors Does Not Affect Attention

Presenter Information

Rachel Poyle, Oberlin College

Location

Science Center, Bent Corridor

Start Date

10-27-2017 6:40 PM

End Date

10-27-2017 7:20 PM

Poster Number

2

Abstract

Attention deficits are common in psychiatric conditions such as schizophrenia and autism, but the biological basis of these deficits is not understood. Previous studies have shown that blocking GABAA receptors within the prefrontal cortex impairs attention, but there are a variety of different types of GABAA receptors which differ in their subunit composition. It is not known which GABAA receptor subtypes contribute to the attention deficit. The goal of this research was to investigate the role of GABAA receptors containing α1 subunits (i.e., GABAA-α1 receptors) in attention using the GABAA-α1 receptor agonist zolpidem (AmbienTM). We used the 5 Choice Serial Reaction Time Task (5CSRTT) to test the attention of rats while under the influence of zolpidem. We found that administration of zolpidem did not seem to significantly increase attention, but did increase the number of omitted trials. It is possible that the increase in omissions is related to a sedative effect, but zolpidem did not affect the number of magazine entries or response latencies, suggesting that the effect is not purely due to sedation. Zolpidem does appear to decrease impulsive behaviors, as indicated by a decrease in premature responses. This research is important because it could lead to better, more effective medication for disorders such as schizophrenia and autism because they are characterized by both deficits in attention and changes in signaling of the inhibitory neurotransmitter GABA.

Major

Biology; Neuroscience

Project Mentor(s)

Tracie Paine, Neuroscience

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Oct 27th, 6:40 PM Oct 27th, 7:20 PM

Stimulating GABAA-α1 Receptors Does Not Affect Attention

Science Center, Bent Corridor

Attention deficits are common in psychiatric conditions such as schizophrenia and autism, but the biological basis of these deficits is not understood. Previous studies have shown that blocking GABAA receptors within the prefrontal cortex impairs attention, but there are a variety of different types of GABAA receptors which differ in their subunit composition. It is not known which GABAA receptor subtypes contribute to the attention deficit. The goal of this research was to investigate the role of GABAA receptors containing α1 subunits (i.e., GABAA-α1 receptors) in attention using the GABAA-α1 receptor agonist zolpidem (AmbienTM). We used the 5 Choice Serial Reaction Time Task (5CSRTT) to test the attention of rats while under the influence of zolpidem. We found that administration of zolpidem did not seem to significantly increase attention, but did increase the number of omitted trials. It is possible that the increase in omissions is related to a sedative effect, but zolpidem did not affect the number of magazine entries or response latencies, suggesting that the effect is not purely due to sedation. Zolpidem does appear to decrease impulsive behaviors, as indicated by a decrease in premature responses. This research is important because it could lead to better, more effective medication for disorders such as schizophrenia and autism because they are characterized by both deficits in attention and changes in signaling of the inhibitory neurotransmitter GABA.