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Evidence for GABA-BZ receptor modulation in short-term memory passive avoidance task paradigm in mice.
Methods Find Exp Clin Pharmacol. 1990 Apr; 12(3):175-80.MF

Abstract

The possible involvement of gamma-aminobutyric acid/benzodiazepine (GABA-BZ) receptor modulation in scopolamine-induced short-term memory deficit was investigated in mice. Passive avoidance step-down task behavior was observed. Latency of mice to reach shock-free zone (SFZ) and number of mistakes the animal made in 15 min were used as separate parameters for acquisition and memory retention, respectively. Scopolamine (0.3 mg/kg) caused a delay in reaching SFZ and an increased number of mistakes. Physostigmine reversed the scopolamine-induced increase in number of mistakes; however, it caused a delay in the time to reach SFZ. Subeffective dose of GABA, when combined with physostigmine, further delayed the latency to reach SFZ, but reduced the number of mistakes very significantly. GABA (50, 75 and 100 mg/kg, i.p.) and GABA agonists sodium valproate (30 and 60 mg/kg, i.p.), fengabine (5 and 10 mg/kg, i.p.), (+/-)baclofen (0.25, 0.5 and 1.0 mg/kg, i.p.) and (-)baclofen (0.25 and 0.5 mg/kg i.p.) reversed the scopolamine-induced effect; however, sodium valproate at higher dose delayed time to reach SFZ. Combined administration of lower dose (+/-)baclofen and subeffective dose of GABA showed significant decrease in latency and number of mistakes in scopolamine-treated animals. The specific benzodiazepine antagonist flumazenil (Ro-15-1788) (5 and 10 mg/kg, i.p.) and inverse agonist FG-7142 (10 mg/kg, i.p.) very significantly reversed scopolamine-induced increase in number of mistakes, but Ro-15-1788 failed to show any effect on latency per se and in scopolamine-treated experiments, as well.(ABSTRACT TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Department of Pharmaceutical Sciences, Panjab University, Chandigarh, India.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

2161973

Citation

Sharma, A C., and S K. Kulkarni. "Evidence for GABA-BZ Receptor Modulation in Short-term Memory Passive Avoidance Task Paradigm in Mice." Methods and Findings in Experimental and Clinical Pharmacology, vol. 12, no. 3, 1990, pp. 175-80.
Sharma AC, Kulkarni SK. Evidence for GABA-BZ receptor modulation in short-term memory passive avoidance task paradigm in mice. Methods Find Exp Clin Pharmacol. 1990;12(3):175-80.
Sharma, A. C., & Kulkarni, S. K. (1990). Evidence for GABA-BZ receptor modulation in short-term memory passive avoidance task paradigm in mice. Methods and Findings in Experimental and Clinical Pharmacology, 12(3), 175-80.
Sharma AC, Kulkarni SK. Evidence for GABA-BZ Receptor Modulation in Short-term Memory Passive Avoidance Task Paradigm in Mice. Methods Find Exp Clin Pharmacol. 1990;12(3):175-80. PubMed PMID: 2161973.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence for GABA-BZ receptor modulation in short-term memory passive avoidance task paradigm in mice. AU - Sharma,A C, AU - Kulkarni,S K, PY - 1990/4/1/pubmed PY - 1990/4/1/medline PY - 1990/4/1/entrez SP - 175 EP - 80 JF - Methods and findings in experimental and clinical pharmacology JO - Methods Find Exp Clin Pharmacol VL - 12 IS - 3 N2 - The possible involvement of gamma-aminobutyric acid/benzodiazepine (GABA-BZ) receptor modulation in scopolamine-induced short-term memory deficit was investigated in mice. Passive avoidance step-down task behavior was observed. Latency of mice to reach shock-free zone (SFZ) and number of mistakes the animal made in 15 min were used as separate parameters for acquisition and memory retention, respectively. Scopolamine (0.3 mg/kg) caused a delay in reaching SFZ and an increased number of mistakes. Physostigmine reversed the scopolamine-induced increase in number of mistakes; however, it caused a delay in the time to reach SFZ. Subeffective dose of GABA, when combined with physostigmine, further delayed the latency to reach SFZ, but reduced the number of mistakes very significantly. GABA (50, 75 and 100 mg/kg, i.p.) and GABA agonists sodium valproate (30 and 60 mg/kg, i.p.), fengabine (5 and 10 mg/kg, i.p.), (+/-)baclofen (0.25, 0.5 and 1.0 mg/kg, i.p.) and (-)baclofen (0.25 and 0.5 mg/kg i.p.) reversed the scopolamine-induced effect; however, sodium valproate at higher dose delayed time to reach SFZ. Combined administration of lower dose (+/-)baclofen and subeffective dose of GABA showed significant decrease in latency and number of mistakes in scopolamine-treated animals. The specific benzodiazepine antagonist flumazenil (Ro-15-1788) (5 and 10 mg/kg, i.p.) and inverse agonist FG-7142 (10 mg/kg, i.p.) very significantly reversed scopolamine-induced increase in number of mistakes, but Ro-15-1788 failed to show any effect on latency per se and in scopolamine-treated experiments, as well.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0379-0355 UR - https://www.unboundmedicine.com/medline/citation/2161973/Evidence_for_GABA_BZ_receptor_modulation_in_short_term_memory_passive_avoidance_task_paradigm_in_mice_ L2 - https://antibodies.cancer.gov/detail/CPTC-CALR-1 DB - PRIME DP - Unbound Medicine ER -