Different outcomes after acute and chronic treatment with nicotine in pre-pulse inhibition in Lister hooded rats

• Published in: European journal of pharmacology Vol. 407; no. 1; pp. 73 - 81
• Main Authors: Mirza, Naheed R, Misra, Anil, Bright, Joanne L
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 27.10.2000; Elsevier
• Subjects: Animals; Biological and medical sciences; Brain - metabolism; Drug toxicity and drugs side effects treatment; Information processing; Medical sciences; Mental Processes - drug effects; Mental Processes - physiology; Motor Activity - drug effects; Motor Activity - physiology; Nicotine; Nicotine - administration & dosage; Nicotine - pharmacokinetics; Nicotinic Agonists - administration & dosage; Nicotinic Agonists - pharmacokinetics; Pharmacology. Drug treatments; Pre-pulse inhibition; Rat; Rats; Reflex, Startle - drug effects; Reflex, Startle - physiology; Schizophrenia; Schizophrenia - drug therapy; Toxicity: nervous system and muscle; Schizophrenia; Rat; Pre-pulse inhibition; Information processing; Nicotine; Human; Nervous system diseases; Neuroleptic; Psychotropic; Toxicity; Acute; Rodentia; Tobacco smoking; Biological activity; Cerebral disorder; Psychosis; Prevention; Vertebrata; Chronic; Cholinergic receptor; Mammalia; Animal; Central nervous system disease; Mechanism of action; Nicotinic receptor; Extrapyramidal syndrome
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(00)00658-0

Excessive tobacco consumption by schizophrenic patients may be a form of self-medication, and nicotine in tobacco may alleviate deficits in information processing. We tested this hypothesis by determining whether nicotine (acute/chronic) would improve information processing in the rat using pre-pulse inhibition as a model. In study 1, rats were injected with nicotine 10 min prior to placement in startle chambers (0.001–0.1 or 0.03–0.3 mg/kg, s.c.). In study 2, rats were injected with either saline or nicotine (0.4 mg/kg, s.c.) for 21 consecutive days and assessed for locomotor activity, pre-pulse inhibition and changes in [ 3H]nicotine binding in whole brain. Acutely, nicotine had no effect on pre-pulse inhibition. By contrast, after chronic nicotine treatment, rats demonstrated a robust deficit in pre-pulse inhibition and significant increases in locomotor activity and [ 3H]nicotine binding. The deficit in pre-pulse inhibition after chronic treatment with nicotine may be the result of non-specific behavioural activation due to increased mesolimbic dopamine release or, possibly, nicotine may rapidly desensitize nicotinic receptors important for normal information processing.