Different outcomes after acute and chronic treatment with nicotine in pre-pulse inhibition in Lister hooded rats.
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.
Mirza
N R
NR
Department of Neuropharmacology, Vernalis PLC, Oakdene Court, 613 Reading Road, Winnersh, RG41 5UA, Wokingham, UK. max@neuroserach.dk
Misra
A
A
Bright
J L
JL
D000818:Animals; D001921:Brain / Q000378:metabolism; D008606:Mental Processes / Q000187:drug effects / Q000502:physiology; D009043:Motor Activity / Q000187:drug effects* / Q000502:physiology; D009538:Nicotine / Q000008:administration & dosage* / Q000493:pharmacokinetics; D018722:Nicotinic Agonists / Q000008:administration & dosage* / Q000493:pharmacokinetics; D051381:Rats; D013216:Reflex, Startle / Q000187:drug effects* / Q000502:physiology; D012559:Schizophrenia / Q000188:drug therapy
D018722:Nicotinic Agonists; D009538:Nicotine