Trevor Archer

Galanin impairs acquisition but not retrieval of spatial memory in rats studied in the Morris swim maze.

The effect of intraventricular administration of the neuropeptide galanin on acquisition and retrieval in a modified Morris swim maze was studied in rats. Galanin induced a significant deficit in the acquisition of the task while no effects on the retrieval were observed. No deficits were seen 24 h after the last treatment. Galanin did not increase the number of failures to reach the platform. It is suggested that endogenous galanin modulates learning possibly via the galanin-containing cholinergic neurons in the septum-basal forebrain area projecting to the hippocampus and cortex.

Role of central noradrenaline neurons in the contextual control of latent inhibition in taste aversion learning.

Three experiments were performed to examine the effects of noradrenaline (NA) depletion, using 3 different methods: lesions of the dorsal noradrenergic bundle (DB) with 6-hydroxydopamine (6-OHDA), lesions induced by neonatal treatment with 6-OHDA and lesions induced by systemic DSP4 upon latent inhibition, using the taste-aversion learning procedure. NA depleted and control (sham, vehicle or saline) rats were given pre-exposure trials to either novel saccharin or to novel saccharin in a novel type of drinking bottle (the noisy bottle). Later, during conditioning trials saccharin was presented in the noisy bottles for all the rats, followed by lithium chloride injections. Saccharin aversions, tested for in the noisy bottles, indicated considerably weaker saccharin aversions (i.e. more latent inhibition) by the control groups pre-exposed to both saccharin and the noisy bottles. These context-dependent latent inhibition effects were clearly attenuated by all 3 treatments that depleted central NA. Biochemical assays confirmed the NA depletions in each case. The results, demonstrating the intimate role of central NA neurons in contextual control of latent inhibition in taste-aversion learning, appear to conform with current attentional theories of NA function in the forebrain.

Noradrenaline and the context-dependent extinction effect

Three experiments were performed to examine the effects of noradrenaline (NA) depletion upon the context-dependent extinction effects in conditioned taste-aversion learning. Three different methods were used to deplete NA: lesions of the dorsal noradrenergic bundle (DNAB) with 6-hydroxydopamine (6-OHDA), lesions induced by neonatal treatment with 6-OHDA and lesions induced by systemic administration with the NA neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). In each experiment, novel saccharin was presented in novel noisy bottle followed by lithium chloride. Later, during the extinction phase, half the control and half the NA depleted rats received saccharin in noisy bottles while the other half received saccharin in silent bottles. In the control condition, the rats that received saccharin in the noisy bottles (same context as conditioning) showed considerably more aversion than those that received saccharin in the silent bottles (different context to conditioning); NA depletion attenuated this effect. Reinstatement of the conditioning context (noisy bottle) resulted in a stronger aversion in the case where the different context (silent bottle) was present during extinction; this effect was attenuated in the NA depletion condition. These findings maintain a role for noradrenaline in compound conditioning tasks.

Attenuation of sensory preconditioning by noradrenaline depletion in the rat

In order to investigate the effect of noradrenaline (NA) depletion upon an associative learning phenomenon, sensory preconditioning, rats were inflicted with either 6-hydroxydopamine-induced lesions of the dorsal noradrenergic bundle (DNAB) or the locus coeruleus (LC), or with systemic injections of the NA neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). Using appropriate controls (the UP groups) sensory preconditioning was demonstrated clearly in the non-lesion conditions (Sham or saline), but was blocked or strongly attenuated in the DNAB and DSP4 conditions. LC lesions did not affect sensory preconditioning. These findings suggest that the loss of central NA may cause some disruption of some aspects of complex associative learning. The role of NA in sensory preconditioning may be relevant to current notions of NA function.