A rapid and simple cannulation technique for repeated sampling of cerebrospinal fluid in freely moving rats

A cannulation technique for frequent sampling of cerebrospinal fluid (CSF) in unanaesthetized freely moving rats is described. A permanent stainless steel cannula, constructed in such a way that no loss of CSF occurs, is placed into the rat's cisterna magna and fixed to the skull by anchoring screws and dental cement. A special CSF outflow opening of the cannula is connected to polyethylene tubing for CSF sampling. Amounts of 50–150 μl CSF can be collected repeatedly without any sign of disturbing the animal. The technique lends itself not only to pilot studies in which within a short period of time a large amount of CSF is wanted, but also to experiments in which physiological conditions are required

Excessive grooming induced by somatostatin or its analog SMS 201-995

Intracerebroventricular (i.c.v.) administration of somatostatin or SMS 201-995 induces excessive grooming behavior in rats. The grooming inducing effect of somatostatin is rather weak, as doses of 300 ng or less did not result in increased total grooming scores. In contrast a dose of 10 ng SMS 201-995 already significantly the increased total grooming scores. However, doses of 100 ng and more did not further increase the total grooming scores reached with a 50 ng dose of this peptide. Systemic administration of SMS 201-995 in doses up to 900 μg did not result in excessive grooming behavior. The patterns of excessive grooming induced by i.c.v. SMS 201-995 and somatostatin were characterized by a predominant display of scratching. Since peptide-induced scratching is mainly due to activation of opiate receptor systems it is suggested that opiate receptors are involved in the behavioral response to SMS 201-995 and somatostatin administration. This suggestion is further supported by the suppressive effect of naloxone on excessive grooming induced by these peptides. Haloperidol and neurotensin also suppress the excessive grooming induced by somatostatin but not that induced by SMS 201-995. Finally, tolerance developed to the grooming-inducing effect of SMS 201-995 and somatostatin. In addition there was cross tolerance between somatostatin and SMS 201-995

Effects of intracerebral implantation of corticosteroids on extinction of an avoidance response in rats

Intracerebral implantation of dexamethasone phosphate facilitated the rate of extinction of a pole jumping avoidance response when implanted into various areas in the median and posterior thalamus and in the ventriculus lateralis. Corticosterone, the rat's natural corticosteroid, also facilitated extinction of the avoidance response, but mainly if implanted in or near the nucleus parafascicularis. Implantations of either dexamethasone phosphate or corticosterone in other areas like hippocampus, nucleus septi lateralis, nucleus caudatus putamen, nucleus interstitialis striae terminalis and nucleus ventralis thalami did not result in a modification of the extinction rat

Fornix transection: Discrimination between neuropeptide effects on attention and memory

Transection of the fornix and the stria terminalis completely blocks the inhibitory action of ACTH 4–10 on extinction of a conditioned avoidance response (CAR), whereas this effect of the vasopressin analogue des-glycinamide-lysine-vasopressin (DG-LVP) is not affected. These data indicate that the behavioral effect of DG-LVP may be localized to certain anatomical substrates, while ACTH 4–10 needs an intact limbic system as a functional substrate for its effect on avoidance behavior. This differential effect of fornicotomy may also be interpreted as a discrimination between the effects of these neuropeptides on attention or on memory consolidation. Additionally, transection of the fornix and the stria terminalis induces an increase in motor responsiveness to an electric footshock (EFS) and a facilitation of acquisition of a CAR

Microinjection of anti-vasopressin serum into limbic structures of the rat brain: effects on passive avoidance responding and on local catecholamine utilization

Rats which had received bilateral microinjections of 1:50 diluted anti-vasopressin serum into the dorsal or ventral hippocampus, immediately after the learning trial of a one-trial passive avoidance test, showed a reduction in avoidance latency scores during subsequent retention tests 24 and 48 h later. Postlearning microinjection of anti-vasopressin serum into either the dorsalateral septum or the caudate nucleus was without effect on the retention of passive avoidance behavior. Microinjection of anti-vasopressin serum 1 h before the 24-h retention session into either the dorsal hippocampus, the ventral hippocampus or the dorsolateral septum attenuated avoidance responding during both the 24-h and 48-h retention sessions, whereas preretention microinjection of the serum into the caudate nucleus was not effective. Intracerebroventricular administration of the anti-vasopressin serum in amounts similar to those used in the microinjection experiments did not affect retention scores when given either immediately after the learning trial or before the first retention session. One week after the behavioral experiments, a repeated microinjection of anti-vasopressin serum decreased the local α-methyl-p-tyrosine methylester (α-MPT)-induced disappearance of noradrenaline in the ventral hippocampus and the dorsal hippocampus respectively. Microinjection of the antiserum in the dorsolateral septum enhanced noradrenaline disappearance in this brain region. No effect was found on α-MPT-induced dopamine disappearance in the caudate nucleus following local microinjection of anti-vasopressin serum. These data show that endogenous vasopressin in both the dorsal and the ventral hippocampus is functionally involved in consolidation processes as well as in retrieval processes related to passive avoidance behavior, while that in the dorsolateral septum seems to be involved in retrieval processes only. They also show that noradrenergic mechanisms in these 3 brain regions respond to the local reduction of the amount of bioavailable vasopressin in a direction opposite to that observed after local microinjection of vasopressin, which suggests that vasopressin might act by modulating noradrenergic neurotransmission

Microinjection of anti-vasopressin serum into limbic structures of the rat brain: effects on passive avoidance responding and on local catecholamine utilization

Rats which had received bilateral microinjections of 1:50 diluted anti-vasopressin serum into the dorsal or ventral hippocampus, immediately after the learning trial of a one-trial passive avoidance test, showed a reduction in avoidance latency scores during subsequent retention tests 24 and 48 h later. Postlearning microinjection of anti-vasopressin serum into either the dorsalateral septum or the caudate nucleus was without effect on the retention of passive avoidance behavior. Microinjection of anti-vasopressin serum 1 h before the 24-h retention session into either the dorsal hippocampus, the ventral hippocampus or the dorsolateral septum attenuated avoidance responding during both the 24-h and 48-h retention sessions, whereas preretention microinjection of the serum into the caudate nucleus was not effective. Intracerebroventricular administration of the anti-vasopressin serum in amounts similar to those used in the microinjection experiments did not affect retention scores when given either immediately after the learning trial or before the first retention session. One week after the behavioral experiments, a repeated microinjection of anti-vasopressin serum decreased the local α-methyl-p-tyrosine methylester (α-MPT)-induced disappearance of noradrenaline in the ventral hippocampus and the dorsal hippocampus respectively. Microinjection of the antiserum in the dorsolateral septum enhanced noradrenaline disappearance in this brain region. No effect was found on α-MPT-induced dopamine disappearance in the caudate nucleus following local microinjection of anti-vasopressin serum. These data show that endogenous vasopressin in both the dorsal and the ventral hippocampus is functionally involved in consolidation processes as well as in retrieval processes related to passive avoidance behavior, while that in the dorsolateral septum seems to be involved in retrieval processes only. They also show that noradrenergic mechanisms in these 3 brain regions respond to the local reduction of the amount of bioavailable vasopressin in a direction opposite to that observed after local microinjection of vasopressin, which suggests that vasopressin might act by modulating noradrenergic neurotransmission

Plasma and cerebrospinal fluid α-MSH levels in the rat after hypophysectomy and stimulation of pituitary α-MSH secretion

Immunoreactive α-MSH was measured in cerebrospinal fluid (CSF) and plasma of rats. While treatment with haloperidol increased α-MSH levels in the plasma concentration of α-MSH in the CSF showed little change. Hypophysectomy also had little effect on the concentration of α-MSH in the CSF despite the fall in plasma α-MSH levels. This lack of correlation between α-MSH levels in the CSF and plasma suggests that the systemic circulation does not deliver α-MSH to the CSF. The apparently normal levels of α-MSH in the hypothalamus after hypophysectomy suggests that this tissue is able to synthesize α-MSH and it is possible that the hypothalamus is a source of the α-MSH in the CSF

Changes in cerebrospinal fluid levels of vasopressin and oxytocin of the rat during various light-dark regimes

Levels of arginine-vasopressin (AVP) and oxytocin (OXT) in cerebrospinal fluid (CSF) of rats were determined at various times of the day and the night under normal and changed light-dark conditions. During a regular daily 14 h and 10 h dark cycle (lights on 06.00 h, off 20.00 h), AVP in CSF reached a peak at 13.00 h, while the lowest levels were found at 19.00 h), AVP in CSF light-dark cycle into a 14 h dark and 10 h light cycle (lights on 20.00 h, off 06.00 h) did not change the normal AVP rhythm. These lighting conditions elevated the OXT levels in the CSF as compared to those found during a normal light-dark regine, but again no differences were observed between the OXT levels determined at the various time-points. A shift of 6 h of the light-dark cycle (lights on 12.00 h, lights off 02.00 h), completely disrupted the AVP rhythm. However, after 3 weeks of adaptation to this new light-dark regime a high level of AVP in CSF was again observed at 13.00 h, and a low level at 19.00 h. The present data suggest that changes in the normal light-dark conditions affect the levels of neurohypophyseal peptides in the CSF. The results are of interest because of reported changes in memory function induced by alterations in the light-dark cycle

Effects of hypophysectomy and ACTH1–10 on responsiveness to electric shock in rats

Response behavior of rats to unescapable electric shock was studied in intact and hypophysectomized animals. The threshold for flinch, jerk, run and jump was significantly lowered in hypophysectomized rats as compared to that of intact controls. Treatment with the ACTH analogue ACTH1–10 did not affect threshold levels in hypophysectomized nor in intact rats. It is concluded that the stimulating effect of ACTH1–10 on conditioned avoidance acquisition in hypophysectomized rats is not caused by an influence on sensory capacities