Septal and Hippocampal Glutamate Receptors Modulate the Output of Acetylcholine in Hippocampus: A Microdialysis Study

Moor, E; Auth, Ferenc; Deboer, P; Westerink, Ben H.C.

doi:10.1046/j.1471-4159.1996.67010310.x

Cited by 37 publications

(12 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cholinergic neurons synapse onto glutamatergic cells in the hippocampus (Moor et al 1996). The individual roles of glutamatergic and cholinergic processes in the hippocampus have been well demonstrated (Izquierdo et al 1993;Staubli et al 1994;Ohno and Watanabe 1996).…”

Section: Acetylcholine Gaba and Spontaneous Alternationmentioning

confidence: 99%

Increasing Acetylcholine Levels in the Hippocampus or Entorhinal Cortex Reverses the Impairing Effects of Septal GABA Receptor Activation on Spontaneous Alternation

Degroot¹,

Parent²

2000

Learn. Mem.

View full text Add to dashboard Cite

Intra-septal infusions of the ␥-aminobutyric acid (GABA) agonist muscimol impair learning and memory in a variety of tasks. This experiment determined whether hippocampal or entorhinal infusions of the acetylcholinesterase inhibitor physostigmine would reverse such impairing effects on spontaneous alternation performance, a measure of spatial working memory. Male Sprague-Dawley rats were given intra-septal infusions of vehicle or muscimol (1 nmole/0.5 µL) combined with unilateral intra-hippocampal or intraentorhinal infusions of vehicle or physostigmine (10 µg/µL for the hippocampus; 7.5 µg/µL or 1.875 µg/0.25 µL for the entorhinal cortex). Fifteen minutes later, spontaneous alternation performance was assessed. The results indicated that intra-septal infusions of muscimol significantly decreased percentage-of-alternation scores, whereas intra-hippocampal or intra-entorhinal infusions of physostigmine had no effect. More importantly, intra-hippocampal or intra-entorhinal infusions of physostigmine, at doses that did not influence performance when administered alone, completely reversed the impairing effects of the muscimol infusions. These findings indicate that increasing cholinergic levels in the hippocampus or entorhinal cortex is sufficient to reverse the impairing effects of septal GABA receptor activation and support the hypothesis that the impairing effects of septal GABAergic activity involve cholinergic processes in the hippocampus and the entorhinal cortex.Extensive evidence has implicated the medial septum in learning and memory. Lesions of the medial septum impair acquisition and retention performance in a variety of behavioral paradigms (Mitchell et al. 1982;Bolhuis et al. 1988;Fibiger et al. 1991;M'Harzi and Jarrard 1992). Furthermore, memory can be enhanced or impaired by intra-septal infusions of drugs that act at a variety of neurotransmitter systems (Brioni et al. 1990;Givens and Olton 1990;Markowska et al. 1990). For example, intra-septal infusions of ␥-aminobutyric acid (GABA)ergic agonists impair memory during numerous tasks, including radial arm maze performance, inhibitory avoidance, water maze performance, spontaneous alternation, rewarded alternation, and visual discrimination (Brioni et

show abstract

Section: Acetylcholine Gaba and Spontaneous Alternationmentioning

confidence: 99%

Increasing Acetylcholine Levels in the Hippocampus or Entorhinal Cortex Reverses the Impairing Effects of Septal GABA Receptor Activation on Spontaneous Alternation

Degroot¹,

Parent²

2000

Learn. Mem.

View full text Add to dashboard Cite

show abstract

“…Although several microdialysis studies have provided evidence that intraseptal infusions of different glutamatergic drugs are capable of increasing hippocampal acetylcholine outflow by as much as 500% (Giovannini et al, 1994;Moor et al, 1996;Giovannini et al, 1998;Moor et al, 1998), relatively little is known about the effect of glutamate on GABA release. It has been reported that perfusing the septum with an N-methyl-D-aspartate (NMDA)-receptor antagonist results in a decreased septal GABA outflow (Giovannini et al, 1994), suggesting a tonic glutamatergic activation of septal GABA neurons.…”

Section: Functional Considerationsmentioning

confidence: 99%

Intrinsic vesicular glutamate transporter 2‐immunoreactive input to septohippocampal parvalbumin‐containing neurons: Novel glutamatergic local circuit cells

2004

View full text Add to dashboard Cite

Glutamatergic influence on the medial septum diagonal band of Broca complex (MSDB) is a crucial and powerful driver of hippocampal theta rhythm and associated memory processes, in the rat. The recent discovery of vesicular glutamate transporters (VGLUT) provided a specific marker for glutamatergic neuronal elements. Therefore, this study aimed to address two specific questions: (1) do glutamatergic axons innervate MSDB gamma-aminobutyric acid (GABA)ergic, parvalbumin (PV)-containing septohippocampal neurons that are known to have a great influence on the electric activity of the hippocampus; and (2) is the origin of these glutamatergic axons extrinsic and/or intrinsic to the septum. The results of the correlated light and electron microscopic double-labeling immunohistochemistry for VGLUT2 and PV, and single immunostaining for VGLUT2 in colchicine-treated animals, showed that (1) VGLUT2-containing boutons establish asymmetric synaptic contacts with PV-positive perikarya and dendrites; (2) a large population of VGLUT2-immunoreactive neurons is located primarily in the posterior division of the septum; and (3) following surgical fimbria/fornix transection and septal undercut, most VGLUT2-containing axons, including those terminating on MSDB PV cells, remains intact. The latter two observations suggest that the major portion of MSDB glutamate axons have an intraseptal origin and raise a novel functional aspect of glutamatergic cells as local circuit neurons. A constant impulse flow in the septohippocampal GABA pathway is essential for the generation of theta rhythm. Thus, the heavy glutamatergic innervation of these septohippocampal GABA cells establishes the morphological basis for the powerful glutamatergic influence upon theta rhythm and hippocampus-associated memory processes.

show abstract

“…The needle was 1 mm from the front and rear, and the ends of these two needles were 3 mm apart. The needles were slowly embedded into the right side of the hippocampus (stereotactic site: AP, Ϫ5.3 mm; R/L, 4.8; H, Ϫ6.8 mm) (Balcioglu and Maher, 1993;Moor et al, 1996;Alabadi et al, 1999;Sierra-Paredes et al, 2000). The microinjection needle was used for kainate and GDNF administration; the microdialysis probe dialyzed the salicylic acid/Ringer's solution on the one part and drew out the dialysate on the other part in order to detect the hydroxyl radicals.…”

Section: Stereotactic Surgerymentioning

confidence: 99%

Ability of GDNF to diminish free radical production leads to protection against kainate‐induced excitotoxicity in hippocampus

Cheng¹,

Fu²,

Guo³

2003

Hippocampus

View full text Add to dashboard Cite

The primary aim of this study is to explore the protective mechanisms of glial-derived neurotrophic factor (GDNF) during excitotoxicity by kainate in the hippocampus. After a 15-min microinjection with kainate, excitotoxicity was induced in the rat hippocampus. The protective effect of GDNF in the hippocampus was evaluated by administering GDNF 14 min after injection of kainate. The resulting hydroxyl free radicals were quantified by microdialysis of the hippocampus. The results show that GDNF can effectively suppress the production of kainate-induced hydroxyl free radical production. In addition, histological observation indicated the ability of GDNF to decrease the damage level of pyramidal neurons in the CA3 and CA4 areas of the hippocampus. Superoxide dismutase (SOD) activity in the hippocampus was elevated significantly at 30 min and 7 days after kainate induction, while glutathione peroxidase (cGPx) activity did not increase significantly until the seventh day. With GDNF treatment, SOD and cGPx activity in the hippocampus was elevated significantly 7 days after kainate induction. We suggest that mechanisms including a decrease in free radical generation and scavenging of free radicals might be involved in GDNF protection against kainate-induced excitotoxicity.

show abstract

Septal and Hippocampal Glutamate Receptors Modulate the Output of Acetylcholine in Hippocampus: A Microdialysis Study

Cited by 37 publications

References 26 publications

Increasing Acetylcholine Levels in the Hippocampus or Entorhinal Cortex Reverses the Impairing Effects of Septal GABA Receptor Activation on Spontaneous Alternation

Increasing Acetylcholine Levels in the Hippocampus or Entorhinal Cortex Reverses the Impairing Effects of Septal GABA Receptor Activation on Spontaneous Alternation

Intrinsic vesicular glutamate transporter 2‐immunoreactive input to septohippocampal parvalbumin‐containing neurons: Novel glutamatergic local circuit cells

Ability of GDNF to diminish free radical production leads to protection against kainate‐induced excitotoxicity in hippocampus

Contact Info

Product

Resources

About