Morphology and physiology of neurons in the rat perirhinal-lateral amygdala area

Faulkner, Billie; Brown, Thomas H.

doi:10.1002/(sici)1096-9861(19990906)411:4<613::aid-cne7>3.0.co;2-u

Cited by 75 publications

(66 citation statements)

References 63 publications

(78 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As previously reported (Faulkner and Brown, 1999;D'Antuono et al, 2001;Martina et al, 2001), these neurons could be characterized as either "intrinsically bursting" or "regular firing" depending on their responses to intracellular depolarizing pulses (Figs. 4Ab,Bb,Cb).…”

Section: Electrophysiological Recordingsmentioning

confidence: 58%

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

et al. 2011

View full text Add to dashboard Cite

The perirhinal cortex (PC), which is heavily connected with several epileptogenic regions of the limbic system such as the entorhinal cortex and amygdala, is involved in the generation and spread of seizures. However, the functional alterations occurring within an epileptic PC network are unknown. Here, we analyzed this issue by using in vitro electrophysiology and immunohistochemistry in brain tissue obtained from pilocarpine-treated epileptic rats and agematched, nonepileptic controls (NECs). Neurons recorded intracellularly from the PC deep layers in the two experimental groups had similar intrinsic and firing properties and generated spontaneous depolarizing and hyperpolarizing postsynaptic potentials with comparable duration and amplitude. However, spontaneous and stimulus-induced epileptiform discharges were seen with field potential recordings in over one-fifth of pilocarpine-treated slices but never in NEC tissue. These network events were reduced in duration by antagonizing NMDA receptors and abolished by NMDA + non-NMDA glutamatergic receptor antagonists. Pharmacologically isolated isolated inhibitory postsynaptic potentials had reversal potentials for the early GABA A receptor-mediated component that were significantly more depolarized in pilocarpine-treated cells. Experiments with a potassium-chloride cotransporter 2 antibody identified, in pilocarpine-treated PC, a significant immunostaining decrease that could not be explained by neuronal loss. However, interneurons expressing parvalbumin and neuropeptide Y were found to be decreased throughout the PC, whereas cholecystokinin-positive cells were diminished in superficial layers. These findings demonstrate synaptic hyper-excitability that is contributed by attenuated inhibition in the PC of pilocarpine-treated epileptic rats and underscore the role of PC networks in temporal lobe epilepsy.

show abstract

Section: Electrophysiological Recordingsmentioning

confidence: 58%

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

et al. 2011

View full text Add to dashboard Cite

show abstract

“…The brain was removed from the skull and stored in 10% formalin for a minimum of 24 hr, followed by storage in a 30% sucrose solution for 3-4 d. The brain was sectioned at 60 m with a freezing-stage microtome and mounted on gelatin-coated slides. Lesions were sectioned in the horizontal plane to be in register with studies of the cellular neuroanatomy and neurophysiology of the PR (Moyer and Brown, 1998;Faulkner and Brown, 1999;Beggs et al, 2000;Furtak et al, 2001;McGann et al, 2001;Moyer et al, 2002). Microscopic examination (Zeiss Axioskop, 2.5ϫ objective; Carl Zeiss Microimaging, Thornwood, NY) of each thionine-stained section identified the extent of each lesion, which was then traced, using a camera lucida, onto appropriately matched plates from the brain atlas of Paxinos and Watson (1998).…”

Section: Methodsmentioning

confidence: 99%

Perirhinal Cortex Supports Delay Fear Conditioning to Rat Ultrasonic Social Signals

Lindquist¹,

Jarrard²,

Brown³

2004

J. Neurosci.

View full text Add to dashboard Cite

Auditory information can reach the lateral nucleus of the amygdala (LA) through a monosynaptic thalamic projection or a polysynaptic cortical route. The polymodal input from the perirhinal cortex (PR) is a major informational gateway to the LA and nearby structures. Pretraining PR lesions impair fear conditioning to a context, but there have been no reports that they cause deficits in delay conditioning to an auditory cue. The direct subcortical projection to the LA seems sufficient to support delay conditioning to a tone conditional stimulus (CS). We examined the effect of PR lesions on delay conditioning to two different tone conditional stimuli (4 and 22 kHz tones; both 10 sec duration) and two different rat ultrasonic vocalization (USV) conditional stimuli (10 sec of "22 kHz USVs"). The two USV conditional stimuli were multi-call segments that were recorded (digitized at 100 kHz) from two different rats. One USV CS was a continuous sequence of eight calls, and the other was a portion of a continuous sequence of six calls. PR lesions significantly impaired conditioning to both USV conditional stimuli and to the training context but had no significant effect on conditioning to either tone CS. The role of PR in fear conditioning appears not to be determined by whether the conditional stimuli serve as contexts or cues, but instead by the nature or complexity of the stimuli or stimulus configurations. These cue-specific effects of PR lesions are suggested to reflect differences in the stimulus features that are encoded in the two CS pathways to the LA.

show abstract

“…Burst-spiking neurons exhibit two or more spikes with a short inter-spike interval in response to current injection [21] .…”

Section: Classifi Cation By Action Potential Firingmentioning

confidence: 99%

Dysfunction of hippocampal interneurons in epilepsy

Liu

et al. 2014

Neurosci. Bull.

View full text Add to dashboard Cite

Gamma-amino-butyric acid (GABA)-containing interneurons are crucial to both development and function of the brain. Down-regulation of GABAergic inhibition may result in the generation of epileptiform activity. Loss, axonal sprouting, and dysfunction of interneurons are regarded as mechanisms involved in epileptogenesis. Recent evidence suggests that network connectivity and the properties of interneurons are responsible for excitatory-inhibitory neuronal circuits. The balance between excitation and inhibition in CA1 neuronal circuitry is considerably altered during epileptic changes. This review discusses interneuron diversity, the causes of interneuron dysfunction in epilepsy, and the possibility of using GABAergic neuronal progenitors for the treatment of epilepsy.

show abstract

Morphology and physiology of neurons in the rat perirhinal-lateral amygdala area

Cited by 75 publications

References 63 publications

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

Perirhinal cortex hyperexcitability in pilocarpine‐treated epileptic rats

Perirhinal Cortex Supports Delay Fear Conditioning to Rat Ultrasonic Social Signals

Dysfunction of hippocampal interneurons in epilepsy

Contact Info

Product

Resources

About