The rhinal cortices (perirhinal areas 35-36 and entorhinal cortex, EC) play a critical role in high-order perceptual/mnemonic functions and constitute the main route for impulse traffic in and out of the hippocampus. However, there is a discrepancy between anatomical and physiological data about this network. Indeed, tracing studies indicate that the perirhinal cortex forms strong reciprocal connections with the neocortex and EC. In contrast, physiological findings indicate that perirhinal transmission of neocortical and entorhinal inputs occur with an extremely low probability. The general objectives of this proposal are: (A) to shed light on the inhibitory mechanisms that limit impulse traffic through the rhinal cortices and (B) to identify the afferents that allow the rhinal cortices to overcome this inhibition, focusing on inputs from the medial prefrontal cortex (mPFC) and amygdala. To these ends, we will: (1) identify the transmitter and synaptic targets of neocortical and entorhinal axons to areas 35, 36 and EC using anterograde (or retrograde) tracer injections in the temporal neocortex or particular rhinal fields coupled to immunocytochemistry at the electron microscopic level. (2) determine the effect of neocortical and entorhinal stimuli on rhinal neurons recorded in vitro with the whole cell patch method and in vivo with sharp micropipettes. (3-4) determine how the mPFC and amygdala affect impulse traffic across the rhinal cortices. This will be studied using a combination of anatomical and physiological experiments. Anatomical experiments will require anterograde tracer injections restricted to particular regions of the mPFC and amygdala, and the same methods as in (1). Physiological experiments will involve inverse dialysis of picrotoxin in mPFC or amygdala and multiple simultaneous extra- and intracellular neuronal recordings of rhinal neurons in vivo. Since the rhinal cortices are primarily damaged during early stages of Alzheimer's disease, this basic research program may improve our understanding of memory disorders.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
1R01MH073610-01
Application #
6896291
Study Section
Neurobiology of Learning and Memory Study Section (LAM)
Program Officer
Vicentic, Aleksandra
Project Start
2005-06-01
Project End
2010-05-31
Budget Start
2005-06-01
Budget End
2006-05-31
Support Year
1
Fiscal Year
2005
Total Cost
$308,250
Indirect Cost
Name
Rutgers University
Department
Type
Organized Research Units
DUNS #
130029205
City
Newark
State
NJ
Country
United States
Zip Code
07102
Headley, Drew B; Kanta, Vasiliki; Paré, Denis (2017) Intra- and interregional cortical interactions related to sharp-wave ripples and dentate spikes. J Neurophysiol 117:556-565
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Headley, Drew B; DeLucca, Michael V; Haufler, Darrell et al. (2015) Incorporating 3D-printing technology in the design of head-caps and electrode drives for recording neurons in multiple brain regions. J Neurophysiol 113:2721-32
Unal, Gunes; Paré, Jean-Francois; Smith, Yoland et al. (2014) Cortical inputs innervate calbindin-immunoreactive interneurons of the rat basolateral amygdaloid complex. J Comp Neurol 522:1915-28
Headley, Drew B; Paré, Denis (2013) In sync: gamma oscillations and emotional memory. Front Behav Neurosci 7:170
Unal, Gunes; Pare, Jean-Francois; Smith, Yoland et al. (2013) Differential connectivity of short- vs. long-range extrinsic and intrinsic cortical inputs to perirhinal neurons. J Comp Neurol 521:2538-50
Paz, Rony; Pare, Denis (2013) Physiological basis for emotional modulation of memory circuits by the amygdala. Curr Opin Neurobiol 23:381-6
Unal, Gunes; Apergis-Schoute, John; Pare, Denis (2012) Associative properties of the perirhinal network. Cereb Cortex 22:1318-32
Popescu, Andrei T; Pare, Denis (2011) Synaptic interactions underlying synchronized inhibition in the basal amygdala: evidence for existence of two types of projection cells. J Neurophysiol 105:687-96
Popa, Daniela; Duvarci, Sevil; Popescu, Andrei T et al. (2010) Coherent amygdalocortical theta promotes fear memory consolidation during paradoxical sleep. Proc Natl Acad Sci U S A 107:6516-9

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